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STEP1 > Neuro Part 2 > Flashcards

Neuro Part 2 Flashcards

1
Q

Describe the structures on the dorsal brainstem in order from rostral to caudal.

A
  • pineal body
  • superior colliculi
  • inferior colliculi
  • superior cerebellar peduncles
  • middle cerebellar peduncles
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2
Q

What is the role of the pineal gland?

A

it is involved in melatonin secretion according to circadian rhythms

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3
Q

What is the function of the superior colliculi?

A

it is the conjugate vertical gaze center

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4
Q

What is the function of the inferior colliculi?

A

it is a relay station for auditory information

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5
Q

What is Parinaud syndrome?

A

paralysis of the conjugate vertical tase due to lesions of the superior colliculi (e.g. stroke, hydrocephalus, pinealoma)

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6
Q

Which cranial nerves are organized more medially and which are located more laterally?

A
  • medial: motor nuclei

- lateral: sensory nuclei

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7
Q

Which cranial nerve nuclei are in the midbrain?

A

CN III and IV

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8
Q

Which cranial nerve nuclei are in the pons?

A

CN V, VI, VII, and VIII

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9
Q

Which cranial nerve nuclei are in the medulla?

A

CN IX, X, XII

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10
Q

Which cranial nerve nuclei are in the spinal cord?

A

CN XI

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11
Q

What is the cribriform plate?

A

the medial portion of the anterior cranial fossa though which olfactory nerves extend

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12
Q

What is the optic canal?

A

a foramen in the middle cranial fossa (sphenoid bone) through which CN II and the ophthalmic artery pass

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13
Q

What is the superior orbital fissure?

A

a foramen in the middle cranial fossa through which CN III, IV, V1, and VI pass

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14
Q

What is the foramen rotundum?

A

a foramen in the middle cranial fossa through which CN V2 passes

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15
Q

What is the foramen ovale?

A

a foramen in the middle cranial fossa through which CN V3 passes

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16
Q

What is the foramen spinous?

A

a foramen just behind the sphenoid in the middle cranial fossa through which the middle meningeal artery passes

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17
Q

What is the internal auditory meatus?

A

a foramen in the posterior cranial fossa through which CN VII and VIII pass

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18
Q

What is the jugular foramen?

A

a foramen lateral to the foramen magnum and hypoglossal canal in the posterior cranial fossa through which CN IX, X, and XI pass

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19
Q

What is the hypoglossal canal?

A

a foramen in the posterior cranial fossa, just lateral to the foramen magnum, through which CN XII passes

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20
Q

What is the foramen magnum?

A

a foramen in the posterior cranial fossa through which the brainstem extends

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21
Q

What is the function of CN III?

A
  • most eye movements and eyelid opening by action of the elevator palpebrae via the oculomotor nucleus
  • parasympathetic innervation of the eye (accommodation and pupillary constriction) via the Edinger-Westphal nucleus
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22
Q

What is the function of CN IV?

A

control of the superior oblique muscle of the eye

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23
Q

What is the function of CN V?

A

control muscles of mastication, somatosensation from the anterior ⅔ of the tongue, and facial sensation

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24
Q

What is the function of CN VI?

A

control of the lateral rectus muscle of the eye

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25
Q

What is the function of CN VII?

A

facial movement, taste from the anterior ⅔ of the tongue, lacrimation, salivation (submandibular and sublingual glands), eyelid closing (orbicularis oculi), auditory volume modulation (stapedius)

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26
Q

What is the function of CN VIII?

A

hearing and balance

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27
Q

What is the function of CN IX?

A
  • taste and sensation from the posterior ⅓ tongue
  • swallowing and salivation of the parotid gland
  • monitoring the carotid body and sinus chemo-/baroreceptors
  • elevation of the pharynx and larynx via the stylopharyngeus
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28
Q

What is the function of CN X?

A
  • taste from the supraglottic region
  • swallowing
  • soft palate elevation
  • midline uvula
  • talking
  • coughing
  • parasympathetics to the thoracoabdominal viscera
  • monitoring aortic arch chemo- and baroreceptors
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29
Q

What is the function of CN XI?

A

head turning and shoulder shrugging via motor innervation of the SCM and trapezius

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30
Q

What is the function of CN XII?

A

tongue movement

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31
Q

What are the three vagal nuclei?

A
  • nucleus solitarius
  • nucleus ambiguus
  • dorsal motor nucleus
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32
Q

What is the function of the nucleus solitarius and what cranial nerves contribute?

A
  • it is a purely sensory vagal nucleus in the medulla
  • processes primarily taste and some other visceral sensory information (e.g. taste, baroreceptors, gut distention)
  • CN VII, IX, and X contribute
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33
Q

What is the function of the nucleus ambiguus and what cranial nerves does it contribute to?

A
  • a motor nucleus that innervates the soft palate, larynx, pharynx, and upper esophagus
  • located in the medulla
  • functions in swallowing and speech
  • contributes to CN IX, X, and XI
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34
Q

What is the function of the dorsal motor nucleus and what cranial nerves contribute?

A
  • a cranial nerve in the medulla
  • sends parasympathetic fibers to the heart, lungs, and upper GI tract
  • contributes to the CN X
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35
Q

Describe the corneal reflex.

A
  • initiated by touching the cornea with a cotton swab
  • afferent: V1
  • efferent: VII to the orbiculares oculi to initiate a blink
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36
Q

Describe the lacrimation reflex.

A
  • initiated by irritation of the eye
  • afferent: V1
  • efferent: VII elicits lacrimation
  • even if dysfunction, you may see emotional tears
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37
Q

Describe the jaw jerk reflex.

A
  • a stretch reflex in which the mandible is tapped downward just below the lips while the mouth is slightly open
  • normally the master muscles pull the mandible upward only slightly or not at all
  • damage to upper motor neurons, however, cause this reflex to be very pronounced
  • afferent: V3 (muscle spindle)
  • efferent: V3 (motor)
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38
Q

Describe the pupillary reflex.

A
  • afferent: CN II
  • efferent: CN III
  • shining a light in the eye should elicit constriction of the pupil
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39
Q

Describe the gag reflex.

A
  • afferent: CN IX
  • efferent: CN X
  • normal response is reflex contraction of the back of the throat in response to touching the roof of the mouth in the back of the throat
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40
Q

What does a direct pupillary response without consensual response indicate?

A

that it isn’t a sensory problem in the direct eye, but rather a deficit in the connection between the left and right pathway

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41
Q

What would signify a CN V motor lesion.

A

deviation of the jaw to the side of the lesion

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42
Q

What would signify a CN X lesion?

A

the uvula deviates away from the side of the lesion

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43
Q

What would signify a CN XI lesion?

A

weakness when turning the head to the contralateral side with shoulder droop on the ipsilateral side

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44
Q

What would signify a CN XII lesion?

A

the tongue would deviate toward the side of the lesion

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45
Q

What are the muscles of mastication? Do they open or close the jaw?

A
  • masseter and temporalis close the jaw

- medial pterygoid opens the jaw

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46
Q

The muscles of mastication are innervated by what nerve?

A

CN V3

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47
Q

Describe the corticobulbar tract.

A
  • upper motor neurons form the corticobulbar tract and decussate in the genu of the internal capsule
  • they project to LMNs located in the contralateral facial nucleus
  • LMNs are divided into an upper division and lower division
  • LMNs in the upper division receive ipsilateral input as well as contralateral
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48
Q

Damage to the facial nucleus or CN VII leads to what deficits?

A
  • ipsilateral paralysis of the upper and lower muscles of facial expression (UMNs have already decussated)
  • ipsilateral hyperacusis (loss of stapedius muscle function)
  • ipsilateral loss of taste on the anterior ⅔ of the tongue
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49
Q

What is the stapedius muscle?

A
  • a muscle, innervated by CN VII, in the middle ear which serves to dampen oscillation and control volume
  • damage to the facial nucleus or CN VII, then, results in hyperacusis
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50
Q

Bell’s Palsy

A
  • an idiopathic clinical syndrome caused by a peripheral CN VII lesion
  • similar syndromes can be caused by Lyme disease, herpes simplex, and herpes zoster
  • treat with corticosteroids and acyclovir; most patients have gradual recovery
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51
Q

What virus is known for causing Bell’s palsy?

A

herpes simplex

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52
Q

What are the cavernous sinuses?

A

a collection of venous sinuses on either side of the pituitary, which drains into the internal jugular vein

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53
Q

Cavernous Sinus Syndrome

A
  • caused by a pituitary tumor mass effect, carotid-cavernous fistula, or cavernous sinus thrombosis related to infection
  • compresses some combination of CNs III, IV, V1, V2, VI, and post-ganglionic sympathetic pupillary fibers en route to the orbit
  • presents with variable ophthalmoplegia, reduced corneal sensation, Horner syndrome, and occasional decreased maxillary sensation
  • CN VI is most susceptible to injury
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54
Q

Sympathetic stimulation to the eye runs through which cranial nerve?

A

V1

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55
Q

What is the order of the ossicles in the middle ear?

A
  • malleus
  • incus
  • stapes
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56
Q

What is the purpose of the middle ear ossicles?

A

conduct and amplify sound

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57
Q

What is the function of inner and outer hair cells?

A
  • inner cells transduce sound as their hair cells are displaced by movement against the tectorial membrane
  • outer cells modify basilar membrane movement to fine tune hearing
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58
Q

What is the function of the basilar membrane?

A

it vibrates secondary to sound waves and moves inner hair cell cilia against the tectorial membrane

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59
Q

Describe the tonotopy of the basilar membrane.

A
  • low frequency sounds vibrate the basilar membrane best at the apex where it is wide and flexible
  • high frequency sounds vibrate the basilar membrane best at the base, near the stapes, where it is thin and rigid
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60
Q

Describe the Rinne test.

A
  • air conduction should be better than bone conduction
  • so the test begins with the tuning fork against the mastoid bone and then is moved to beside the ear when the patient can no longer hear it pressed against the mastoid
  • if the patient can’t hear the tuning fork after it is moved, this indicates their bone conduction is better than air conduction; this indicates conductive hearing loss
  • if the patient can hear the tuning fork after it is moved, this indicates air conduction is still better; this indicates sensorineural hearing loss
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61
Q

Describe the Weber test.

A
  • a tuning fork is placed in the center of the head and the patient is asked which side the sound is better on
  • if it localizes to the affected ear, this indicates a conductive hearing loss
  • if it localizes to the unaffected ear, this indicates a sensorineural hearing loss
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62
Q

Describe the innervation of inner and outer hair cells in the ear.

A
  • inner cells contact several afferents

- outer cells are innervated by efferents which change their shape to modify tuning

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63
Q

Unilateral sensorineural hearing loss can be localized where? Why is this?

A
  • it is due to a lesion in the cochlear nucleus or more distally
  • above this level, there is bilateral input and hearing loss would be bilateral
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64
Q

What frequency of hearing is lost first in response to noise damage?

A

high frequency

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65
Q

What is a cholesteatoma and what are the major complications?

A

an overgrowth of desquamated keratin debris within the middle ear space, which may erode ossicles or mastoid air cells and contribute to conductive hearing loss

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66
Q

The ciliary body is connected to the lens by what?

A

zonular fibers

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67
Q

What is the posterior chamber of the eye?

A

the area between the iris and lens

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68
Q

Describe the sympathetic innervation of the eye.

A
  • a1 receptors are expressed by the dilator pupillae muscle
  • B1 receptors are expressed by the non pigmented epithelium of the ciliary body and induce aqueous humor production
  • sympathetics stimulate dilation of the pupil, flattening of the lens for far sight, and production of aqueous humor
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69
Q

Describe the parasympathetic innervation of the eye.

A
  • M3 receptors are expressed by the sphincter pupillae muscle
  • M3 receptors are also expressed by the ciliary body and induce constriction
  • parasympathetics, then, stimulate constriction of the pupil, rounding of the lens for near sight, and drainage fo aqueous humor through the canal of Schlemm
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70
Q

What is hyperopia?

A
  • essentially the eye is too short for the refractive power of the cornea and lens, so light is focused behind the retina
  • aka far sightedness
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71
Q

What is myopia?

A
  • essentially the eye is too long for the refractive power of the cornea and lens, so light is focused in front of the retina
  • aka near sightedness
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72
Q

What is astigmatism?

A

an abnormal curvature of the cornea which leads to different refractive powers at different axes

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73
Q

What is presbyopia?

A

an age-related impaired accommodation primarily due to diminished lens elasticity, which often necessitates reading glasses

74
Q

Cataracts

A
  • a painless, often bilateral opacification of the lens, which impairs normal vision
  • acquired risk factors include age, alcohol, smoking, sunlight, prolonged corticosteroid use, diabetes, trauma, and infection
  • congenital risk factors include classic galactosemia, galactokinase deficiency, trisomies, TORCHES infection, Marfan syndrome, Alport syndrome, myotonic dystrophy, and neurofibromatosis 2
75
Q

What is glaucoma?

A

optic disc atrophy with characteristic cupping of the optic nerve head, usually due to elevated intraocular pressure and with progressive peripheral visual field loss

76
Q

Open-Angle Glaucoma

A
  • optic disc atrophy that arises due to elevated intraocular pressure secondary to impaired drainage of humor
  • is painless with peripheral visual field defects, and you can visualize cupping of the optic nerve head upon fundoscopic examination
  • most often due to blocked trabecular meshwork by WBCs in the case of uveitis, RBCs in the case of vitreous hemorrhage, or retinal elements in the case of a detachment
  • associated with increased age, AA race, and family history
77
Q

Closed-Angle Glaucoma

A
  • can be primary in which enlargement or anterior displacement of the lens prevents flow from the posterior to the anterior chamber, building pressure that pushes the iris forward against the cornea and impedes flow through the trabecular meshwork
  • or it can be secondary due retinal hypoxia, which induces vasoproliferation in the iris that contracts the angle
  • chronic is often painless
  • acute is a true emergency and presents as a very painful, red eye with sudden vision loss, halos around light, a frontal headache, and a fixed and mid-dilated pupil
  • in the case of acute closed-angle glaucoma mydriatic agents are contraindicated
78
Q

Conjunctivitis

A
  • inflammation of the conjunctiva
  • presents as a red, very vascular eye
  • most commonly viral, specifically due to adenovirus, with sparse mucous discharge and a swollen preauricular node; usually self-resolves
  • can also be allergic, which is usually characterized by pruritus and a bilateral nature
  • or bacterial, which is usually accompanied by pus and should be treated with anti-biotics
79
Q

Uveitis

A
  • inflammation fo the pigmented layer beneath the sclera and cornea
  • may present with hypopyon (accumulation of pus in the anterior chamber) or conjunctival redness
  • associated with systemic inflammatory disorders
80
Q

Age-Related Macular Degeneration

A
  • degeneration of the macula, causing distortion and eventual loss of central vision
  • most cases are “dry”, meaning non-exudative, with deposition of yellowish extracellular material in and between the Bruch membrane and retinal pigment epithelium with gradual vision loss
  • some cases are “wet”, meaning exudative, with rapid loss of vision secondary to bleeding caused by choroidal neovascularization
  • treat the dry form with multivitamin and antioxidants; treat the wet form with anti-VEGF like ranibizumab
81
Q

What is scotomas?

A

loss of central vision

82
Q

What is ranibizumab?

A

an anti-VEGF injection used to treat wet macular degeneration

83
Q

What is the difference between dry and wet macular degeneration?

A
  • dry is non-exudative and characterized by yellowish deposits between the Bruch membrane and retinal pigment with gradual vision loss, best treated by antioxidants and multivitamins
  • wet is exudative and characterized by choroidal neovascularization, which causes bleeding and rapid vision loss, best treated with anti-VEGF (ranibizumab)
84
Q

Diabetic Retinopathy

A
  • retinal damage due to chronic hyperglycemia
  • can be of the non-proliferative or proliferative form
  • non-proliferative is characterized by leaking capillaries and macular edema
  • non-proliferative is best treated with blood sugar control
  • proliferative is characterized by neovascularization in the setting of chronic hypoxia with resultant traction on the retina
  • proliferative is best treated with peripheral retinal photocoagulation, surgery, and anti-VEGF (ranibizumab)
85
Q

Retinal Vein Occlusion

A
  • blockage of the central or a branch of the retinal vein due to compression from nearby arterial atherosclerosis
  • causes retinal hemorrhage, venous engorgement, and edema
86
Q

Retinal Detachment

A
  • a separation of the neurosensory layer of the retina from the pigmented epithelium, leading to degeneration of photoreceptors and subsequent vision loss
  • can see “crinkling of retinal tissue” on fudoscopy with changes in vessel direction
  • often preceded by posterior vitreous detachment (seen as “flashes” and “floaters”) and eventual monocular loss of vision like a curtain being drawn
  • may be secondary to retinal breaks, diabetic traction, or inflammatory effusions
  • breaks are more common in patients with high myopia or a history of head trauma
  • surgical emergency
87
Q

Central Retinal Artery Occlusion

A
  • presents as an acute, painless monocular vision loss
  • the retina becomes cloudy with attenuated vessels and a “cherry-red” fovea
  • treatment requires evaluation for the embolic source
88
Q

Retinitis Pigmentosa

A
  • an inherited retinal degeneratoin

- presents with painless, progressive vision loss beginning with night blindness since rods are affected first

89
Q

Retinitis

A
  • retinal edema and necrosis leading to a scar
  • most often viral but can be bacterial or parasitic in nature
  • associated with immunosuppression
90
Q

Papilledema

A
  • optic disc swelling, usually bilateral, due to increased ICP
  • presents with an enlarged, elevated optic disc with blurred margins
91
Q

Describe the neural pathway responsible for constriction of the pupil in response to light.

A
  • light enters either retina and sends a signal via CN II to the pretectal nucleus in the midbrain
  • projections from this pretectal nucleus then stimulate the Edinger-Westphal nuclei bilaterally
  • neurons in the Edinger-Westphal nuclei project to the ciliary ganglion via CN III where they synapse on short ciliary nerves
  • these second order neurons in the ciliary ganglion project to the pupillary sphincter muscles where they activate M3 receptors on the sphincter pupillae muscle
92
Q

Describe the neural pathway responsible for dilation of the pupil.

A
  • a first order neuron is located in the hypothalamus and projects to the ciliospinal center of Budge in the lateral horn of C8-T2
  • these second order neurons exit at T1 and project to the superior cervical ganglion
  • third order neurons located in the superior cervical ganglion form a plexus along the internal carotid, which travels through the cavernous sinus and enters the orbit as the long ciliary nerve
  • these nerves release NE, which stimulates a1 receptors on the dilator pupillae muscle and induce mydriasis
93
Q

What is Marcus Gunn pupil?

A
  • an afferent pupillary defect that arises due to optic nerve damage or severe retinal injury
  • results in a poor bilateral pupillary constriction when light is shone in the affected eye
  • there is a proper direct and consensual response when a light is shone in the unaffected eye
94
Q

What is Horner syndrome?

A
  • a sympathetic denervation of the face presenting as ptosis, anhidrosis, and miosis
  • most commonly associated with a lesion of the spinal cord above T1
95
Q

CN IV innervates which ocular muscle?

A

superior oblique

96
Q

CN VI innervates which ocular muscle?

A

the lateral rectus

97
Q

What is the function of the superior oblique ocular muscle?

A

abduct, introit, and depress the eye

98
Q

How is functioning of the oblique ocular muscles tested?

A

by having the patient look down (SO) and up (IO) while their eye is adducted

99
Q

Why is the motor component of CN III more likely to be damaged by vascular disease?

A
  • because CN III is organized with the motor components within and surrounded by the parasympathetic components with the vessels exterior to that
  • as a result they are most sensitive to changes in oxygen because they are the interior fibers
100
Q

What sort of disease is most likely to affect the motor component of CN III? The parasympathetic component?

A
  • motor: vascular disease

- parasympathetic: compression

101
Q

What are the signs of damage to the motor component of CN III?

A

ptosis and a “down and out” gaze

102
Q

What are the signs of damage to the parasympathetic component of CN III?

A

diminished or absent pupillary light reflex

103
Q

What are signs of CN IV damage?

A

eye moves upward, particularly with contralateral gaze and the head tilts toward the side of the lesion

104
Q

What are signs of CN VI damage?

A

the eye is pointed medially and cannot be abducted

105
Q

What is Meyer’s loop?

A
  • temporal lobe projections between the LGN and inferior portion of the visual cortex, which carries input from the inferior retina and superior visual field
  • loops around the inferior horn of the lateral ventricle
106
Q

What is the dorsal optic radiation?

A
  • parietal lobe projections between the LGN and superior portion of the visual cortex, which carries input from the superior retina and inferior visual field
  • travels within the internal capsule
107
Q

Where would a lesion be that causes a visual field defect on the left side in each eye?

A

the right optic tract between the chiasm and LGN

108
Q

Where would a lesion be that causes a bilateral temporal hemianopsia?

A

at the optic chiasm

109
Q

Where would a lesion be that caused a central visual field defect in the right eye?

A

the macula of the right eye

110
Q

Where would a lesion be that caused a defect in the left, inferior portion of each visual field?

A

in the dorsal optic radiation on the right side

111
Q

What is the medial longitudinal fasciculus?

A
  • a pair of tracts that allow for crosstalk between CN VI and CN III nuclei in order to coordinate the movement of both eyes
  • consist of projections from CN IV nuclei to CN III medial rectus subnuclei
  • highly myelinated for movement at the same time
112
Q

What disease classically presents with a bilateral lesion to the medial longitudinal fasciculus?

A

multiple sclerosis

113
Q

Internuclear Ophthalmoplegia

A
  • a conjugate horizontal gaze palsy
  • uncoordinated movement of the two eyes arises from damage to one or both medial longitudinal fasciculi between CN VI and CN III nuclei
  • when C VI activates the ipsilateral lateral recuts, CN III does not stimulate the contralateral medial rectus to fire
  • presents with nystagmus of the abducting eye since CN VI overtires in an attempt to stimulate the contralateral medial rectus via the MLF
  • named with the directional term indicating the paralyzed eye
114
Q

How is epinephrine used in the treatment of glaucoma?

A
  • it is used for it’s a1 agonist activity, which causes vasoconstriction and restricts aqueous humor production
  • not used in closed-angle glaucoma because it also induces mydriasis, which pushes the iris into the angle and limits drainage of humor
115
Q

What role do beta-blockers play in the treatment of glaucoma?

A

they reduce aqueous humor synthesis

116
Q

Which diuretic is used for the treatment of glaucoma? How does it work?

A
  • acetazolamide

- it inhibits carbonic anhydrase, the activity of which is required for aqueous humor production

117
Q

What kind of cholinergic drugs are used in the treatment of glaucoma?

A

direct and indirect M3 agonists

118
Q

Which cholinergic is reserved for emergent cases of glaucoma and opens up the canal of Schlemm exceedingly well?

A

pilocarpine

119
Q

Which prostaglandins are used in the treatment of glaucoma? What is their mechanism of action and adverse effects?

A
  • bimatoprost and iatanoprost (PGF2a)
  • increase the outflow of aqueous humor
  • but may darken the color of the iris (aka browning) or cause eyelashes to grow
120
Q

What is dextromethorphan and how is it used clinically?

A

it is an opioid analgesic used for cough suppression

121
Q

Which opioids are used for as anti-diarrheal agents?

A
  • loperamide

- diphenoxylate

122
Q

Tolerance doesn’t develop to which effects of opioids?

A

miosis and constipation

123
Q

What is pentazocine, how is it used, and what are it’s adverse effects?

A
  • it is a kappa-opioid receptor agonist and mu-opioid receptor antagonist
  • used for analgesia of moderate-to-severe pain
  • may cause withdrawal if patient is also taking a full opioid antagonist via competitive inhibition
124
Q

What is butorphanol, how is it used, and what are it’s adverse effects?

A
  • a kappa-opioid and mu-opioid receptor partial agonist
  • produces analgesia for severe pain in the setting of migraines and labor with less respiratory depression than full opioid agonists
  • can cause withdrawal if patient is also taking a full opioid agonist via competitive inhibition and overdose is not easily reversed with naloxone
125
Q

What is tramadol, how is it used, and what are it’s adverse effects?

A
  • a very weak opioid agonist that also inhibits serotonin and NE reuptake
  • used for the treatment of chronic paian
  • adverse effects mimic other opioids, there is a risk for serotonin syndrome, and the drug decreases the seizure threshold
126
Q

Give the clinical use, mechanism, and adverse effects of ethosuximide.

A
  • indicated for absence seizures
  • works by blocking thalamic T-type calcium channels
  • side effects are recalled by EFGHIJ: Ethosuximide causes Fatigue, Gi distress, Headache, Itching, and stevens-johnson syndrome
127
Q

Give the clinical use, mechanism, and adverse effects of benzodiazepines in the setting of epilepsy.

A
  • indicated as first line therapy for status epilepticus
  • increases frequency of GABA(A) channel opening
  • may cause sedation, tolerance, dependence, and respiratory depression
  • includes diazepam, midazolam, and lorazepam
128
Q

What is the preferred treatment for status epilepticus?

A

benzodiazepines

129
Q

What is the preferred treatment for eclampsia seizures?

A

MgSO4, followed by benzodiazepines

130
Q

Give the clinical use, mechanism, and adverse effects of phenobarbital in the setting of epilepsy.

A
  • indicated for partial and tonic-clonic seizures
  • increases duration of GABA(A) channel opening
  • may cause sedation, tolerance, dependence, induction of CYPs, and cardiorespiratory depression
  • considered first line for neonates
131
Q

What is the first line therapy for epilepsy in neonates?

A

phenobarbital

132
Q

Give the clinical use, mechanism, and adverse effects of phenytoin and fosphenytoin.

A
  • indicated as first line therapy for tonic-clonic seizures and status epilepticus prophylaxis in addition to suitable treatment for partial seizures
  • functions by blocking sodium channels
  • may cause diplopia, ataxia, n/v, rashes, hyperplasia of the gums, megaloblastic anemia, hirsutism, or have teratogenic effects
  • has zero-order kinetics and induces CYP
133
Q

Give the clinical use, mechanism, and adverse effects of carbamazepine.

A
  • indicated as first line therapy for partial seizures and also as suitable therapy for tonic-clonic seizures
  • functions by blocking sodium channels
  • may cause diplopia, ataxia, blood dycrasias, liver toxicity, teratogenesis, SIDA, or Stevens-Johnson
  • induces CYP
  • indicated for first line treatment of trigeminal neuralgia
134
Q

What is first line therapy for trigeminal neuralgia?

A

carbamazepine

135
Q

Give the clinical use, mechanism, and adverse effects of Valproic Acid.

A
  • indicated as first line therapy for tonic-clonic seizures and as suitable therapy for all others
  • causes sodium channel inactivation and inhibits GABA transaminase to increase GABA activity
  • may cause GI distress, pancreatitis, neural tube defects, tremor, weight gain, or a rare but fatal hepatotoxicity
  • contraindicated in pregnancy
136
Q

Give the clinical use and mechanism of Vigabatrin.

A
  • indicated for partial seizures

- works by irreversibly inhibiting GABA transaminase to increase GABA activity

137
Q

Give the clinical use, mechanism, and adverse effects of gabapentin in the setting of epilepsy.

A
  • indicated for partial seizures
  • designed as a GABA analog but mostly inhibits voltage-gated calcium channels
  • may cause sedation or ataxia
138
Q

Give the clinical use, mechanism, and adverse effects of topiramate.

A
  • indicated for partial and tonic-clonic seizures as well as migraine prevention
  • blocks sodium channels and increases GABA activity
  • may cause sedation, mental dulling, kidney stones, or weight loss
139
Q

Give the clinical use, mechanism, and adverse effects of lamotrigine.

A
  • indicated for all forms of seizures
  • functions by blocking voltage-gated sodium channels
  • may cause Stevens-Johnson syndrome and therefore has to be titrated slowly
140
Q

Give the clinical use, mechanism, and adverse effects of levetiracetam.

A
  • indicated for partial and tonic-clonic seizures

- unknown mechanism

141
Q

Give the clinical use, mechanism, and adverse effects of tiagabine.

A
  • indicated for partial seizures

- increases GABA activity by inhibiting re-uptake

142
Q

Thiopental

A
  • a barbiturate with rapid onset and cessation of acting used in the induction of anesthesia and short surgical procedures
  • high potency and high lipid solubility
  • effect is terminated quickly by rapid redistribution into fat
143
Q

Give the clinical use, mechanism, and adverse effects of tiagabine.

A
  • includes the -“barbital” drugs and thiopental
  • they increase the duration of GABA(A) channel opening
  • indicated for anxiety, seizures, insomnia, and induction of anesthesia
  • may cause fatal respiratory, cardiovascular, and CNS depression without an antidote; induce CYPs; dependence
  • contraindicated in those with porphyria
144
Q

Which benzos have a short half-life and are more prone to addiction?

A
  • alprazolam
  • triazolam
  • oxazepam
  • midazolam
145
Q

How do benzos work?

A

they increase the frequency with which GABA(A) channels open

146
Q

What are the indications for benzos?

A

anxiety, spasticity, status epilepticus, eclampsia, alcohol withdrawal and DTs, night terrors, sleepwalking, general anesthetic (amnesia and muscle relaxation for conscious sedation), insomnia

147
Q

What is flumazenil?

A

the antidote for benzodiazepine overdose

148
Q

What is the danger associated with flumazenil?

A

may cause acute benzodiazepine withdrawal and precipitate a seizure

149
Q

Zolpidem, Zaleplon, Eszopiclone

A
  • nonbenzodiazepine hypnotics
  • act via the BZ1 subtype of GABA receptor
  • indicated for inducing sleep and don’t affect the sleep cycle as much as benzos
  • may cause ataxia, headaches, confusion
  • can be reversed with flumazenil
150
Q

How do the non-benzo hypnotics compare to benzodiazepines?

A
  • non-benzos have a short duration of action so they don’t affect the sleep cycle as much
  • non-benzos have fewer day-after effects when used as hypnotics
  • non-benzos have a lower risk for dependence
151
Q

How does solubility related to the kinetics of inhaled anesthetics?

A

lower blood solubility means they distribute to the brain faster but have lower potency (higher MAC)

152
Q

Wha tis the minimal alveolar concentration of an inhaled anesthetic?

A

the concentration required to induce unconsciousness or anesthesia in 50% of patients

153
Q

Halothane

A

an old inhaled anesthetic with high lipid and blood solubility (therefore has high potency and slow induction)

154
Q

What are the adverse effects associated with inhaled anesthetics?

A
  • halothane is known for hepatotoxicity
  • methoxyflurane for nephrotoxicity
  • enflurane for seizures
155
Q

Malignant Hyperthermia

A
  • a rare, life-threatening complication of inhaled anesthetics or succinylcholine
  • characterized by fever and severe muscle contractions
  • susceptibility is inherited in an autosomal dominant fashion with variable penetrance
  • genetics relate to mutations in voltage-sensitive ryanodine receptors, which cause an increase in calcium release form the sarcoplasmic reticulum in response to these agents
  • treat with dantrolene, a ryanodine receptor antagonist
156
Q

Midazolam

A
  • a benzodiazepine used as anesthesia for endoscopy or as an adjunct to gaseous anesthetics and narcotics
  • may cause severe post-op respiratory depression, hypotension, and anterograde amnesia
157
Q

Ketamine

A
  • a PCP analog aka arylcyclohexylamine, used as an IV anesthetic
  • functions by blocking NMDA receptors
  • causes cardiovascular stimulation and increases cerebral blood flow
  • but has dissociative properties and may cause disorientation, hallucinations, or bad dreams, collectively known as a “re-emergence effect”
158
Q

Propofol

A
  • the preferred agent for induction of anesthesia as well as maintenance in the ICU and during short surgical procedures
  • functions by potentiating GABA(A) activity
  • produces less post-op nausea than thiopental
159
Q

What are the mechanisms and uses of dantrolene?

A
  • a drug that prevents release of calcium from the sarcoplasmic reticulum
  • used in the treatment of malignant hyperthermia induced by inhaled anesthetics and in neuroleptic malignant syndrome, a toxicity of antipsychotics
160
Q

What is the mechanism and clinical use of baclofen?

A
  • it activates GABA(B) receptors at the level of the spinal cord and includes skeletal muscle relaxation
  • it is used to treat muscle spasm, especially those sen in acute low back pain
161
Q

What is the mechanism, clinical use, and side effect profile of cyclobenzaprine?

A
  • it is a centrally acting skeletal muscle relaxant
  • it is indicated for muscle spasms
  • it’s structure is related to TCAs, so it has similar anticholinergic side effects
162
Q

What is the mechanism, clinical use, and side effect profile of succinylcholine?

A
  • it is a strong ACh receptor agonist selective for nicotinic receptors at the NMJ, which produces a sustained depolarization and prevents muscle contraction
  • indicated for muscle paralysis in surgery and mechanical ventilation
  • cannot be reversed in the initial stage and is potentiated by cholinesterase inhibitors during this time
  • in phase II, the receptors are available but desensitized and this can be reversed with cholinesterase inhibitors
163
Q

Non-depolarizing Neuromuscular Blockades

A
  • includes drugs with the suffix “-curarine,” “-curonium,” or “curium”
  • serve as competitive antagonists at nicotinic receptors at the neuromuscular junction
  • indicated for muscle paralysis in surgery and mechanical ventilation
  • can be reversed with cholinesterase inhibitors in all stages but should be given alongside atropine to prevent the muscarinic effects of cholinesterase inhibitors
164
Q

Local Anesthetics

A
  • include esters such as procaine, cocaine, tetracaine, and benzocaine as well as amides like lidocaine, mepivacaine, bupivacaine (all with 2 I’s in the name)
  • function by blocking sodium channels from the inside; therefore, esters are most effective in rapidly firing neurons because they are taken up first in those (tertiary amides penetrate the membrane readily)
  • need more anesthetic in infected tissues because the environment is acidic and these alkaline anesthetics become charged, unable to penetrate the membrnae
  • they block small-diameter fibers first; and myelinated fibers before unmyelinated (but size is the predominant determinant so small unmyelinated before large myelinated); and this means that pain is lost before temp, touch, and pressure last
  • often given with vasoconstrictors (e.g. epinephrine) to reduce local bleeding and diffusion of the anesthetic
165
Q

What is the mechanism, clinical use, and side effect profile of levodopa?

A
  • it crosses the BBB where it is converted to dopamine
  • indicated for treatment of Parkinson’s disease
  • often given with a peripheral DOPA decarboxylase inhibitor to increase availability in the brain and limit peripheral side effects
  • may cause arrhythmias from peripheral formation of catecholamines, long-term use may lead to dyskinesia known as the “on off” phenomenon, and there may be akinesia between doses
166
Q

What is the mechanism, clinical use, and side effect profile of selegiline?

A
  • a selective MAO-B inhibitor, which increase the availability of dopamine
  • used as an adjunct to levodopa in the treatment of Parkinson’s disease
  • but may enhance the adverse effects of levodopa
167
Q

What is the mechanism, clinical use, and side effect profile of rasagiline?

A
  • a selective MAO-B inhibitor, which increase the availability of dopamine
  • used as an adjunct to levodopa in the treatment of Parkinson’s disease
  • but may enhance the adverse effects of levodopa
168
Q

What is the mechanism, clinical use, and side effect profile of memantine?

A
  • an NMDA receptor antagonist
  • helps prevent excitotoxicity in the treatment of Alzheimer’s disease
  • may cause dizziness, confusion, and hallucinations
169
Q

Name two classes of drugs used in the treatment of Alzheimer’s disease.

A
  • memantine, an NMDA antagonist used to prevent excitotoxicity
  • acetylcholinesterase inhibitors
170
Q

What is the preferred treatment for Huntington’s disease?

A
  • tetrabenazine and reserpine, which inhibit VMAT to reduce DA packaging for release
  • haloperidol, a D2 receptor antagonist
171
Q

What is the mechanism of action of haloperidol?

A

it is an antipsychotic that blocks D2 receptors

172
Q

What is riluzole?

A

the preferred treatment for ALS that modestly increases survival by reducing glutamate excitotoxicity

173
Q

What is the mechanism, clinical use, and side effect profile of triptans?

A
  • they are serotonin 1B/1D receptor agonists, which inhibit trigeminal nerve activation, prevent vasoactive peptide release, and induce vasoconstriction
  • they are indicated for the acute treatment of migraines and cluster headaches
  • may cause coronary vasospasm, thus they are contraindicated in patients with CAD or prinzmetal angina
  • also have the potential for causing paresthesia
174
Q

What is the treatment regiment for Parkinson’s disease?

A

BALSA

  • bromocriptine (dopamine agonist)
  • amantadine (increase availability of endogenous DA)
  • levodopa
  • selegiline (selective MAO-B inhibitor)
  • antimuscarinics (limit side effects)
175
Q

What is the preferred dopamine agonist for Parkinson’s patients?

A

non-ergot agonists like pramipexole and ropinirole are preferred over ergots like bromocriptine

176
Q

What is pramipexole?

A

a non-ergot DA agonist used in the treatment of Parkinson’s disease

177
Q

What is ropinirole?

A

a non-ergot DA agonist used in the treatment of Parkinson’s disease

178
Q

What is amantadine?

A
  • a drug used in the treatment of Parkinson’s which increases DA release and reduces uptake
  • may cause ataxia or lived reticularis at toxic doses
179
Q

What is carbidopa?

A

a drug co-administered with levodopa to inhibit peripheral DOPA decarboxylase, thereby increasing availability in the CNS and reducing peripheral side effects

180
Q

What is entacapone?

A

inhibits peripheral COMT to prevent peripheral degradation of L-DOPA

181
Q

What is tolcapone?

A

inhibits peripheral COMT to prevent peripheral degradation of L-DOPA

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