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Clin med II Eye and Cardio > Eye disorders > Flashcards

Eye disorders Flashcards

1
Q

Most common cause of orbital fx in kids and adults

A
  • Children, Adolescents
  • Sports trauma Projectiles- baseball
  • Adults
  • Assaults MVC Industrial accidents
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2
Q

What is the most common fracture of the orbital rim

A

Orbital Zygomatic fx

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3
Q

Orbital Zygomatic fx is often associated w/ fracture of _____________ fracture

A

orbital floor Zygomaticomaxillary complex (tripod)

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4
Q

Disruption of the medial canthal ligament and lacrimal duct system is what type of fx

A

Nasoethmoid Fx

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5
Q

type of injury associated w Nasoethmoid Fx

A

Medial rectus muscle entrapment

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6
Q

type of fracture that results from high impact blow to lateral orbit

A

Orbital Zygomatic fx

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7
Q

describe an Orbital floor / “blow out” fx

A

Displacement of the globe

Entrapment of the inferior rectus muscle à Resulting ischemia and loss of muscle function

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8
Q

fx resulting from a small round object hitting eye or direct blow to infraorbital rim

A

Orbital floor / “blow out” fx

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9
Q

what type of fx

A

Orbital floor / “blow out” fx

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10
Q

what type of fx has a High association with intracranial injury

A

Orbital Roof Fx

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11
Q

Injury to infraorbital nerve decreased sensation along the ____, ____ ___, and _____.

A

cheek upper lip and gingiva

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12
Q

gold standard for imaging orbital fx

A
  • CT Orbit Gold Standard 1-2 mm cuts
  • Axial and coronal through orbits
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13
Q

what is hyphema

MOI?

A

Blood in anterior chamber

Typically caused by blunt trauma or penetrating injury to orbit or globe

  • Finger, hockey stick, racquet, ball
  • Deployed airbag
  • Paintball
  • Assault
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14
Q

tx of hyphema

A

Goal is to prevent secondary hemorrhage and intraocular hypertension, increase absorption of blood

Limit activity

Daily monitoring of IOP

Eye shield

Topical glucocorticoids- prednisone acetate, dexamethasone sodium phosphatate QID- lowers risk of re-bleeds

+/- Cycloplegics and Mydriatics

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15
Q

Regarding hyphema the most common source of blood is tear in the anterior face of the ____ ____.

A

ciliary body

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16
Q

Pt presents with:

Vision loss

Eye pain with pupillary constriction

Photophobia

dx?

A

hyphema

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17
Q

what nerve is affected in a corneal abrasion

A

Trigeminal CN 5

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18
Q

Most frequent cause of visits for ophthalmic emergencies is

A

FB with corneal abrasion

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19
Q

Tx of corneal abrasion

A

Topical antibiotics

Erythromycin • Polymyxin • Sulfacetamide

No patching recommended

No ophtho f/u for small abrasions

Contact Wearers: anti-psuedemonals

Ciproflox drops • Oxiflox drops • Gentamicin • Tobramicin

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20
Q

when treating a corneal abrasion in a contact lense wearer what must you conisder adding to tx

A

Contact Wearers: anti-psuedemonals

Ciproflox drops

Oxiflox drops

Gentamicin

Tobramicin

opth f/u

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21
Q

Indication for ophthalmologist f/u in corneal abrasions

A

Large abrasions

Contact lens wearer

Young children

Vision changes

Rust ring

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22
Q

Flourescein is an important diagnostic tool that can be used after _____.

A

after open globe ruled out

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23
Q

common bacterial causes of corneal ulcers

A

pseudomonas staph strep MRSA Moraxella liquefaciens (DM, alcoholics)

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24
Q

common causes of viral and fungal corneal ulcers

A

Viral HSV/Zoster

Fungal (Amoebas)

Acanthamoeba- contaminated water

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25
Q

risk factors of corneal ulcers

A

Contact lens wearer

Previous eye surgery

Eye injury

Hx of herpes- Type 1 and 2

Use of topical or systemic steroids

Immune compromised

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26
Q

tx of corneal ulcer

A

Aggressively with topical antibiotics

Fluoroquinolone: Ciloxin, Ocuflox

Topical antifungal

Natamycin

Amphoteracin b

Fluconazole

Topical antiviral

Ganciclovir

Acyclovir

NO EYE PATCHES

All suspected corneal ulcers should be referred to ophthalmologist • Within 12-24 hours

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27
Q

open globe injury is considered a ___ prone wound

A

tetnus

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28
Q

tx for open globe injury

A

Assess any life-threatening injuries

NPO – may need to go to OR

Do not remove any FB

Avoid any eye manipulation

Nothing in the eye

Patch

Place head at 30 degrees

Treat nausea and pain aggressively

Provide sedation

Begin IV antibiotics

Ophthalmic consult

Needs surgical repair within 24 hours

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29
Q

Sever the inferior arm of lateral canthal tendon results in

A

Retrobulbar Hemorrhage

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30
Q

why MUST we identify and evacuate septal hematomas

A

Produces avascular necrosis if not evacuated

Blood collects in space between cartilage and mucoperichondrium and obstructs blood flow

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31
Q

Fracture of the midface that involves the zygoma, lateral orbit and maxilla

Caused by direct blow

A

Tripod fx

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32
Q

describe the Lefort Injuries classifcation system

A

I- transverse fx through maxilla above teeth

II- bilateral extend superiorly include nasal bridge, maxilla, lacrimal bones, orbital floor and rim

III- discontinuity between face and skullcranio-facial dissociation

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33
Q

Ethmoid bone fractures often associated with___ _____- head ______ important

A

CSF leakage

elevation

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34
Q

tx of tripod injury

A

Needs surgical repair due to instability

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35
Q

describe the classifcation system for tooth fx

A

Ellis System:

Class I- enamel- not painful

Class II- expose yellow dentin painful

Class III- expose dental pulp seen as red line or dot exquisitely painful

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36
Q

indications for repair of tongue lac

A
  • >2 cm that extend into muscular layers or pass completely through the tongue deep at the lateral border
  • large flaps or gaps significant hemorrhage lacerations that may cause dysfunction if healed improperly
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37
Q

tx of tongue lacs

A

Have suction ready

Closed in LAYERS

Absorbable sutures 3-0 or 4-0 chromic gut or Vicryl

Direct infiltration with 2% lido

IV sedation

Tetanus

Complications

Edema /Hemorrhage

Aspiration

IV decadron

Ice chips, popsicles

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38
Q

try to handle tooth fx

A

Stored in milk if cannot be immediately reimplanted

Handle tooth by the crown

Don’t wipe or handle the root

Rinse gently with tap water or saline

Replace in socket

Have patient put in between gum and buccal mucosa

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39
Q

Name 3 types of anterior blephritis

A

Ulcerative – usually associated with Staphylococcus

  • Seborrheic – usually associated with seborrhea of other areas
  • Parasitic -dermodex follicularum
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40
Q

name si/sx associated w/ anterior blephritis

A

Red-rimmed” eyes

Scales or granulations on lashes

“Greasy” appearance

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41
Q

tx of anterior blephritis

A

Routine cleaning of lid margins, eyelashes, with warm H2O/cotton, baby soap

In acute exacerbations – bacitracin or erythromycin eye ointment daily

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42
Q

posterior blephritis is caused by?

A

Caused by inflammation of the Meibomian gland

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43
Q

blephritis mostly occur in assoc w/ ?

A

Most occur in association with acne, rosacea or seborrheic dermatitis

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44
Q

tx of posterior bleph?

A

Regular Meibomian gland expression

  • Inflammation of the conjunctiva indicates need for long-term low dose oral antibiotics and possibly short-term topical corticosteroids
  • Tetracycline 250mg BID/
  • Doxycycline 100mg daily
  • Prednisolone 0.125% BID

Short-term treatment with ciprofloxacin 0.3% ophthalmic solution BID can be used for exacerbations

Treatment of dermodex is with tea tree oil

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45
Q

most common causes of viral and bacterial conjuncivitis

A

viral

Adenovirus is the most common cause

Other causes are HSV, enterovirus, and coxsackie

bacterial

Most common causes is Staphylococci, including MRSA

Other causes- Strep pneumoniae, Haemophilus, Pseudomonas, and Moraxella

Gonococcal conjunctivitis –emergency can lead to corneal perforation

•Diagnosis is confirmed by stain smear and culture

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46
Q

difference in discharge between viral and bacterial and allergic conjuncivitis

A

viral - watery

bacterial purulent

allergy - string like white discharge (Hallmark sign)

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47
Q

tx of viral conj

A

Although viral, many providers prescribe erythromycin ophthalmic ointment to prevent bacterial co-infection: 1/2in ribbon TID x 7 days. •

HSV – Ganciclovir 0.15% gel

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48
Q

tx of bacterial conj

A

Topical antibiotic ointment will usually clear infection in 2-3 days

  • Bacitracin ointment
  • Erythromycin ointment

Gonococcal – Ceftriaxone IM and topical antibiotics

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49
Q

tx for allergic conj

A

Cold compresses

  • Topical vasoconstrictors: Visene
  • Antihistamines: diphenhydramine
  • Mast cell stabilizers: olopatadine
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50
Q

Inflammation of the lacrimal drainage system usually due to congenital or acquired obstruction

risk fx?

A

Dacryocystitis

age, trauma, surgery, systemic disease, certain medications.

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51
Q

acute vs chronic si/sx of Dacryocystitis

A

Acute signs and symptoms:

  • Pain and Swelling
  • Tenderness and redness over lacrimal sac area
  • Purulent material may be expressed

Chronic signs and symptoms:

  • Tearing
  • Discharge
  • Mucus or pus may be expressed
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52
Q

tx of Dacryocystitis

A

Systemic antibiotics like Augmentin

Surgery to fix underlying obstruction

• Dacryocystorhinostomy – removes obstruction and formation of a fistula into the nasal cavity

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53
Q

enropin vs ectropin

A

entropin Inwardly turning eyelid, usually the lower lid

ectropin

Outwardly turned eyelid, sagging lid

Usually the lower lid

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54
Q

tx of entropin

A

Ointment for lubrication

Eye patching

Surgery may be used to repair muscle laxity

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55
Q

tx of ectropin

A

Artificial tears

Surgery is indicated if there is excessive tearing, exposure keratitis, or cosmetic problem

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56
Q

name 2 types of Hordeolum (stye)

A

Internal: blockage of the Meibomian gland (conjunctival side)

External: blockage of the Zeis (sebaceous) or Moll (sweat) glands

57
Q

si/sx of Hordeolum (stye)

A

Localized redness

Swelling

tenderness

58
Q

tx of stye

A

Antibacterial ointment

Erythromycin ointment: ½ inch ribbon TID x7 days

I&D by ophthalmologist in 1-2 weeks if not improved

May develop into a chalazion

59
Q

Firm cyst of the upper or lower eyelid

dx and cause?

A

chalazion

Caused by inflammation or blockage of the Meibomian gland

60
Q

tx of chalazion

A

Warm compresses • 2-3 weeks

Incision and drainage

Refer to ophthalmologist

Corticosteroid injection • Triamcinalone (Kenalog)

61
Q

si/sx of chalazion

A

Granulomatous

Erythematous

Non-tender

Slow growing

Same risk factors as for hordeolum

62
Q

risk factors for chalazion and hordeum (stye)

A

Can affect anyone but increased in patients with diabetes, contact and eye make-up wearers, blepharitis

63
Q

define Periorbital / Preseptal Cellulitis

A

Infection anterior to the orbital septum

Cellulitis of eyelid

Most common in children

64
Q

pathogens responsible for Periorbital / Preseptal Cellulitis vs Orbital cellulitis

A

Peri

Staph aureus

Strep

H. flu

orbital

Strep pneumoniae

H. Flu

s. Aureus

occasionally fungi or mycobacterium

65
Q

PE finding differentiating Periorbital / Preseptal Cellulitis vs orbital

A

peri

No proptosis

No pain or restriction of EOM

orbital

Proptosis

Restriction of EOM

Pain in EOM

Dx confirmed w/

CT or MRI

66
Q

tx of Periorbital / Preseptal Cellulitis

A

Oral abx

•Augmentin 10 days

Daily f/u bc it can spread deeper

67
Q

tx of orbital cellulitis

A

Ocular emergency – needs rapid dx and tx

Immediate IV abx

•Zosyn or vanco

Admit to hospital

Opth consult

Surgery sometimes needed to drain paranasal sinuses, to decompress pressure on the optic nerve and vessels, or if not improving on antibiotics

68
Q

what can occur if orbital cellulitis goes untreated

A

If untreated can lead to optic nerve damage and can spread infection to cavernous sinuses, meninges and brain

69
Q

expalin the role of retina rods and cones

A
  • Retina transduces patterns of light energy into neuronal signals
  • Rods: operate in dim illumination
  • Cones: operate in daylight; color perception and high spatial resolution
70
Q

pt describes as vision being “looking through a frosty or fogged-up window”

A

cataracts

71
Q

where is “myopic shift” seen

what is myopic shift

A

more difficulty with distance vision

cataracts

72
Q

on fundascopic exam you seeImpaired red reflex* - opacities within the red reflex in an elderly person

dx?

A

cataracts

73
Q

describe patho of cataracts

A

degradation and denaturing of crystallin proteins in the lens

• Compression over time leads to loss of transparency and opacification

74
Q

what are 2 types of macular degeneration

A

dry and wet

75
Q

degenerative dz characterized by loss of central vision

A

macular degen

76
Q

leading cause of adult blindness in industrialized countries

A

macular degen

77
Q

subretinal drusen deposits are characteristically seen in?

A

dry AMD

78
Q

describe the idfference b/w dry and wet macular degen

A

dry

80-90% of cases - Slow and gradual vision loss

Unknown etiology

wet

Less common, more SEVERE and RAPID vision loss

Growth of abnormal vessels into the subretinal space, usually from the choroidal circulation and less frequently from the retinal circulation

Leakage from these vessels produces elevation of the retina, collections of subretinal fluid and/or blood beneath the retina with distortion (metamorphopsia) and blurring of vision

79
Q

focal or widespread geographic atrophy of the retinal pigment epithelium and pigment epithelial detachments

dx?

A

dry AMD

80
Q

gradual loss of vision in one or both eyes

•first noticed as difficulty reading or driving

scotomas

reliance on brighter light or a magnifying lens for tasks that require fine visual acuity

A

dry Amd

81
Q

tx of dry amd

A

Smoking cessation

Antioxidant vitamins

  • Ocuvite or Preservision
  • Studies found patients with more extensive dry AMD may benefit
82
Q

metamorphisia is seen in

A

wet amd

distortion of straight lines

•Patients may perceive straight edges (such as doors or window blinds) as curved or distorted

83
Q

tx of wet amd

A

VEGF Inhibitors

•Bevacizumab, ranibizumab, aflibercept

Antioxidants and vitamins

•Zinc, Vitamin C, Vitamin E, and others

Photodynamic therapy

•Used in patients who fail VEGF inhibitors

84
Q

An eye disease that results in damage to the optic nerve – not always in the presence of elevated intraocular pressure

A

glaucoma

85
Q

after cataracts the leading cause of blindnesss is

A

glaucoma

86
Q

describe open angle glaucoma

A

•optic neuropathy characterized by progressive peripheral visual field loss followed by central field loss in a typical pattern

87
Q

patho of open angle galucoma

A
  • Increased aqueous production and/or decreased outflow are possible mechanisms
  • anatomic or physiologic features of the trabecular meshwork and other outflow structures
88
Q

myocillin gene (MYOC) is assoc w/

A

open angle glaucoma

89
Q

describe angle closure glaucoma

A
  • characterized by narrowing or closure of the anterior chamber angle – presents acutely
  • lens is located too far forward anatomically and rests against the iris, resulting in “pupillary block” of aqueous humor
90
Q

patho of angle closure glaucoma

A
  • Pressure behind the iris causes the peripheral iris to bow forward and cover the anterior chamber angle
  • can lead to scarring and functional damage to the trabecular meshwork
91
Q

si/sx of open angle glaucoma

A

Usually asymptomatic

May or may not be elevated IOP

progressive peripheral vision loss

Central vision loss is a late presentation

92
Q

si/sx of angle closure glaucoma

A

Usually unilateral

Decreased vision

Halos around lights

Headache

Severe eye pain

Nausea and vomiting

often occur in the evening or low light causing mydriasis and folds of the peripheral iris block the narrow angle*

93
Q

gold standard diagnostic test for angle closure glaucoma

A

Gonioscopy

94
Q

“cupping” on fundoscopic exam is ?

A
  • “Cupping”, asymmetry of the cup-to-disc ratio between the eyes
  • thinning or notching of the disc rim, progressive change of the size or shape of the cup

open angle glaucoma

95
Q

tx of open angle glaucoma

A

If IOP is elevated, treatment to lower IOP may delay or prevent the onset of open-angle glaucoma

Topical Prostaglandins*(Preferred) Latanoprost, bimatoprost, tafluprost

Topical Beta-blockers

• Timolol, Betaxolol

Alpha-adrenergic agonists

• Brimonidine

Laser therapy- trabeculoplasty

Surgery – trabeculectomy

•first-line approach only for patients with severe visual field loss at baseline

96
Q

tx fo acute angle closure glaucoma

A

Medical therapy:

one drop each, one minute apart:

  • 0.5% timolol maleate;
  • 1% apraclonidine; and
  • 2% pilocarpine, especially immediately prior to laser peripheral iridotomy
  • And 500 mg of oral or IV acetazolamide
  • Check pressure in 30 and 60 minutes
97
Q

tx for chronic angle closure glaucoma

A

Laser peripheral iridotomy

•tiny hole in the peripheral iris through which aqueous humor can flow

Surgical peripheral iridotomy

•incision into the anterior chamber and surgically excises a small amount of iris tissue to create a passage

98
Q

standard of care in open angle glaucoma

A

Visual Field Testing - Automated Perimetry

  • Standard of care
  • More accurate than confrontational field testing
99
Q

leading cause of blindness in American adults (aged 20–74 years)*

A

diabetic retinopathy

100
Q

primary preventative measure for diabetic retin

A

Good glycemic control is the primary preventive measure**

101
Q

explain the 2 types of diabetic retinopathy

A

Proliferative

presence of neovascularization arising from the disc and/or retinal vessels, preretinal and vitreous hemorrhage, subsequent fibrosis, and traction retinal detachment

Nonproliferative

nerve-fiber layer infarcts (cotton wool spots), intraretinal hemorrhages, and hard exudates and microvascular abnormalities

102
Q

on fundascopi exam of a pt with diabetic retinopathy you will see?

A
  • flame-shaped and blot hemorrhages
  • intraretinal infarcts - “cotton wool” or “soft exudates“
  • formation of tortuous loops of the veins
  • Change in caliber of the veins
  • neovascularization
103
Q

tx of diabetic retinopathy

A

Intravitreal Anti-VEGF agents

Focal photocoagulation

  • Highly effective
  • Often used in poorly compliant patients or patients who have difficulty with follow-up

Combination of the two can be used depending on the patient – treatment individualized

104
Q

fundascopic exam on HTN retin

A
  • Evidence of retinal hemorrhages, exudates, and/or papilledema
  • Arteriovenous nicking, “AV nicking”
  • Copper wire arterioles – central light reflex occupies most of the width of the arteriole
105
Q

tx of htn retinopahty

A

Rapidly lower the mean arterial pressure by approximately 10 to 15 percent, and no more than 25 % compared with baseline during the 1 st day of therapy

• IV Labetolol • IV Nicardipine • IV Nitroprusside

Gradually reduction of systolic BP to <130 and the diastolic pressure being gradually reduced to <80 over two to three months

Retinopathy may regress with good BP control

106
Q

what is strabismus snd what are 2 types

A

Misalignment of the eyes

“Comitant“: describes a deviation that is of the same size in all positions of gaze.

“Incomitant”: deviation that changes depending upon the position of gaze.

107
Q

common complicatiosn of strabismus

A

Amblyopia – lazy eye

Diplopia

Secondary contracture of extraocular muscles

Adverse psychosocial consequences

108
Q

tests in strabismus

A

Corneal light reflex test - Initial screening test*

Cover test - Manifest strabismus

Cover/uncover test

•Performed if cover test is normal – can detect Latent strabismus

109
Q

tx of strabismus

A

Ophthalmology referral – decrease risk of amblyopia

Aimed at treating visual impairment(amblyopia) and misalignment

  • Corrective glasses
  • Occlusion therapy
  • Visual training exercises

•

Surgery

•Reposition or shorten certain extraocular muscles

110
Q

tx of Pterygium

A

Artificial tears for symptoms relief

Surgical excision

• Recurrence rate up to 80%, not recommended for small pterygium or cosmetic purposes

111
Q

Pterygium is caused by

A

UV radiation may trigger events that produce damage to cellular DNA, RNA, and extracellular matrix composition

112
Q

what is Pterygium

A

triangular wedge of fibrovascular conjunctival tissue that typically starts medially on the nasal conjunctiva and extends laterally onto the cornea

113
Q

visual impairment that results from Pterygium

A

•Astigmatism – results in blurred vision

114
Q

define

Acute Transient Visual Loss (Amaurosis fugax)

and

Acute Persistent Visual Loss

A

acute transient sudden deficit in visual function lasting < 24hours (monocular or binocular

  • Temporary vascular occlusion
  • Neuronal depression (after seizure or migraine)

acute persistant > 24hours

115
Q

Characterized by a normal fundus exam initially “The doctor sees nothing, and the patient sees nothing

A

optic nueritis

116
Q

highly associated with delyelinating conditions such as MS

A

optic nuetitis

117
Q

opth exam of retinal detachment shows

A

retinal hydration lines;

“billowing sail” or “ripple on a pond”

118
Q

Retinal detachment often starts with ______and_____ ____ ____ which are warning signs

A

flashes of light and floaters

warning signs

119
Q

risk factors for retinal detachment

A
  • Myopia (near sighted)
  • Previous ocular surgery (cataract extraction)
  • Use of fluoroquinolones •Trauma to the eye
  • Family history (i.e. lattice degeneration)
  • Marfan Disease
120
Q

pt shows unilateral vision loss and pain exacerbated by movement

dx?

A

optic nueritis

121
Q

tx of MS

A

•Treatment with interferon Beta-1a can retard the development of more lesions

122
Q

tx of optic nuetitis

A

Gradual recovery in vision without treatment typically

Consult neurologist, or neuro-ophthalmologist

Plasmapheresis

Systemic corticosteroids is controversial

  • If steroids are prescribed; methylprednisolone followed by tapering dose of oral prednisone
  • Steroids accelerate recovery but do not change end point
123
Q

Physical exam finding during fundoscopic exam

Associated w/ increased IOP = only TRUE cause

A

papiledema

124
Q

explain early, fully developed and later papilledeam

A

1.Early

  • Loss of spontaneous venous pulsations
  • Optic cup is retained early on.
  1. Fully Developed

*Optic disc elevated *Cup is obliterated *Disc margins obscured *Blood vessels buried. * Engorged veins. *Flame hemorrhages *Cotton wool spots (result from nerve fiber infarction)

  1. Late

*Cup remains obliterated. *Hemorrhagic and exudative components resolve. *Nerve appears flat with irregular margins. *Disc pallor.

125
Q

management of Idiopathic intracranial ht

A

Many cases self limited

  • Careful observation/brief hospitalization
  • Weight loss
  • Serial lumbar punctures
  • Acetazolamide (Diamox) –inhibits carbonic anhydrase
  • High dose corticosteroids if rapid vision loss
  • Surgery for severe, refractory cases; optic nerve sheath decompression or lumbar peritoneal shunt
126
Q

dz assoc w pregnant and obese women

A

Idiopathic Intracranial Hypertension

127
Q

si/sx of Idiopathic Intracranial Hypertension

A

Nausea, vomiting, headaches, blurred vision

  • Cranial nerve VI paresis/horizontal diplopia (double vision on lateral gaze). •Papilledema
  • Spontaneous venous pulsations (retinal vein pulsations) are absent

Visual field defects

128
Q

explain 2 types of retinal artery occlusion

A

1.Central retinal artery occlusion (CRAO)

Sudden, profound vision loss in one eye

  • Usually painless
  • Occasionally preceded by transient monocular blindness (amaurosis fugax), stuttering or fluctuating course
  • Rarely ‘flashing lights’ in visual field
  1. Branch retinal artery occlusion (BRAO)

Monocular vision loss, which may be restricted to just part of the visual field

129
Q

fundascopic exam shows

Ischemic retinal whitening

• “Cherry red spot” in the macula

A

retinal a. occlusion

130
Q

tx of retinal a occlusion

A

Check ESR and CRP to r/o GCA

Consult opth

There is no definitive therapy to improve vision

131
Q

PE exam of retinal a occlusion

A

Visual acuity reduced -severity ranges from loss of part of visual field (BRAO) to nearly complete visual loss (can not tell how many fingers clinician is holding up) -check peripheral fields!

•-afferent pupillary defect (Marcus Gunn pupil) (pupil does not constrict appropriately to light)

132
Q

findings assoc w GCA

A

Often very high ESR or CRP

Diagnosis – temporal artery biopsy

• Panarteritis, CD4+ lymphocytes and macrophages

133
Q

retinal vein occlusion fundascopic findings

A

features vary from a few scattered retinal hemorrhages and cotton wool spots to a marked hemorrhagic appearance

134
Q

explain 3 types of retinal vein occlusion

A
  1. Branch retinal vein occlusion (BRVO) distal vein is occluded leading to hemorrhage along the distribution of a small vessel
  2. Central retinal vein occlusion (CRVO) occurs due to thrombus within central retinal vein leading to involvement of the entire retina
  3. Hemiretinal vein occlusion (HRVO) occurs when blockage is in a vein that drains the superior or inferior hemiretina
135
Q

sudden vision loss that may present w

Possible unilateral numbness, weakness, slurred speech if related to carotid disease

a form of stroke

A

retinal a occlusion

136
Q

si/sx of GCA

A
  • New temporal headache
  • Abrupt transient monocular vision disturbance
  • Jaw claudication
  • Fever, anemia, other constitutional symptoms
137
Q

risk factors for rental v. occlusion

A

HTN, diabetes, sickle cell anemia, conditions that slow venous blood flow.

138
Q

_____ ______ is often described as papilledema but should NOT be

A

Hypertensive Retinopathy

139
Q

normal intracranial pressure

A

(Normal Pressure: 70 - 180 mm H20)

Clin med II Eye and Cardio (2 decks)

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