Neuro Part 15

Front 1

Bruch's membranes

Back 1

innermost layer of the choroid plexus

Front 2

conjunctival injection =

Back 2

dilatation of the conjunctival vessels

Front 3

diabetic retinopathy = dz of retinal blood vessels in which:

Back 3

sugar glycosylates to vessel walls

=> weakening

=> breakdown (microangiopathy)

=> blindness

Front 4

microangiopathy

Back 4

dz of the small blood vessels, where the walls of said vessels become so thick and weak that they bleed, leak protein, and slow the flow of blood

Front 5

glycosylation happens everywhere, but _________________________________ are most sensitive

Back 5

microvasculature of kidney and eye

Front 6

3 extra risk factors for diabetic retinopathy:

Back 6

1. HTN

2. smoking

3. preg

Front 7

2 types of Diabetic Retinopathy:

Back 7

1. Non-proliferative DR

2. Proliferative DR

Front 8

Non-Proliferative DR ~~

(5)

Back 8

1. 95% of pts

2. **progressive** microangiopathy

3. => microaneurysms on fundoscope

4. *cotton-wool spots* if severe

5. venous beading (funny-looking vessels)

Front 9

Proliferative DR ~~

(2)

Back 9

1. neovascularization

2. scarring

Front 10

2 serious complications of Proliferative DR:

Back 10

1. vitreal hemorrhage
(blood in the back of the eye)

2. retinal detachment

Front 11

treatment of Diabetic Retinopathy =

Back 11

laser photocoagulation

- easily treatable if caught early

Front 12

Laser Photocoagulation seals:

(2)

Back 12

blood vessels or coagulate tissue

Front 13

Macular Degeneration:

(3)

Back 13

1. >55 yo

2. => loss/blurriness of central vision

3. two types (dry and wet)

Front 14

4 risk factors for Macular Degeneration:

(apart from age)

Back 14

1. Caucasian

2. female

3. smoking

4. FH of AMD

Front 15

Dry Mac D:

(4)

Back 15

1. aka atrophic Mac D

2. much m.c.

3. PAINLESS loss of central vision

4. ~~drusens in Bruch's membrane

Front 16

drusens =

Back 16

yellow lipid deposits that form in Bruch's membrane in the retina

Front 17

treatment of Dry/Atrophic Mac D =

Back 17

combo of Vits C, E, beta-carotene, and zinc

- slows progression

Front 18

Wet Mac D:

(6)

Back 18

1. aka exudative form

2. *more rapid/severe*

3. ~BREAKS in Bruch's memb

4. => neovascularization

5. => pot. for hemorrhage

6. => sub-retinal fluid accum.

Front 19

treatment of Wet/Exudative Mac D =

(3)

Back 19

1. VEGF inhibitors (e.g. Bevacizumab)

2. +/- photodynamic therapy

3. +/- laser

Front 20

aqueous fluid pathway:

(6)

Back 20

1. produced by ciliary body, in posterior chamber

2. flows forward around the lens into the anterior chamber

3. then into angle formed by iris and cornea

4. => trabecular meshwork

5. => canal of Schlemm within said angle

6. venous circulation

Front 21

even though it has a lot to do with the aqueous fluid, glaucoma is ultimately a dz of the:

Back 21

optic nerve

Front 22

4 risk factors for open-angle glaucoma:

Back 22

1. FH

2. AfAm's

3. inc. IOP

4. large vertical nerve cupping

Front 23

main symp of open-angle glaucoma =

Back 23

GRADUAL loss of vision, over many YEARS

- PAINLESS

Front 24

cause of open-angle glaucoma =

Back 24

*clogged trabecular meshwork*

Front 25

4 signs of open-angle glaucoma:

Back 25

1. inc. IOP

2. cup-to-disk ratio >0.5
(nl = o.3)

3. papilledema

4. repeatable visual field loss patterns

Front 26

treatment for open-angle glaucoma =

(1 => 2)

Back 26

dec. IOP, via:

1. meds

- B-blockers,
- carbonic anhydrase inhibitors

2. trabeculectomy

Front 27

closed-angle glaucoma = acute glaucoma, due to:

Back 27

pupillary block of aqueous humor

***an EM - can lose ALL vision within hours***

Front 28

how does the block of aqueous humor in closed-angle glaucoma occur?

Back 28

- lens attaches to iris, pushes it outward

=> *closes iro-corneal angle*

=> trabecular meshwork is blocked

=> **rapid** inc. in IOP

Front 29

symps of closed-angle glaucoma:

(7)

Back 29

1. extremely pain

2. red eye

3. n/v

4. **halos around lights**

5. ciliary, conjunctival injection

6. pupil sluggish, dilated

7. P up to 60 mmHg

Front 30

treatment of closed-angle glaucoma = dec. IOP, via:

(4)

Back 30

1. iridotomy
(hole in iris, allowing communication b/w the chambers)

2. oral glycerin + IV mannitol to drain aqueous humor

3. Pilocarpine to constrict pupil/iris, open up angle

4. B-blocker or CAI to dec. production

Front 31

cataract =

Back 31

ANY opacity of the lens

tx = lens replacement

Front 32

mature cataract =

Back 32

ALL of lens is opaque

Front 33

4 risk factors for cataracts:

Back 33

1. age

2. smoking

3. DM

4. hereditary

Front 34

Temporal Arteritis might result in blindness of one or BOTH eyes, due to:

Back 34

occlusion of central retinal artery

Front 35

features of Temporal Arteritis:

(5)

Back 35

1. ~elderly

2. pain chewing

3. pain in temples

4. HA

5. associated with Polymyalgia Rheumatica, aortic aneurysm, aortic dissection

Front 36

treatment of Temporal Arteritis =

Back 36

systemic corticosteroids like Prednisone

- the sooner the better

Front 37

Polymyalgia rheumatica

Back 37

Inflammatory disorder that causes muscle pain and stiffness, that is associated with temporal arteritis

Front 38

anything that increases ICP will cause:

Back 38

papilledema,

by pressing on the optic nerve

Front 39

symps of papilledema:

(3)

Back 39

1. HA

2. n/v

3. visual problems

Front 40

dx of papilledema =

Back 40

bulging optic disk

Front 41

next steps after seeing papilledema:

(3)

Back 41

1. m. BP

2. MRI of heard (or CT if unavailable)

3. LP to check opening pressure

Front 42

eye emergencies:

(5)

Back 42

1. closed-angle glaucoma

2. papilledema

3. central retinal artery occlusion

4. Temporal Arteritis (sort of)

5. suspected retinoblastoma

Front 43

Central Retinal Artery Occlusion =>

Back 43

***sudden, painless, often complete, loss of vision***

Front 44

2 causes of CRA Occlusion:

Back 44

1. inc. ICP

2. thromboses

Front 45

****signs of CRA Occlusion:****

(3)

Back 45

1. cherry red spot on fovea

2. whitish optic disc

3. bloodless arteries

- treat immediately is suspected

Front 46

Central Retinal Vein Occlusion is NOT an emergency; usually occurs in:

Back 46

elderly,

esp with HTN/athero/CV dz's

Front 47

rarely, CRV Occlusion can be induced by:

(2)

Back 47

1. polycythemia vera (thickened blood)

2. lymphoma-leukemia

Front 48

Polycythemia Vera =

Back 48

myeloproliferative blood disorder that results in an overproduction of red blood cells

Front 49

symp of CRV Occlusion =

Back 49

*sub*acute onset of painless loss of vision

Front 50

3 signs of CRV Occlusion:

Back 50

1. *diffuse* retinal hemorrhages

2. cotton-wool spots

3. optic disk swelling

Front 51

amblyopia = lazy eye =

Back 51

decreased vision due to failure of growth of afferent neurons due to decreased use

=> strong eye's neurons grow while disused eye's disappear

Front 52

3 main causes of amblyopia:

Back 52

1. strabismus

2. anisometropia

3. visual deprivation
(e.g. congrenital cataracts)

Front 53

tx for amblyopia, in general:

Back 53

patch the strong eye or blur it with drops, giving the weak one a competitive advantage/be used more

Front 54

strabismus =

Back 54

misaligned eyes

(objects NOT visualized simultaneously in both fovea)

Front 55

anisometropia =

Back 55

big difference in prescriptions between the eyes

Front 56

strabismus =>

Back 56

diplopia in adults,

amblyopia in kids

Front 57

strabismus that occurs when NOT fixating on an object is called:

Back 57

"-phoria"

Front 58

strabismus that's always present is called:

Back 58

manifest,

"-tropia"

Front 59

treatment for strabismus =

Back 59

surgery, to make EOM's either stronger or weaker

Front 60

pseudostrabismus (most commonly pseudoesotropia) =

Back 60

optical illusion of eyes seeming misaligned b/c of wide nasal bridge

Front 61

leukocoria =

Back 61

white-colored pupil

Front 62

3 causes of leukocoria:

Back 62

1. congenital cataracts

2. ROP

3. retinoblastoma

Front 63

congenital cataracts have many causes, including:

Back 63

TORCH

tx = remove ASAP

Front 64

ROP = retinopathy of prematurity; in premature kids, vascularization of the retina hasn't:

Back 64

finished spreading

=> ischemia of parts of retina not vascularized

=> neovascularization

=> bleeding

=> retinal detachment

Front 65

born more premature =

Back 65

worse ROP

Front 66

treatment of ROP =

(2)

Back 66

1. ablate ischemic retina

2. Bevacizumab

Front 67

Retinoblastoma =

Back 67

mc. ocular primary malignancy of kids

Front 68

**sign of Retinoblastoma:**

Back 68

white/cream-colored mass on retina, causing a

***white iris***

Front 69

the tumor can fill the entire retina, =>

Back 69

retinal detachment

- CANNOT miss - often causes death, esp. around 18 months

Front 70

treatment of Retinoblastoma =

Back 70

enucleation of the eye

Front 71

Weber and Rinne results in conduction loss:

(2)

Back 71

1. Weber would lateralize to the *affected* side

2. negative Rinne test (BC > AC)

Front 72

in normal conditions, there is considerable background noise, which reaches the tympanic membrane by air conduction. This tends to mask the sound of the tuning fork heard by bone conduction.

(**background noise masks sound heard by bone conduction**)

Back 72

In an ear with a conductive hearing loss, the air conduction is decreased, and the **masking effect is therefore diminished.** Thus, the affected ear's BC is > AC (i.e. it hears and feels the vibrating tuning fork better than does the normal ear)

Front 73

Weber and Rinne results in sensorineural hearing loss:

Back 73

1. Weber would lateralize to the good (unaffected) ear

2. Rinne would be AC > BC in both ears.

Front 74

**Conduction loss ~~

Back 74

middle ear,

sensorineural ~~ INNER ear

Front 75

Moraxella species are:

Back 75

oxidase +

Front 76

Solid objects _________ better

Back 76

conduct better