Neuro VIII

Question 1

What happens with CN V motor lesion?

Answer 1

Jaw deviates TOWARD side of lesion due to unopposed opposite pterygoid

Question 2

What happens with CN X lesion?

Answer 2

1) uvula deviates AWAY from side of lesion (SCM)

Weak side collapses and uvula points away

Question 3

What happens with CN XII lesion?

Answer 3

Tongue deviates TOWARD side of lesion (“lick your wounds”) due to weakened tongue muscles on affected side.

Question 4

What happens with facial nerve UMN lesion?

Answer 4

Contralateral paralysis of lower muscles of facial expression, sparing forehead due to bilateral UMN innervation

Question 5

Presentation of facial nerve LMN lesion?

Answer 5

1) ipsilateral paralysis of upper and lower muscles of facial expression.
2) hyperacusis + loss of taste sensation to anterior tongue.

Question 6

most common facial nerve palsy?

Answer 6

Idiopathic (aka Bell palsy)

Question 7

other causes of facial nerve palsy?

Answer 7

1) lyme disease
2) HSV
3) herpes zoster (Ramsay hunt syndrome)
4) sarcoidosis
5) tumors
6) DM

Question 8

path of venous drainage from eye and superficial cortex

Answer 8

eye and superficial cortex –> cavernous sinus –> internal jugular vein.

Question 9

Cavernous sinus syndrome presentation

Answer 9

1) Variable ophthalmoplegia
2) decreased corneal sensation 3) Horner syndrome
4) occasional deceased maxillary sensation

Question 10

CN most susceptible to injury with cavernous sinus syndrome

Answer 10

CN VI

Question 11

Causes of cavernous sinus syndrome

Answer 11

1) mass effect from tumor
2) carotid-cavernous fistula
3) cavernous sinus thrombosis related to infection

Question 12

tonotopy concept

Answer 12

Each frequency of vibration of hair cells leads to vibration at specific location on basilar membrane.

Question 13

Where are frequencies heard in cochlea?

Answer 13

1) Low frequency heard at apex near helicotrema (wide and flexible).
2) High frequency heard base at base of cochlea (thin and rigid).

Question 14

Rinne test findings with conductive hearing loss

Answer 14

Abnormal (bone greater than air)

Question 15

Rinne test findings with sensorineural hearing loss

Answer 15

Normal (air greater than bone)

Question 16

weber test results

Answer 16

Localizes to affected ear with conductive, and normal ear with sensorineural.

Question 17

How do sudden extremely loud noises produce hearing loss?

Answer 17

Due to tympanic membrane rupture.

Question 18

Where do cholesteatomas occur?

Answer 18

middle ear

Question 19

What is a cholesteatoma?

Answer 19

overgrowth of desquamated keratin debris

Question 20

Sequela of cholesteatoma?

Answer 20

Can erode ossicles and mastoid air cells causing conductive hearing loss.

Question 21

Inner to outer layers of eye

Answer 21

Retina –> choroid –> sclera

Question 22

what inhibits aqueous humor production?

Answer 22

1) beta blockers
2) A2 agonists
3) carbonic anhydrase inhibitors

Question 23

Receptors on Iris dilator muscle?

Answer 23

alpha2

Question 24

Receptors on iris sphincter muscle?

Answer 24

M3

Question 25

Aqueous humor pathway

Answer 25

produced in ciliary body --> flows through posterior chamber up and over lens --> flows above iris --> then flows through trabecular meshwork and into canal of scheme and into episcleral vasculature (90% OR drains into urea and sclera (uveoscleral outflow)

Question 26

With do M3 agonists affect?

Answer 26

trabecular outflow.

Question 27

What do prostaglandin agonists affect?

Answer 27

Uveoscleral outflow

Question 28

Hyperopia pathophys

Answer 28

Eye too short for refractive power of cornea and lens --> light focused behind retina.

Question 29

Myopia pathophys

Answer 29

Eye too long for refractive power of cornea and lens --> light focused in front of retina.

Question 30

astigmatism etiology and sequela

Answer 30

Abnormal curvature of cornea leading to different refractive power at different axes.

Question 31

What is presbyopia caused by?

Answer 31

Decreased lens elasticity

Question 32

cataracts?

Answer 32

painless, often bilateral opacification of lens.

Question 33

cataracts RFs

Answer 33

1) age 2) smoking 3) excessive alcohol use 4) excessive sunlight 5) chronic corticosteroid use 6) DM 7) trauma 8) infection

Question 34

congenital RFs for cataracts

Answer 34

1) classic galactosemia 2) galactokinase deficiency 3) trisomies 13,18,21 4) rubella 5) Marfan 6) Alport syndrome 7) myotonic dystrophy 8) NF2

Question 35

Glaucoma etiology?

Answer 35

Optic disc atrophy with cupping + elevated IOP usually

Question 36

visual manifestation of glaucoma?

Answer 36

Progressive peripheral visual field loss

Question 37

What is cupping?

Answer 37

Thinning of outer rim of optic nerve head.

Question 38

open-angle glaucoma RF's

Answer 38

1) increased age 2) AA race 3) family history

Question 39

Which glaucoma type is more common in US?

Answer 39

open-angle

Question 40

Cause of secondary open-angle glaucoma

Answer 40

1) blocked trabecular meshwork from WBCs (uveitis), RBCs (vitreous hemorrhage), retinal elements (retinal detachment).

Question 41

primary closed angle glaucoma pathophys

Answer 41

Enlargement or forward movement of lens against central iris (pupil margin) leads to obstruction of normal aqueous flow through pupil --> fluid builds up behind iris, pushing peripheral iris against cornea and impeding flow through trabecular meshwork.

Question 42

Secodnary closed angle glaucoma pathophys

Answer 42

Hypoxia from retinal disease induces vasoproliferation in iris that contracts angle.

Question 43

causes of secondary closed angle glaucoma

Answer 43

1) DM | 2) vein occlusion

Question 44

chronic closed angle closure glaucoma pathophys

Answer 44

often asymptomatic with damage to optic nerve and peripheral vision.

Question 45

acute closure glaucoma pathophys

Answer 45

Increased IOP pushes iris forward --> angle closes abruptly.

Question 46

acute closure glaucoma presentation

Answer 46

very painful, red eye, sudden vision loss + halos around light + rock-hard eye + frontal headache

Question 47

Drug contraindicated with acute closure glaucoma

Answer 47

epinephrine (mydriatic effect)

Question 48

How to differentiate allergic, bacterial, viral conjunctivitis?

Answer 48

Allergic --> itchy eyes and bilateral Bacterial --> pus Viral --> sparse mucous discharge, swollen pre auricular node.

Question 49

most common cause of conjunctivitis?

Answer 49

viral (adenovirus)

Question 50

anterior uveitis

Answer 50

iritis

Question 51

intermediate uveitis

Answer 51

pars planitis inflammation

Question 52

posterior uveitis

Answer 52

choroidits and/or retinitis

Question 53

other findings in uveitis

Answer 53

1) hypopyon | 2) conjunctival redness

Question 54

hypopyon

Answer 54

accumulation of pus in anterior chamber

Question 55

Uveitis associations

Answer 55

* systemic inflammatory disorders 1) sarcoidosis 2) RA 3) JRA 4) HLA-B27 associations

Question 56

Visual effects of macular degeneration?

Answer 56

1) metamorphopsia | 2) loss of central vision (scotomas)

Question 57

metamorphopsia

Answer 57

distortion of vision

Question 58

dry mac degeneration prophylaxis

Answer 58

multivitamin + antioxidants

Question 59

more common type of macular degeneration?

Answer 59

Dry (over 80%)

Question 60

where does drusen deposit with macular degeneration?

Answer 60

In and between Bruch membrane and retinal pigment epithelium.

Question 61

difference in presentation between wet and dry macular degeneration?

Answer 61

Dry presents with gradual loss vision; wet with rapid loss of vision

Question 62

cause of wet macular degeneration?

Answer 62

Bleeding secondary to choroidal neovascularization.

Question 63

wet macular degeneration treatment

Answer 63

ranibizumab

Question 64

non proliferative diabetic retinopathy pathophys..

Answer 64

Damaged capillaries leak blood --> lipids and fluid seep into retina --> hemorrhages and macular edema occur.

Question 65

treatment for non proliferative diabetic retinopathy pathophys..

Answer 65

blood sugar control

Question 66

proliferative diabetic retinopathy pathophys..

Answer 66

Chronic hypoxia results in new blood vessel formation with resultant traction on retina.

Question 67

proliferative diabetic retinopathy treatment

Answer 67

1) peripheral retinal photocoagulation 2) surgery 3) anti-VEGF

Question 68

Retinal vein occlusion pathophys

Answer 68

Blockage of central or branch retinal vein due to compression from nearby arterial atherosclerosis.

Question 69

Retinal vein occlusion presentation on fundoscopy

Answer 69

Retinal hemorrhage and venous engorgment. Edema in affected area.

Question 70

retinal detachment pathophys

Answer 70

Separation of neurosensory layer of retina (photoreceptor layer with rods and cones) from outermost pigmented epithelium --> degeneration of photoreceptors --> vision loss.

Question 71

normal function of pigmented retinal epithelium

Answer 71

Shields retina from excess light and supports retina.

Question 72

Causes of retinal detachment

Answer 72

1) retinal breaks 2) diabetic traction 3) inflammatory effusions

Question 73

fundoscopy findings with retinal detachment?

Answer 73

1) Crinkling of retinal tissue | 2) changes in vessel direction

Question 74

Rss for retinal detachment

Answer 74

1) high myopia | 2) history of head trauma

Question 75

retinal detachment presentation

Answer 75

1) often preceded by posterior vitreous detachment (flashes and floaters) 2) eventual monocular vision loss like curtain drawn down.

Question 76

CN XI lesion

Answer 76

1) Weakness turning head to contralateral side of lesion (SCM). Shoulder droop on side of lesion (trapezius). 2) Left SCM contracts to help turn the head to the right.