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Second Pass Half Blood Prince > Optho > Flashcards

Optho Flashcards

1
Q

What innervates the cornea? What then causes the eye to blink?

A

CN 5 provides the corneal reflex
CN 7 contracts the orbicularis oculi to close the eye shut

Remember 5 is the senation and 7 is the muscle

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2
Q

What are the three parts of the uvea?

A

Iris
Cilliary body
Choiroid

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3
Q

What does the choroid do?

A

Vascular layer that supplies the retina and the sclera

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4
Q

What is the cilliary body and what does it do?

A

Circular strcuture of the uvea that is made up of muscle, fibrous connective tissue and epithelial cells. It attaches the choroid to the circumference of the iris

Think of it in three main parts:
Cilliary processes are projections that attach to the zonular fibers that make up the suspensatory ligament for the lens
Ciliary muscle - helps lens to contract and strech to accomodate objects
Ciliary epithelial cells - make aqeous humor and then secrete it through processes so it can go through the pupil and into the anterior chamber

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5
Q

What is the iris and what does it do?

A

It is a thin ring like structure in the front of the eye that control the amount of light that is able to travel in through the pupil.

It is made up of two layers - a pigmented fibromuscular layer or stroma that connects to two muscles (the spincter papilae - constricts, and the dilator papilae that opens it up) and a highly pigemnted epithelial layer underneath that stop light getting through.

The outer edge of the iris that attaches to the sclera is called the root. Just in front of the root is the trabecular network that props open and draws aqueous humor into the canal of schelm which drains it. Also attaches to ciliary body.

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6
Q

What is the boarder between the anterior and posterior chamber of the eye? Outline the path of aqeous humor (this is relevent to understand pupilary block)

A

The Iris - in front is anterior, behind is posterior
This is clinically relevent because the ciliary bodies are in the posterior chamber and the aqeous humor flows forward through the pupil.

Made by the ciliary process in the posterior chamber
Enters anterior chamber through the pupil
Moves peripherally, then through trabecular meshwork
From meshwork to Canals of Schlemm to episcleral veins

There are two ways your pupil gets big - sympathetic stimulation or absence of parasynpathetic stimulation.

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7
Q

What is the fundus?

A

Interior portion of the eye where light enters and is focused
The retina is something that we see when we look at the fundus

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8
Q

What is the optic disc? Explain what you are looking at when you do fundoscopy (theoretically, if you were good at it)

A

Optic disc - circular area that corresponds to the exit of the optic nerve and the central retinal vein, entrace of central retinal artery. No photoreceptors here so it is a blind spot in our vision. From the optic disc you will see retinal arterioles (thinner) and venoles.

Macula is lateral the optic disc with a high photoreceptor concentration that specialized in acute vision (without this everything would be blurry)
The central area of the macula is the fovea - most acute vision is here.

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9
Q

What is the difference between the anterior and posterior chamber and the anterior and posterior segment?

A

Anterior segment has anterior and posterior chamber seperated by the iris. The posterior segment is everything behind the lens.

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10
Q

What does aqeous humor and vitreous humor do?

A

AH - supplies nutrients, oxygena and removes waste from the cornea because it does not have its own blood supply

VH - thicker gel like transparent fluid that supports the lens and holds the reinta in place (why you can get vitreous detachment).

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11
Q

What are the four big categories of eye complaints?

A

Pain, redness, disordered vision, swelling

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12
Q

What is a cataract?

A

A cataract is a cloudy area in the lens of the eye that leads to a decrease in vision of the eye.Cataracts often develop slowly and can affect one or both eyes

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13
Q

What is the levator tendon? What does it do?

A

Tendon attached to a muscle that sits above the eye and conencts to the eyelid to keep it open. (Why you need optho to repair if laceration)

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14
Q

What are the canthal tendons? What do they do?

A

The medial and lateral canthal ligaments contain the eye within the orbit and eyelids.

The lateral canthal tendon has two branches: a superior and an inferior. Cutting one, or both, loosens the eyelids and allows the globe to expand out of the orbit and thus relieve pressure on the eye.

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15
Q

Eyelid laceration does not meet criteria for optho repair - what do you use to repair it?

A

6-0 or 7-0 proline have it come out in a week

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16
Q

What is one reassuring feature that you have a sunconjunctival hemmorage and not something deeper (conjunctival laceration or scleral laceration)

A

If you can’t see any blood vessels. This is because it means the blood is in the most superficial layer. Use cold compresses, artifical tears, should heal up on its own in 2 weeks.

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17
Q

Which corneal abrasions get topical antibiotics? Which get a call to optho?

A

Deep
Heavily contaminated
Contact lens wearer
Immunocompromised
(Otherwise infection rate is only 0.7%)

Optho if large, concern for FB, central area of visual axis is involved.

Give additional coverage for pseduomonas with cipro or tobra drops

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18
Q

What is the risk with giving someone topical tetracaine to take home?

A

Erosive keratopathy - most likely from emerging infection masked by anesthetic. Will present with corneal infiltration and ulceration.

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19
Q

What is cyclodialysis?

A

Tear where the cilliary muscle is avulsed from a scleral spur

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20
Q

What are signs of a lens dislocation? What is one predisposing factor?

A

Might see on slit lamp exam as edge of natural lens which is normally not visible, shimmering of the lens with eye movement and shimmering or iris with movements

Weakening of lense zonule complex with trauma

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21
Q

What is commotio retinae?

A

Also known as Berlin’s edema is a traumatic retinopathy caused by the eye being hit.
most often occurs after blunt trauma that results in a bony injury to the orbit causing the retina to be damaged
Mechanism can be at areas of scleral impact (coup) and or distant sites (contrecoup) including the macula.

Get decreased vision in the injured eye a few hours after the injury. Under examination the retina appears opaque and white in colour in the periphery but the blood vessels are normally seen along with “cherry red spot” in the foveal region
Usually will get better on its own in a few weeks

?like an optho version of a concussion

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22
Q

Why is retinal detachment painless?

A

Retina does not have pain receptors

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23
Q

What is sympathetic ophthalmia?

A

A vision threatening autoimmune response in the remaining healthy eye after open globe triggered by exposure of the naive immune system to intraoccular contents

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24
Q

What is the difference between intra orbital and intra occular foreign bodies? When do they need to come out?

A

Orbital is in the wall but not inside the actual eye. If enert can stay, if organic needs to come out.

Everything that’s truly in needs to come out (open globe)

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25
Q

Two specific consequences of metal in the eye?

A

Siderous oxidation from iron
Chalcosis sterile inflammatory reaction to copper containing compounds

26
Q

Antibiotics for open globe

A

Ceftaz and Vanco

(Per uptodate, rosens say ancef but that doesnt give you pseudo coverage

27
Q

What are clinical signs that strongly suggest the presence of a retrobulbar hematoma?

A

The presence of 3 or more = strong suggestion
decreased vision
proptosis with resistance to retropulsion,
chemosis
limited extraocular
motility,
diplopia,
diffuse subconjunctival hemorrhage,
increased IOP,
and an APD

28
Q

Two signs on xray of orbital floor fracture

A

Tear drop
Air fluid level in the maxillary sinus

29
Q

What are general precautions for orbital floor frature?

A

Dont blow nose
Abx if you also have sinusitus
Nasal decongestants
Ice pack 48 hours

30
Q

Which orbital floor fractures need optho?

A

Pediatric trapdoor
Entrapement with gaze restriction
Non resolving occulo-cardiac reflex
Persistnat diplopia
Chemosis
Persistant cosmetic concerns after swelling resolves

31
Q

What is an occular-cardio reflex?

A

Rare complication of orbital fracture or retrobulbar pathology
occurs due to pressure exerted on the periorbital soft tissues
Afferent signal from CN5 and efferent from vagus leads to brady, junctional and even asystole with vomitting/ nausea

32
Q

Worrisome signs of chemical injury? What are you irrigating with? What are some long term complications?

A

periorbital edema
Depithelizied skin
Loss of eylashes or brows
Conjunctival epithelial defects
Chemosis
Corneal clouding
Ulceration
Perforation

Ideally ringers lactate (tap water is hypotonic). Start right away becuase the longer you wait the harder it will be to wash out.

Corneal injury
Glaucoma
Adhesions
Cataracts

33
Q

How do you manage someone who has glued their eye shut

A

Glue wont stick to a surface that is wet so its usually eyelids and lashes affect.
Dont use acetone to open (can do more damage)
Gently cut away lashes to try and open - if you can look for corneal abrasion and if none outpatient optho
If you cant or there is malposition, corneal abrasion underneath optho same day

34
Q

When do you send conjunctivits to optho?

A

Severe symptoms like pseudomembrane formation or bleeding. They will consider steroids and arrange follow-up.

35
Q

What is opathalmia neonatorum?

A

Conjunctivtis in the first 30 days of life
Infection is what you are worried about, can lead to sepsis or scarring and blindness.
Agent you worry about are those with the risk of vertical transmission like gonorrhea, chlamydia, HSV
Patients get a full septic workup, admitted, cetrixzone, optho consult ?topical acyclovir ointment

36
Q

What makes corneal ulcers different from abrasions? Who might you worry about a fungal ulceration in? What is one cause that can be reccurent?

A

Invovle the epithelial layer and the stroma underneath of the cornea

Chronic steroid use or agricultural workers (vegtable matter, soil)

HSV can be recurrent

37
Q

What is Hepres Zoster Opthalmicus?
How is it different from HSV?

A

Reactivation of Herpes Zoster virus alone CN 5
Present with deramtome rash in that distribution
Hutchinson sign is lesion on tip of nose indicates higher risk of optho invovlement

HSV might get topical agents or systemic depending on severity. Topical dont work for herpes zoster opthimalicus - needs systemic - if immunocompromised or retinal invovlement needs to be admitted.

38
Q

What do lesions around the eyes warn you about?

A

irit, uvetits, chroiditis - probably send to optho

39
Q

What is the orbital septum? Why is this relevent for peds?

A

Thin fibrous membrane that acts as a barrier between the superficial lids and the orbit.

Relevent for peds because they have an underdeveloped orbital septum so it makes distinguishing between pre and post septal really hard

40
Q

Who is dacrocystitis actually an emergency in?

A

Neonates - can lead to orbital cellulitis they need to be admitted. Occasionally will get surgical consult so optho needs to come see them as well.

41
Q

3 ways you can get endophtamaitis and 1 bedside test?

A

Post occular surgery - most common, can get cons with things like cataract repair
Penetrating trauma
Endogenous spread

Ultrasound might show numerous heterogenous strands and membranes. (vitreous fluid should be uniformly hypoechoic anything else is worrisome)

Remember this gets IV and intravitreal antibiotics (optho)

42
Q

What is open angle glaucoma? Is it a pre-requisite for AACG?

A

Chronic condition of asymptomatic elevated IOP causing an enlarged ratio of diameter of optic cup to diameter of optic disc and peripheral vision loss

Not required for AACG. People can get that with tumor, shallow chamber, big lens with aging, or pupil dilating from low light, topical agents, anti-cholinergic or sympathometic

43
Q

What is the blood supply to the retina? How is this clinically relevent?

A

Duel - inner layers solitary central retinal artery. Outer are choroid. (Why you get a cherry red spot - the central retinal artery is gone but the choiroid is still perfusing the fovea and the rest looks super pale.

44
Q

What is the classic story for optic neuritis?

A

Young person 14 to 45, monooccular blurry or foggy vision worse over severeal days. May get worse with heat or have other signs of MS (presenting symptoms in 1/4 of cases)

Causes can be infectious, autoimmune, metabolic (hyperglycemia with large osmotic shifts), methanol (metabolizes to formic acid accumuulates in optic nerve get edema bad flow).

Treatment depends on cause, remove toxin, correct metabolics, steroids, IVIG, plasmapharesis

45
Q

What are 5 causes of vision loss from a toxicologic cause?

A

Methanol, ethylene glycol
Isonized, heavy metals
Barbituates

46
Q

What is papiledema?

What can minic it?

A

Swelling of the optic nerve as it enters the back of the eye due to increaed intracranial pressure (different from occular compartment syndrome which is increased IOP)

Occurs because subarachnoid space is continuous with optic nerve sheath so if CSF pressure goes up affects the eye. Why its so worrisome if you get vision loss with IIH - there is enough pressure the optic nerve is getting squished.

Anything that leads to optic nerve swelling can mimic papiledema such as ischemic optic neuropathy, optic disc vasculitis, diabetic papilitis (palpitis = optic disc swelling)

47
Q

What are signs on fundoscopy of increased IOP?

A

Loss of cupping (pressure coming from the back)
Optic disc margins blurring
Hyperemia
Obliateration of spontanous venous pulsations
Flame shapped hemorages and yellow exudates

48
Q

What is the optic disc?

A

Round spot on the back of the eye where the optic nerve and the retina connect. Also where the central retinal artery and central reintal vein come out.

49
Q

What causes floaters? What causes bright flashes of light with retinal hemmroage?

A

Floaters - objects in the field of vision caused by material obstructing the light path. Often caused by vitreous hemmroage from longstand dibetic retinopathy and tears. Management is expectant sleep with head of bed up to let blood settle.

Flashing light is seen with retinal detachment. Occurs because the abnormal stimulation of the photoreceptors creates action potentials that your brain just interprets as flashes of light.

50
Q

What type of reitnal detachment is the most worrisome?

A

If it involves the macula (presents with loss of central vision). The longer it is off the worse your prognosis.

51
Q

What are three mechanisms of retinal detachement?

A

Rheumatogenous - tear in neuronal layer where fluids from vitreous cavity leaks between and seperates retinal layers

Exudatvive - fluid or blood leaks from vessels within retina. Think HTN, pre-eclampsia, CRVO

Tractional - contraction of fibrous band that as formed in the vitreous. Get flashes from the traction and floaters.

52
Q

Compare retina and ultrasound findings for vitreous hemmorage and retinal detachment

A

Vitreous hemmorage - reddish haze in mild, black
reflex in severe . Details of the fundus are hard to see, diminished red reflex. Shoudnt have a APD (light gets around blood is everything else fine)

On US - reveal echogenic debris in the vitreous, may be evenly distributed throughout the vitreous, or as a pre-retinal
hemorrhage—may be focal, with a boat shape

Retinal Detachment - can have APD if large, the retina appears out of focus at the site of detachment (cant rule this out could be anterior where you cant see). large retinal detachments with large fluid accumulation,
a bullous detachment with retinal folds

on US - billowing hyperechoic line that may undulate with side-to-
side movements of the eye. Can get flase negative with vitreous hemmorhage

53
Q

Compare RF for CRAO and CRVO

A

CRAO - 50-70 with vascular rRF like vasculitis, sickle cell, collagen vascular disease, cardiac valve problem. Increased IOP like glaucoma, retrobulbar hematoma, hyperthyroidism

CRVO - general vascular risk factors like HTN, high cholesterol, DM, smoking, hyperviscosity

54
Q

What is a CRAO? What is a CRVO?

A

Central retinal artery occulsion - can be non-arteritic and permanent (ischemia), non-arteritic and temporary (TIA or vasospasm), or arteritic (systemic inflammation from GCA).

CRVO is a central retinal veion occlusion where you get congestion fo the venous blood leading to secondary retinal ischemia. It can be non-ischemic, where its just dilated or ischemic where it has vision loss.

I am going to think of CRAO as loss of blood supply in and CRVO as venous statis of the eye, except instead of not perfusing your foot you arent perfusing your retina.

55
Q

What is ION? What is a distinct clinical finding?

A

Ischemic optic neutitis - loss of blood supply to the optic nerve itself (different from CRAO and CRVO because they supply the retina).

Two main types anterior which is the head and posterior which is the rest.
Also divided into arteritic from GCA or non arteritic from a non inflammatory cause.

Distinct finding is visual filed loss that respects horizontal line, symptoms of GCA like cludication weight loss malaise

56
Q

Outline your management of CRAO vs CRVO vs ION

A

CRAO
Call optho
Dislodge any embolus with digital massage (pressure 10 seconds then release
Dilate the artery with elevated CO2
Reduce IOP with paracentesis
HBO
Non-arteritic consider TPA, hypercoagulable work up and stroke prevention clinic

CRVO - optho to consider treatments like heparin, endotheial gorwth factor steroids

ION from GCA is high dose steroids everything else just refer to optho

57
Q

4 ways to spot functional vision loss (conversion or malingering)

A
  1. Rocking a mirror - will induce nystagmus in real not in functional because they cant see it
  2. Rapidly move hand to their eye - if they can see will flinch if not will do nothing
  3. APD - blind will have one functional will not
  4. Raise arms and touch fingers together - actually blind can do it just fine faking it will not to try and seem more legit. Alternative right their name
  5. Hodl picture close to face ask what is missing, then pull it back and ask again. Fucntinal will say same things for consistency real should change based on fixed lesion in visual field.
58
Q

New horner syndrome what are you getting?

A

CTA first will probably need an MRI

59
Q

Meds that will cause a small pupil? A large pupil?

A

Small - organophosphates, pilocarpine, cholinesterase inhibtors, apraclonidine

Large - anticholinergics scopolamine, atrovent, psycdelics, cocaine

60
Q

Places that can give you a horner syndrome

A
61
Q

Outline the following types of pupils:
Argyll
Addie
Tadpole
Marcus Gunn

Two other things that can cause weird pupils?

A

Argyll - doesnt constrict with bright light, but do with a near by object. Problem in brain but machinery to constrict still intact - Neurosyphillis

Adie - doesnt constrict with bright light, cant read up close. - Problem with cilliary nerves so cant do either Lots of causes sarcoid, amyloid, surgery, idiopathic

Tadpole pupil - pupil becomes distorted and pulled in one direction several times a day then resolving. Atraumatic no uvea prolaspe like open globe.

Marcus Gunn - afferent pupillary defect seen on swining flashlight test

Opthalmoplegia migraine - autonomic control of CN 3 messed up. or headache assocaited (make sure no horner)

62
Q

How can you tell if nystagmus is stroke or drugs?

A

Drugs bilateral stroke unilateral

Second Pass Half Blood Prince (13 decks)

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