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ICM Unit 3 HEENT > Eye Manifestation of Systemic Diseases > Flashcards

Eye Manifestation of Systemic Diseases Flashcards

1
Q

Uveal tract and sclera

A

Episcleritis, Scleritis, Uveitis

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2
Q

Vascular Disorders

A

Retinal vein occlusion
Retinal artery occlusion - ischemic optic neuropathy
Temporal arteritis

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3
Q

Retinopathy

A

Diabetic retinopathy
Hypertensive retinochoroidopathy (incl optic disc swelling)
HIV: HIV retinopathy and CMV Retinitis
Blood dyscrasias

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4
Q

Neuropathy/Neuritis

A

Optic Neuritis and ischemic optic neuropathy

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5
Q

simple anatomy

A

medial canthus
lateral canthus
eyelids
conjunctiva (bulbar and palpebral)
cornea (corneal limbus)
Iris
Pupil
Sclera
Meibomian gland

Be able to ID

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6
Q

What is the ciliary body, choroid and iris together called?

A

Uveal tract/ middle of the eye

(vascular layer according to anatomy)

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7
Q

Retina receives a dual blood supply, with the inner retina supplied by the

A

central retinal artery

from ophthalmic artery from internal carotid a.

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8
Q

the outer reti­na supplied by the choroidal circulation

A

via branches of the posterior ciliary arteries

ophthalmic artery branch as well

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9
Q

History questions of importance

A

Photophobia (have lights been bothering your eyes before or after this in the past?)

Diplopia (double vision)

Have you ever had visual loss of both or one eye(s) at the same time?

Haziness of vision

Flashing or flickering of lights/floaters

Decreased vision

Medical Illnesses

Headache? (did you have a HA associated with this before or after these events? Do you have a HA now?)

Pulsating artery near the temple?

Arthralgias?

Nausea/Vomiting

Tearing

Eye irritation (dryness, foreign body sensation, drainage, pruritis)

Any recent medication changes

Do you wear contacts or glasses?

Recent trauma to the eye?

Last 2 should be primary questions

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10
Q

Episcleritis

A

Inflammation localized to the episclera
Typical young – 30’s-40’s
Benign, recurrent and usually self-limiting

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11
Q

Episcleritis increased risk individuals

A

Anyone

Gout, allergic rhinitis, autoimmune (RA, IBD, SLE) (30% will have other autoimmune d/o

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12
Q

Episcleritis - Clin Findings

A

Often sudden onset with red eye, and minor discomfort (not usually painful)

Irritation
Redness (Dilatation of the episcleral vessels)
Watering of eye
Pain is unusual unless associated nodule or is chronic in nature

No affect to vision

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13
Q

Episcleritis - Tx (in order)

A

IN ORDER

Artificial tears
Topical NSAID’s/Oral NSAID’s
Ophthalmology

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14
Q

Scleritis

A

Much more severe of a condition if found

Worse symptoms – especially pain

Can result in structural damage to eye and more association with an underlying condition

Average age of onset ~ 48 but range is high

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15
Q

2 types scleritis

A

Anterior and Posterior

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16
Q

Scleritis causes - autoimmune

A

RA (Rheumatoid arthritis)
SLE (Systemic Lupus Erythematosus)
UC (Ulcerative Colitis)
PsA (Psoriatic arthritis)
Vasculitis

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17
Q

Scleritis causes - infections

A

TB
Syphilis
HSV
HZV
Pseudomonas
Staph/Strep

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18
Q

other causes Scleritis

A

Sarcoidosis
Chemical/Physical agents (burns, acid/alkali)
Trauma
Lymphoma
Gout

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19
Q

Scleritis - Clin Findings (anterior)

A

Boring or piercing pain, even at night

Scleral inflammation with painful EOM’s

Deep violaceous discoloration of the globe often with edema

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20
Q

Scleritis - Clin Findings (Posterior)

A

Involves nonvisible portion of sclera (so sclera is usually white) and can potentially cause blindness

Pain (most but not all)

Visual disturbances such as blurring, diplopia

Visual loss

Proptosis

Optic disk swelling

VERY DIFFICULT TO DIAGNOSE CLINICALLY

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21
Q

Scleritis Dx and Tx

A

Refer to ophtho

Ask questions that may indicate systemic disease (fevers, arthralgias, rashes, etc.)

They will perform specialized testing and slit lamp exam
B-Scan US (looks for edema)
Possible CT/MRI scan

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22
Q

Uveitis (uvea=?)

A

iris, ciliary body, choroid

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23
Q

Uveitis

A

Inflammation of the “middle layer” of the eye (intraocular)

Usually immunologic but possibly infective or neoplastic

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24
Q

4 catergories of Uveitis

A

Anterior, Intermediate, Posterior, Pan uveitis

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25
Q

Iritis

A

Leukocytes/inflammation in the anterior chamber of eye

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26
Q

Cyclitis

A

Leukocytes/inflammation in the middle chamber of eye (intermediate)

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27
Q

Retinitis, choroiditis

A

Leukocytes/inflammation in posterior chamber

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28
Q

Diffuse uveitis

A

Leukocytes/inflammation in all areas of uvea

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29
Q

Uveitis associated more commonly with

A

Systemic inflammatory conditions = (RA, Spondyloarthropathies - AS, Reiter’s syndrome) Psoriatic arthritis, IBD, Sarcoidosis, LE, Sjogren’s)

Other causes – Infections – HSV, CMV, Zika, Cat-Scratch, TB, etc.

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30
Q

Uveitis- Clin Findings

A

generally most often anterior

Pain
Photophobia
Blurred vision
(note posterior may be painless and only have floaters and/or visual loss)

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31
Q

Uveitis - exam

A

Small and/or irregular pupil
Circumcorneal redness
Inflammatory cells or debris may be noted in anterior chamber

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32
Q

Uveitis - Tx

A

Refer to ophthalmology!!

Needs detailed medical history

May need testing according to potential associations (i.e. autoimmune, infectious)

Topical steroids (prednisolone acetate); Cycloplegics/mydriatics (homatropine) – for anterior

Intraocular injections (variable, often steroids) for the remainder

If infectious – treat infectious cause – anti-virals/anti-biotics/anti-parasitics

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33
Q

Transient monocular blindness
(ocular TIA)

A

Monocular vision loss (amaurosis fugax), lasting a few minutes (5-10) with complete recovery

Characteristically: curtain passing vertically across the visual field with complete monocular visual loss lasting a few minutes and a similar curtain effect as the episode passes (which is called “amaurosis fugax” or fleeting blindness

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34
Q

Transient monocular blindness (ocular TIA)
Potential causes

A

Retinal emboli from ipsilateral carotid disease

Central Retinal Artery Occlusion

Giant Cell Arteritis (Temporal arteritis)

Also: Cardiogenic emboli (often with associated atrial fibrillation); Retinal Migraine; Anti-coagulant deficiency states (Protein C, S or others)

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35
Q

Transient monocular blindness (ocular TIA) -
Risk factors

A

HTN
HLD
DM
Atrial fibrillation

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36
Q

Transient monocular blindness (ocular TIA) -
Tx

A

Needs to be treated as a TIA (transient ischemic attack)

ASA 81 mg

Refer immediately to ophthalmology - ED first

Must consider ipsilateral carotid artery stenosis - Carotid US and possible stenting or endarterectomy if needed

ECHO to determine any other abnormalities of heart
Inflammatory markers (CRP/ESR)

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37
Q

Central Retinal Artery Occlusion - Clin Findings

A

Sudden monocular loss of vision (Amaurosis fugax)

Profound….reduced to counting digits or worse,

No pain or redness

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38
Q

Central Retinal Artery Occlusion -
Ophthalmic exam

A

Widespread or sectoral retinal PALLID SWELLING and a CHERRY RED SPOT at the fovea (perifoveal atrophy)

Retinal ARTERIES ATTENUATED (thin), “BOX-CAR” segmentation of blood in the arteries or venules (separation of arterial flow)

Always consider Giant Cell Arteritis (Temporal Arteritis) in patients > 50 yo. Commonly associated with PMR – Polymyalgia Rheumatica (autoimmune)

39
Q

Central Retinal Artery Occlusion -
Tx and referral

A

transient monocular blindness” is a TIA – Treat as such!

Evaluate for Giant Cell Arteritis (if no visible emboli)

Emergent optho referral; Prognosis depends

40
Q

Central Retinal Artery Occlusion -
Tx other options

A

Anterior chamber paracentesis (reduces pressure)

Place patient flat -ocular massage, and high concentration of oxygen administration

IV acetazolamide (Diamox), and/or topical pressure lowering eye drops to reduce intra-ocular pressure (IOP)

Possible thrombolytics

41
Q

Central Retinal Artery Occlusion -others to order

A

Search for sources of carotid and cardiac emboli (this is essentially a stroke)

Check for HTN, DM, HLD, other risk factors
- Duplex US of carotid arteries, ECG, Echocardiography, +/- CT or MRI for carotid artery dissections

42
Q

Temporal artheritis (Giant cell arteritis)

A

Inflammation of the blood vessels around the scalp (often large vessels)

Occurs most often in elderly (>75)

50% found in patients with rheumatic condition – polymyalgia rheumatica

43
Q

Temporal artheritis (Giant cell arteritis)

Clinical findings

A

Headache
Amaurosis fugax
Fever/fatigue
Myalgias
Scalp tenderness/nodularity of artery
Jaw Claudication
Often (not always), tender temporal artery
Some patients can have aneurysms of the subclavian, carotid, basilar and other arteries

44
Q

Temporal artheritis (Giant cell arteritis)

Dx

A

Inflammatory markers (CRP and ESR) – very high
WBC – often normal
Liver function test (alkaline phosphatase)
Ultrasound

45
Q

Temporal artheritis (Giant cell arteritis)

Tx

A

Urgent -> Go to ED
Prednisone (~80mg) then continue for 1 mo
Needs a temporal artery bx

46
Q

Retinal Vein occlusion - 2 types

A

BRVO - Branch of retinal vein

CRVO - central retinal vein

“blood and thunder”

47
Q

Retinal Vein occlusion

A

Blockage of small veins (BRVO) occurs where retinal arteries that have been thickened/hardened by atherosclerosis cross over and place pressure on a retinal vein; also caused by other types of ischemia/thrombosis

Blockage of central vein (CRVO)

48
Q

Retinal Vein occlusion
Clinical findings

A

Sudden monocular loss of vision, commonly first
noted upon awakening (CRVO)

No pain or redness

Poor visual acuity (20/200 or worse)

49
Q

Retinal Vein occlusion - exam

A

Central:
Widespread or sectoral RETINAL HEMORRHAGES

Retinal venous dilation and tortuosity

Retinal cotton wool spots and optic disk swelling (i.e. papilledema)*

50
Q

Retinal Vein occlusion - tX

A

BRVO and CRVO) All patients with RVO should be assessed for DM, HTN, Hyperlipidemia and glaucoma

Tx: REFER!!! (really….laser treatment to prevent growth of new, abnormal blood vessels)

Intravitreal injections of anti-VGEF

May regain useful vision, however vision rarely returns to normal

51
Q

Treatment of vascular disorders- SUMMARY

A

Control disease processes

Assess vascular risk factors (HTN, DM, A-fib, etc.). If found often need anti-coagulants

Occlusions: prompt referral to ophthalmologist for revascularization procedures immediately

52
Q

Diabetic Retinopathy

A

Present in about 33% of Type 2 diabetic patients at time of diagnosis

Risk of development is highest in Type I DM (60-75%)

Most common microvascular complication of diabetes

Primary Risk factors
- Duration of diabetes
- Level of control

53
Q

Diabetic Retinopathy - Types

A

Nonproliferative (Background) retinopathy:
- Mild retinal abnormalities without neovascularization or visual loss
- Small hemorrhages, microaneurysms, hard exudates

Proliferative retinopathy (less common):
- new retinal vessels; causes more severe visual loss

54
Q

Diabetic Retinopathy - Proliferative Clin Pres

A

“neovascularization” from the optic disk or major vascular arcades

Proliferation into the vitreous of blood vessels, -> tractional retinal detachment

Untreated, the prognosis is much worse than non-proliferative disease

55
Q

Diabetic Retinopathy -Tx

A

Focused on PREVENTION

Control DM tightly
Educate patient on risks of NOT controlling DM
Treat HTN and HLD
Annual eye exams with Optometrist +/- ophthalmologist (visual acuity PLUS fundoscopy/retinal scan)

Proliferative retinopathy is usually treated by pan retinal laser photocoagulation

Other options for some include vitrectomy
Injections (specialized anti-VEGF – monoclonal antibody)

56
Q

Diabetic retinopathy - summary

A

All diabetic patients with sudden loss of vision or retinal detachment should be referred emergently to an ophthalmologist

Proliferative retinopathy or macular involvement requires urgent referral to an ophthalmologist

Severe nonproliferative retinopathy or unexplained reduction of visual acuity requires early referral to an ophthalmologist

57
Q

Hypertensive Retinopathy - General

A

Systemic HTN affects both retinal and choroid circulation

Clinical symptoms vary with how fast the BP rises and the underlying state of HTN (how long the damage has been present)

58
Q

Hypertensive Retinopathy - Chronic HTN changes in eye

A

Copper-wire changes = retinal arterioles more tortuous and narrow and develop abnormal light reflexes

AV nicking = increased venous compression at the retinal A/V crossings

Flame shaped hemorrhages = occur in the nerve fiber layer of retina

Chronic HTN accelerates atherosclerosis (everywhere in the body)

59
Q

Hypertensive Retinopathy - Pathogenesis

A

Acute elevations in BP (aka hypertensive crisis) +/- atherosclerosis**

Loss of autoregulation in the retinal circulation causes breakdown of endothelial integrity and occlusion of precapillary arterioles and capillaries

60
Q

Hypertensive Retinopathy - Clin findings

A

retinal manifestations = cotton wool spots; retinal hemorrhages, edema, exudates (flame)

Choroid manifestations = retinal detachment and retinal pigment infarcts; may have optic disc swelling

61
Q

Hypertensive Retinopathy - Tx

A

Need to get HTN under control

Refer to ophthalmology – findings in eye can resolve over weeks/months with proper treatment

62
Q

HIV Retinopathy

A

Most common ophthalmic abnormality in HIV

63
Q

HIV Retinopathy Manifestations

A

Cotton-wool spots
Retinal hemorrhages
Microaneurysms

64
Q

CMV retinitis

A

Less common w/use of ART
Prevalent when CD4 <50

65
Q

CMV retinitis - clinical findings

A

Progressively enlarging yellowish-white patches of retinal opacity w/retinal hemorrhages

Asymptomatic until involvement of fovea or retinal detachment occurs

The initial symptoms of CMV retinitis typically include one or more of the FOUR “F’s”: ((floaters, flashes, field deficits, or failing vision))

66
Q

CMV retinitis - TX

A

Needs infections disease and ophthalmology consultation

67
Q

Other HIV associated infxns of eye

A

Herpes simplex retinitis
Toxoplasmosis
Herpes zoster retinitis
Kaposi’s sarcoma of conjunctiva
Candida

68
Q

Blood Dyscrasias

Severe Anemia/Thrombocytopenia

A

(Retinal and Choroidal hemorrhages)

69
Q

Blood Dyscrasias

Leukemia and Endocarditis

A

“ROTH SPOTS”

cotton wool spot surrounded
by hemorrhage

70
Q

Blood Dyscrasias

Sickle Cell Retinopathy

A

“salmon patch”-

“black sunbursts”

71
Q

Optic Neuritis

Most common etiology is…

A

Multiple Sclerosis (demyelinating disease)

(also lupus, sarcoidosis, complications of varicella infection, encephalitis, and others)

Up to 50% of patients who develop optic neuritis will develop MS within 15 years

In 20-30% of patients who present with MS, optic neuritis is first manifestations

72
Q

Optic Neuritis - Clinical Findings

A

Subacute/Acute unilateral visual loss (w/ signs of optic dysfunc)

Pain: “behind” the eye, worse with EOM

Optic disc usually normal in acute stage but subsequently develops pallor

Later - Optic disc swelling if condition worsens w/flame-shaped peripapillary hemorrhages

73
Q

Optic Neuritis - Tx

A

Refer to ophthalmology
IV Prednisone and then oral prednisone

74
Q

Optic Neuritis - Prognosis

A

Visual acuity usually improves within 2-3 weeks and returns to 20/40 or better for 95%;

if not CT/MRI of head and orbits to exclude lesion compressing optic nerve

75
Q

Graves Ophthalmopathy

A

Related to autoimmune HYPERthyroid disease (Graves)

Dysthyroid eye disease/Exophthalmos

76
Q

Graves Ophthalmopathy - Pathogenesis

A

deposition of mucopolysaccharides and infiltration with chronic inflammatory cells of the orbital tissues, esp. extraocular muscles

Worsened by: Radioactive iodine or smoking cigarettes

77
Q

Graves Ophthalmopathy - Clin findings

A

pt complaints = Surface irritation, dry eyes, diplopia

78
Q

Graves Ophthalmopathy - Exam

A

Proptosis
Lid retraction
Lid lag
Conjunctival chemosis (swelling)
Episcleral inflammation
Extraocular muscle dysfunction (diplopia)

79
Q

Graves Ophthalmopathy - Complications

A

Marked visual loss
Corneal exposure
Optic nerve compression

80
Q

Graves Ophthalmopathy - Tx

A

Artificial tears, “prisms” (special eyeglass lens to stop diplopia)

Selenium 100 mcq daily to reduce progression

Control of thyroid hormone

IV pulse prednisone, immunotherapy

If Optic Nerve compression or severe corneal exposure: Surgical decompression

Lid surgery if significant proptosis

81
Q

Papilledema - Clin Findings

A

Swelling of the optic disc that reflects increased intracranial pressure

Often bilateral

82
Q

Papilledema

Must find and treat underlying cause of …

A

intracranial pressure (encephalitis, hemorrhage, tumor, abscess, glaucoma, etc.)

Think of uncontrolled hypertension

83
Q

Nystagmus

A

Repetitive, uncontrollable movements of the eyes

84
Q

Nystagmus types

A

Horizontal
Vertical
Rotary

85
Q

Nystagmus caused by

A

abnormal function in the areas of the brain that control eye mvmts

Part of inner ear that senses mvmt and position helps control eye mvmts (labyrinth)

86
Q

Nystagmus etiology

A

can be congenital and acquired

MCC of Acquired is certain drugs or medication

Dilantin (anti-seizure), MDMA ecstasy), Alcohol, SSRI’s (i.e.. Lexapro, Prozac, Zoloft) benzodiazepines (i.e. Xanax, Valium, Ativan)

87
Q

other causes Nystagmus

A

Head injury
Stroke
BPPV
Retina or optic nerve disorders

88
Q

Nystagmus Classifications

A

Pendular = speed of mvmt of eyes is in same in both directions

Jerk = eyes move slowly in one direction and then quickly “jerk” back in the other direction

89
Q

Central nystagmus (Brain)

A

either normal or abnormal processes not related to the vestibular organ

ex) lesions of the midbrain or cerebellum can result in up- and down-beat nystagmus

90
Q

Peripheral nystagmus (Usually inner ear)

A

either normal or diseased functional states of the vestibular system

may combine a rotational component with vertical or horizontal eye movements and may be spontaneous, positional, or evoked.

91
Q

nystagmus - Clin FIndings

Peripheral : otologic related

A

Otitis media, BPPV (benign paroxysmal positional vertigo, Meniere’s disease, labyrinthitis

Comes on quickly
Hearing loss
Ear pain
Ear drainage
Tinnitus
Vertigo (spinning sensation)

Nystagmus stops with visual fixation and unidirectional (not vertical)

92
Q

nystagmus - Clin FIndings

Central : Brain related

A

Brainstem stroke, MS, ischemic changes to cerebellum, tumor

Headache
Visual changes
Difficulty with swiping on phone
Motion sensitivity
TV (news ticker at the bottom)
Gait issues (i.e.. Wide based gait)

Nystagmus can be in multiple directions (including vertical) and does not stop with visual fixation

93
Q

Nystagmus Tx

A

depends on cause

ICM Unit 3 HEENT (6 decks)

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