Ocular Manifestations of Systemic disease Flashcards

1
Q

Where do the branching of the vasculature always point to in the eye?

A

the optic disc

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2
Q

What is the basic pathology for hypertensive retinopathy?

A

progressively increasing retinal microvascular changes

Rarely by itself causes significant vision loss

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3
Q

Changes in mild hypertensive retinopathy?

3

A
  1. Retinal artery narrowing (Due to vasospasm)
  2. Arterial wall thickening or opacification (start to get lighter)
  3. Arteriovenous nicking—referred to as “nipping” (artery will cross over vein and because pressure is higher the vein will bulge out)
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4
Q

What is vasospasm?

A

sudden constriction of a blood vessel, reducing its diameter and flow rate.

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5
Q

Changes in moderate hypertensive retinopathy?

4

A
  1. Hemorrhages—either flame or dot shaped
  2. Cotton-wool spots (retinal nerve fiber layer microinfarcts/damage)
  3. Hard exudates (lipid residue from serous leakage from damaged capillaries)
  4. Microaneurysms (bulges in the retina)
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6
Q

Changes in severe hypertensive retinopathy?

A

Some or all of the symptoms in moderate hypertensive rentinopathy and:
1. optic disc edema (cant see the borders very well/yellow) or papilledema

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7
Q

The presence of what mandates lowering of the blood pressure?

A

papilledema

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8
Q

Early hypertensive retinal changes produce what?

A

flame shaped hemorrhages

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9
Q

Long standing hypertension can produce what?
3

the again in your own words

A
  1. arteriolar sclerotic changes w/ arteriolar narrowing (copper wiring= darker branching)
  2. AV nicking

In your own words:

  1. narrowing or hardening of the vessels in the eye that make them darker
  2. AV nicking (artery crosses over vein and makes it buldge on both sides)
  3. silver wiring- arteriolar sclerosis is getting worse/reflecting light more.
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10
Q

Symptoms of HTN retinopathy?

3

A
  1. vision normal or blurred or sudden decrease;
  2. scotoma (waves/spotting visual changes);
  3. diplopia
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11
Q

Signs of HTN retinopathy?

4

A
  1. arteriolar narrowing in chronic HTN
  2. focal spasm in acute HTN
  3. retinal edema
  4. microaneurysm may rupture produce sudden vision loss from hemorrhage
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12
Q

What do we do as a primary care provider to treat HTN retinopathy?

A

control the hypertension- it may reverse some of the effect of the retinopathy. But for everything else involved with it refer to a ophthalmologist

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13
Q

what are ghost vessels?

A

neovascularization of the cornea. (generally in response to a lack of oxygen due to the sclerosis)

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14
Q

AV nicking is what?

A

ischemia

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15
Q

Swelling of the optic disc (papilledema) is a hallmark sign of what kind of pathology?

What is this patient at risk for?
5

A

malignant hypertension

Patient w/ malignant HTN is at risk of developing

  1. heart failure and
  2. renal failure,
  3. stroke, and
  4. hypertensive encephalopathy
  5. if not controlled blindness
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16
Q

Most common ocular manifestation of intracranial HTN is what?

A

optic disc swelling -papilledema

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17
Q

How will vision be affacted by intraccranial hypertension?

A

Visual sxs are transient: can range from mild blurring to complete visual loss, usually lasting only a few seconds

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18
Q

What does a yellow area of the eye indicate?

A

ischemia -larger area

in other slides floaters

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19
Q

Common causes of intracranial hypertension?

7

A
  1. brain tumor
  2. Venous sinus thrombosis (clot)
  3. Meningitis
  4. Hydrocephalus (too much CSF)
  5. pseudotumor cerebri (acts like a tumor-idiopathic in nature)
  6. Tetracycline therapy (used for UTI)
  7. Steroid withdrawal
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20
Q

What is the leading cause of new blindness in the US?

A

diabetic retinopathy

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21
Q

What is the pathology of diabetic retinopathy?

A

sugar in the blood deposits in the vessels starting with the small ones (in the eye for example)

-excess glucose binds with free amino acidsforming irreversible advanced glycolsylation end products (AGEs)

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22
Q

What do high advanced glycolsylation end products (AGEs) result in?

A

high tissue levels of AGEs which can then crosslink with collagen and initiate microvascular complications (blockages)

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23
Q

What does microthrombosis lead to in diabetic retinopathy pathology?

A

leads to capillary thrombosis and then to capillary leakage (blockage = back up and leakage)

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24
Q

What does vascular endothelial growth factor cause (VEGF)?

A

can be excessively synthesized leading to the overgrowth of new blood vessels (neovascularization) - just causes problems = causes pressure in the eye that could lead to glaucoma

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25
Q

Where are VEGFs synthesized?

A

in the retina

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26
Q

What are the symptoms of diabetc retinopathy?

how could it affect vision

A
  1. some patients w/ severe disease can have 20/20 vision
  2. blurring slowly or suddenly
  3. visual distortion (things may appear crooked or wavy)
  4. floaters which can be from vitreous hemorrhage—described as “shower”
  5. scotomata
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27
Q

What is indicated if the patient is showing signs of diabetic retinopathy?

A

Annual exam by ophthalmologist and immediate exam for any new visual symptoms or changes!

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28
Q

What are the types of diabetic retinopathy?

3

A

Early nonproliferative retinopathy
Advanced nonproliferative retinopathy
Proliferative retinopathy

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29
Q

AV nicking =

A

microaneurysm

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30
Q

Symptoms that occur in Early nonproliferative retinopathy?

3

A
  1. microaneurysms, and
  2. intraretinal hemorrhages
  3. Cotton wool spots
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31
Q

How is early nonproliferative retinopathy graded?

A

mild, moderate and severe

32
Q

What are little white spots in the eye?

A

lipid deposits

drusen

33
Q

What symptoms often present in advanced nonproliferative retinopathy?
3

A

Cotton wool spots
Extensive retinal hemorrhaging
area of ischemia

34
Q

What is responsible for the most devastating loss in DM?

A

proliferative retinopathy

35
Q

What symptoms often present in proliferative retinopathy?

3

A
  1. Vitreous hemorrhage, and
  2. tractional retinal detachment
  3. Neovascularization:
36
Q

In proliferative retinopathy neovascularization is not just confined to the retina. Where else can it be found? 2

What does this cause?

A

surface of the iris (rubeosis irides) and the trabecular meshwork (located near the base of the cornea= drains aqueous humor), blocking aqueous outflow and causing a very dangerous form of glaucoma (neovascular glaucoma).

37
Q

Treatment of proliferative retinopathy?

As a primary care PA what are we going to do to treat them?

A
  1. photocoagulation fpr macular edema (stops leaking vessels and vision from getting worse-cant fix it)
  2. Intraocular injection of growth hormone to try to repair it

treat theur blood sugars, get A!C down and treat their diabetes

38
Q

Describe Photocoagulation for Proliferative Diabetic Retinopathy

A

The laser is used to place 1000-2000 burns in an evenly distributed scatter-pattern across the entire retina except at the macula
These burns ablate the retinal tissue and cause the proliferating vessels to disappear

39
Q

What is a vitrectomy used for?

A
  1. Used to remove nonclearing vitreous hemorrhage and to treat or prevent retinal detachment
40
Q

How is it done?

A
  1. Vitreous removed, fibrous bands are cut, and endophotocoagulation may be performed to destroy new retinal vessels
41
Q

Whats a risk factor for grave’s opthalmopathy?

A

smoking

42
Q

Describe the pathogenesis of Grave’s ophthalmopathy?

A

activation of T lymphocytes result in inflammation and infiltration of the orbital connective tissue. The inflammation results in a deposition of collagen and glycosaminoglycan’s in the muscles, which leads to subsequent enlargement and fibrosis
(inflammation of eye msucles push out the eye)

43
Q

What is the most commly affected muscle in Grave’s Ophthalmopathy?

What movement does it restrict and what does it result in?

A

Inferior rectus muscle

restricts upward-gaze
results in vertical diplopia

44
Q

Signs of Grave’s Ophthalmopathy?

2

A
protosis
Periorbital edema (tissue around the eye is swollen)
45
Q

Visual symptoms of Grave’s Ophthalmopathy?

A
  1. Excessive tearing, conjunctivitis, eye or retroorbital pain
  2. Blurred vision, vertical diplopia and occasionally loss of vision
46
Q

Vertical diplopia where are the two images in relation to each other?

A

side by side

47
Q

Complications with proptosis?

2

A

dry eyes

corneal ulceration

48
Q

EOM impairments with grave’s ophthalmopthy?

3

A
  1. Diplopia
  2. Inability to achieve upward vision
  3. Inability to achieve or maintain convergence
49
Q

In a primary care setting how would we treat grave’s ophthalmopthy?

A

Treat underlying hyperthyroidism: surgery or meds*

50
Q

How would we treat the mild symptoms of grave’s ophthalmopthy?

A

dark glasses
artificial tears
Raise the head of the bed and see if gravity helps with closing lids

51
Q

How would we treat severe symptoms of grave’s ophthalmoopathy?
2

A

Glucocorticosteroids—IV or oral**

If vision threatened—radiation then surgery

52
Q

Name the Autoimmune disorder characterized by weakness and fatigue of skeletal muscles

A

Ocular Myasthenia Gravis

53
Q

What is the pathology of Ocular Myasthenia Gravis?

A

Due to dysfunction at the neuromuscular junction:
AChR-Ab (acetyl choline receptor-antibodies)- Ach helps with contraction so in OMG the muscles are relaxed all the time = paralysis (eyelid droop)
Usually only 45-60% positive in OMG

54
Q

In OMG what is ptosis due to?

A

weakness of levator palpebrae superioris

55
Q

In OMG what is binocular diplopia due to?

A

Ophthalmoparesis (weakness of the extraocular muscles)

56
Q

How do we treat OMG?

4

A

Symptomatic—anticholinesterase meds
Chronic immunomodulating
Rapid immunomodulating
Surgical—remove thymus

57
Q

One of the first signs of OMG?

A

eyelid drooping

58
Q

Whats the most common pathology of the eye in HIV pateints?

A

cotton wool spots

59
Q

Infections of the eye that are opportunistic of HIV?

2

A

CMV retinitis

Toxoplasmosis

60
Q

What is the most common serious ocular complication of AIDS?

A

CMV

Cytomegalovirus infection

61
Q

What does CMV cause?

A

retinal detachment

62
Q

Is CMV unilateral or bilateral usually?

A

Starts out unilateral but can become bilateral if not treated

63
Q

Symptoms of CMV?

4

A

floaters,
decreased or blurred vision, scotoma,
photopsia (“flashing lights”)

64
Q

Whats the differential for CMV?

2

A

toxoplasmosis, HIV retinopathy (cotton wool spots & retinal hemorrhages)

65
Q

Whats the treatment for CMV?

2

A

anti-HIV meds,

IV or intravitrial antivirals (such as ganciclovir) or implants of drug

66
Q

What is a potentially blinding, nectrotizing retinitis?

A

Toxoplasmosis

67
Q

Symptoms of toxoplasmosis?

4

A

wavy or distorted vision (metamorphopsia),
floaters,
pain-variable,
decreased or blurred vision

68
Q

Signs of toxoplasmosis?

5

A
  1. may see old scars,
  2. vitreous debris,
  3. yellow-white areas on retina, 4. optic nerve yellow-white &
  4. swollen, macular edema
69
Q

Treatment of toxoplasmosis?

Triple therapy plus alternative therapy listed

A
  1. Pyrimethamine,
  2. sulfadiazine with folate,
  3. corticosteriods (“Triple therapy”)

Alternatives : clindamycin, azithromycin, or Bactrim

70
Q

When would herpes zoster infection involve the retina?

A

immunocompromised pt—such as HIV/AIDS pt or pregnant woman

71
Q

What can herpes zoster infection cause?

A

acute retinal necrosis

72
Q

Symtpoms of acute retinal necrosis caused by HZI?

A

dereased vision

73
Q

How would we diagnose and treat patient with acute retinal necrosis?

A

immediate fundoscopic exam and referral for treatment as potentially blinding

74
Q

What would dark hemorrhages on the retina in babies indicate?

A

shaken baby syndrome (takes severe force to accomplish)

75
Q

How would we diagnose shaken baby symdrome from the eye?

A

A fundoscopic examination may reveal preretinal, intraretinal, or vitreous hemorrhages

76
Q

Further Rheumatological Differential of Ocular Disease?

8

A
Sjogrens Syndrome
Systemic Lupus Erythematosus (SLE)
Behçet's disease
Giant cell arteritis
Granulomatosis with polyangiitis (Wegener's)
Polyarteritis nodosa
Inflammatory bowel disease
Sarcoidosis