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Clinical Medicine 2 > Lecture 13 (HEENT)-Exam 4 > Flashcards

Lecture 13 (HEENT)-Exam 4 Flashcards

1
Q

Nystagmus:
* What is this?
* What are the two types?
* What is the primary symptoms?
* What happens to vision?
* Numerous what?
* How can you get it?
* What is txt based on?

A
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2
Q

What are the three types of nystagmus mvts?

A
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3
Q

Optic Neuritis
* What is it?
* Highly assoicated with what? Presenting in how many cases?
* What is the pathophysio?
* What is the etiology?

A
  • Inflammatory demyelinating condition that causes typically monocular vision loss.
  • Highly associated with Multiple Sclerosis
  • Presenting feature in up to 15% of cases of MS
  • Pathophysiology – demyelination of the optic nerve
  • Etiology – unknown – thought to be autoimmune
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4
Q

Optic Neuritis- Clinical Presentation
* Usually what?
* Vision loss over what?
* What type of pain?
* What may be present?

A
  • Usually monocular
  • Vision loss over a matter of hours to days
  • Eye pain (worse with movement)-> but not any infection
  • Numerous visual deficits may be present
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5
Q

Optic Neuritis
* What happens to light?
* Loss of what?
* What type of pain?

A
  • “Photopsias” – flickering light, flashes of light
  • Loss of color vision out of proportion to loss of vision characteristic of optic nerve pathology.
  • Unilateral painful loss of vision in an adult less than 50 years old

under slide: older patient (>50 years), ischemic optic neuropathy (due, or example, to diabetes mellitus or giant cell arteritis) is a more likely diagnosis than optic neuritis.

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6
Q

Optic Neuritis-
* How do you diagnosis?
* What does it require?
* Confirmed via what?

A
  • Clinical diagnosis
  • Requires an ophthalmologic exam
  • Confirmed via MRI with gadolinium contrast.

Multiple lesions, more suggestive of MS

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7
Q

Optic Neuritis- Prognosis & Treatment
* Typically worsens over what?
* Without treatment,
* What are the MRI findings?
* patients with what will have worse prognosis?
* In adults, 30% will have?
* 50% of MC patients experience?

A
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8
Q

Optic Neuritis-
* What is the txt?

A

IV corticosteroids in some patients (severe vision loss, multiple lesions on MRI) - thought to delay onset of MS

intravenous methylprednisolone

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9
Q

Papilledema
* What it is?
* Any entity that increases what? What are examples?

A
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10
Q

What is this?

A

Papilledema

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11
Q

Papilledema-Clinical Presentation
* Always what?
* Uni or bilateral?
* Usually found when?
* If evaluating a hypertensive emergency – this is what?

A
  • Always abnormal finding
  • Nearly always bilateral
  • Usually found when evaluating conditions causing increased intracranial pressure.
  • If evaluating a hypertensive emergency – this is a pertinent positive, or negative.
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12
Q

Papilledema-Clinical Presentation
* What are the sx?

A
  • Headache (worse lying down and in AM), nausea, vomiting.
  • Horizontal diplopia
  • Pulsatile machinery-like sound in the ear

pulsatile machinery-like sound in the ear, probably due to venous sinus obstruction

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13
Q
A

high-grade disc edema, peripapillary subretinal hemorrhages
* Early-The optic cup is retained when the papilledema is mild. However, splinter hemorrhorrahges
* Fully developed-ptic disc becomes elevated, the cup is obliterated, and the disc margins become obscured. Blood vessels are buried as they course the disc. Serpentine engorgement of retinal veins is evident, and the disc appears hyperemicages in the nerve fiber layer, at or beyond the disc margin, may be seen early
* Chronic—The central cup remains obliterated. Hemorrhagic and exudative components resolve. The appearance of hard exudates in the nerve fiber layer indicate a process of some months’ duration.

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14
Q

What is this?

A
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15
Q

Papilledema- Diagnosis & Treatment
* How do you dx?
* What is the treatment?
* Evalute with what?
* If normal imaging, consider what?
* Refer where?

A
  • Detected on fundoscopic exam
  • Treatment based on etiology
  • Evaluate with MRI with gadolinium contrast (CT if access to MRI limited)
  • If normal imaging, consider LP with opening pressures
  • Refer fast!
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16
Q

Papilledema
* Often what?
* Permanent what is common?
* What people carry higher risk for porr prognosis?

A
  • Often impending morbidity/mortality if untreated
  • Permanent loss of vision is common if untreated or unresponsive to treatment.
  • Anemia, old age, glaucoma and systemic hypertension carry higher risk for poor prognosis
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17
Q

Macular Degeneration
* What type of vision loss?
* What is it the leading caue of?
* What are the two cases?

A
  • Central vision loss
  • Age related MD is leading cause of adult blindness OVER 60 years
  • Classified as “dry” – atrophic, or “wet” – neovascular
  • Dry =85-90% of cases
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18
Q

Dry Acute Macular Degeneration- Exam
* What spots are present and what are they?
* What do large or small sports associated with?

A
  • “Drusen” spots – deposits of extracellular material typically in the macula – small, bright yellow. May be hard, calcific or soft.
  • Large, soft Drusen associated with vision loss
  • Small, hard Drusen observable in most humans over age 50
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19
Q

What is this?

A
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20
Q

Wet Acute Macular Degeneration
* Growth of what?
* Vessels leak causing what?
* More common than what?

A
  • Growth of abnormal vessels into the subretinal space
  • Vessels leak causing collections blood beneath the retina (subretinal hemorrhage)
  • More common than Dry AMD in patients with severe visual loss (cannot see at all)
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21
Q

What is this?

A
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22
Q

Macular Degeneration
* What are the biggest risk factors?

A
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23
Q

Macular Degeneration - Clinical Presentation
* What happens early?
* What are dry sx?

A
  • Asymptomatic early

Dry= slow central vision loss
* First signs – difficulty reading or driving
* Scotomas
* Blurry spots (blind spots)

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24
Q

Macular Degeneration
* What are the sx of wet?

A

Wet=slow OR sudden changes in vision
* May initially be unilateral, progress to bilateral
* may present with loss of central vision and distortion of straight lines

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25
Q

What is this?

A
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26
Q

Macular Degeneration -Diagnosis
* How do you dx it?
* What happens to vision?
* Vision loss over days and weeks requires what?

A
  • History and dilated fundoscopic exam (drusen spots, hemorrhages)
  • Gradual vision loss is detected by careful history
  • Vision loss over days and weeks requires immediate ophthalmology referral
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27
Q

Macular Degeneration -Treatment
* Refer to who?
* What is the txt for dry?
* What is the txt for wet?
* What patients take?

A

VEGF inhibitors, such asranibizumab,bevacizumab,aflibercept, andbrolucizumabcan cause regression of choroidal neovascularization with resorption of subretinal fluid and improvement or stabilization of vision

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28
Q

Retinal Detachment
* What is it
* Without txt typically results in what
* Can be what?
* What type of vision loss?
* Typically preceded by what?
* May experience what?

A
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29
Q
A
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30
Q

Retinal Detachment
* how do you dx?
* What can you use to confirm?
* What do you need to do?
* What is the txt?
* What can 90% of uncomplicated detachments can be cured with what?

A
  • Diagnosis by history, may have abnormal findings on dilated fundoscopic exam
  • Ocular US can confirm
  • Emergent referral to specialist (<24 hours)
  • Treatment- Reattachment of retina by ophthalmology (various methods)
  • ~90% of uncomplicated detachments can be cured with one operation
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31
Q

Retinal Detachment-
* How is the fundi exam?

A

There may be a dulling of the red reflex, and funduscopic examination may reveal the retina to be elevated with folds or cause the retina to be difficult to visualize with a direct ophthalmoscope. If the detachment is extensive, there may be a relative afferent pupillary defect.

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32
Q

What are the different components of diabetic retinopathy?

A
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33
Q

Diabetic Retinopathy
* Principle cause of what?
* Typically NO symptoms until when?
* Devlopment =

A
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34
Q

Diabetic Retinopathy
* What are the two forms?

A
  • Non-proliferative
  • Proliferative- neovascularization (new blood vessel growth), less common but more severe
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35
Q

Nonproliferative Retinopathy
* Variety of what?
* Absence of what?
* What are some sx?

A
  • “NPDR”
  • Variety of nerve-fiber infarcts
  • Absence of abnormal new blood vessels (NO neovascularization… yet!)
  • microaneurysms, retinal hemorrhages, venous beading, retinal edema, and hard exudates
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36
Q

What is this?

A
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37
Q

Proliferative Retinopathy
* What is this?
* What are complications?
What are the 3 stages?

A
  • “PDR”
  • Neovascularization arising from the disc and/or retinal vessels.
  • Complications include: preretinal and vitreous hemorrhage, retinal detachments due to fibrosis
  • 3 stages (early, high risk, severe)
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38
Q

What is this?

A
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39
Q

What does this show?

A
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40
Q

Diabetic Retinopathy
* Screening for what?
* When do you refer type 2 diabetics?
* When do you refer type 1 diabetics?
* Screen and monitor who?
* How do you diagnosis?

A
41
Q

Diabetic Retinopathy-Prevention
* What do you need to control (2)?
* What do they need to quit?
* Optimization of what?
* What do you need to screen for?

A
  • Glycemic control is the most important modifiable factor in treating diabetic retinopathy
  • BP control
  • Quit smoking
  • Optimization of kidney function and serum lipids
  • Yearly screening in diabetics
42
Q

Hypertensive Retinopathy
* What is this?
* What is there a hx of?
* Often what?

A
  • Retinal vascular damage caused by hypertension
  • Hx of longstanding, uncontrolled HTN and medication noncompliance
  • Often asymptomatic
43
Q

Hypertensive Retinopathy
* How do you dx?
* What is the txt?

A

Dx: fundoscopic exam- retinal hemorrhages, AV nicking, cotton wool spots, exudates, and/or papilledema

Treatment- No cure, vision loss is irreversible, BP control
* Evaluate for other forms of end-organ damage (renal, cardiovascular, neuro)

44
Q

Hypertensive Retinopathy

  • What is AV nipping?
  • What are cotton wool spots caused by?
  • What are hard exudates?
  • Retinal haemorrhagesare caused by what?
A
  • Arteriovenous nippingis where the arterioles cause compression of the veins where they cross. This is again due to sclerosis and hardening of the arterioles.
  • Cotton wool spotsare caused by ischemia and infarctionin the retina causing damage to nerve fibres.
  • Hard exudatesare caused by damaged vessels leakinglipidsinto the retina.
  • Retinal haemorrhagesare caused by damaged vessels rupturing and releasing blood into the retina.
45
Q

Amaurosis fugax –Presentation & Etiology
* What type of vision loss?
* How does the Visual loss happen?
* How long?
* What is the most common cause?

A
  • Transient monocular or binocular vision loss
  • “visual loss descending like a curtain or shade”
  • Brief (<10 mins)
  • Ischemia most common cause (not only cause)
46
Q

Amaurosis fugax –Presentation & Etiology
* What are the risk factors?
* you typically see this term applied to what?

A
  • Risk factors – carotid disease (#1), cardiac disease, age, hypoperfusion
  • you typically see this term applied to the diagnosis of retinal artery occlusion
47
Q

Amaurosis fugax- Exam and Diagnostics
* Assess what?
* What happens to fundi exam?
* What happens at the time of exam?
* What do >50 or young with risk factors?

A
  • Assess acuity, visual fields, fundus exam
  • Fundi exam may be normal or may show evidence of vascular disease – (cotton wool spots, retinal emboli, hemorrhages or whitening, or dilated retinal veins)
  • Usually at time of exam, symptoms are resolved and neuro & ophthalmologic exam is normal
  • > 50 or young with risk factors-> ischemic workup, carotid US, ESR (autoimmune: temoral giant cell)

Under: By definition, patients with transient visual loss (TVL) almost always present after the episode has resolved; hence, the neurologic and ophthalmologic examination is usually normal.

48
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A
49
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49
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50
Q

Retinal Vascular Occlusion
* What happens to the vision?
* No what?
* Workup for what?
* Occlusion can be what?
* Can involve what?

A
51
Q

Retinal Venous Occlusion
* Who does this affect?
* What can you see?
* What is the txt?

A
52
Q

Retinal Artery Occlusion
* What type of vision loss?

A

Acute, painless loss of monocular vision

53
Q

Retinal Artery Occlusion
* Considered a form of what?
* Considered a form of what?
* What age?
* What are the risks?
* What is the etiology?
* What are the two types?

A
  • Considered a form of stroke
  • More than 90% of patients are over age 40
  • Risks – HTN, DM, smoking (i.e stroke risk factors)
  • Etiology – carotid artery disease, cardiac, other vascular disease, sickle cell, hypercoagulable states, some leukemias, Giant cell arteritis
  • Central (CRAO) vs Branch (BRAO)
54
Q

Central retinal artery occlusion (CRAO): Presentation & Exam
* What type of vision loss?
* Almost never what?
* What does the exam show?

A
  • Profound vision loss in one eye, usually painless
  • Almost never occurs in both eyes simultaneously - but does sequentially
  • Exam – fundus – “cherry red spot” in the macula, retinal whitening
55
Q

What is this?

A
56
Q

CRAO- Acute Treatment & Prognosis
* emergency or not?
* When should txt occur?
* immediate what?
* What is there a poor prognosis for?
* Consider what?

A
  • Ocular Emergency!!
  • Treatment should occur in first six hours of ischemia
  • Immediate referral, call ahead
  • Poor prognosis for vision recovery
  • Consider ocular massage
57
Q

Retinal Artery Occlusion- Workup & Management
* Workup depends on suspected etiology, consider what?

A

Workup depends on suspected etiology, consider:
* Carotid imaging study
* ECG
* ESR/CRP-> to exclude Giant Cell Arteritis (treatable)
* Coagulation studies (hypercoagulable state?)
* ECHO? (cardioembolic source)

58
Q

Retinal Artery Occlusion- Workup & Management
* Goal of long-term management is to what?

A

Goal of long-term management is to reduce risk of future vascular events
* Arthrosclerosis risk factor modification (BP, HLD, smoking)
* Consider antiplatelet agent
* Endarterectomy for severe carotid disease

59
Q

Branch retinal artery occlusion (BRAO)
* Vision loss may be what?
* What is often less affected?
* What does the exam show?
* What happens with vision?
* What is not offered?

A
  • Vision loss may be restricted to a visual field
  • Visual acuity less often affected
  • Exam – fundus with retinal ischemia sectoral pattern of retinal opacification
  • ~80% with BRAO will recover vision (rarer in CRAO)
  • Acute treatments generally not offered
60
Q

Amblyopia
* What is this?

A

Decreased visual acuity in one or both eyes despite correction of refractive error

61
Q

Amblyopia - Etiology & Epidemiology
* Commonly referred to as what?
* What type of condition?
* What are the classifications? (4)

A
  • Commonly referred to as “lazy eye”
  • Childhood condition

Classification
* Strabismic (50%) are strabismic – misalignment of eyes
* Refractive (15-20%) – unequal focus between eyes
* Deprivational (<5%)– congenital cataracts, ptosis
* 30% combined

62
Q

Amblyopia
* What are the Risk Factors?

A
  • Prematurity
  • Small size compared to gestational age
  • First degree relative with same
  • Neurodevelopmental delay
63
Q

Amblyopia - Presentation
* Usually what?
* Vision?
* Detected by what?
* Amblyopia inducing conditions?

A
  • Usually unilateral
  • Vision in two eyes is unequal
  • Detected by visual acuity testing in older children
  • Amblyopia inducing condition (ex: strabismus, cataracts, visual lesion)

Amblyopia should be suspected if the vision in the two eyes is unequal or if the child has an amblyopia-inducing condition

64
Q

Amblyopia – Screening and Evaluation
* how do you routine screening?
* Early detection does what?
* Refer to who?
* Treatment?

A
  • Routine screening of children < 5 years old
  • Early detection improves prognosis
  • Refer suspected amblyopia to pediatric ophthalmologist or optometrist
  • Treatment depends on etiology

  • Elimination of visual obstruction, correction of refractive errors, pathing or eye drops, surgery (rarely)
  • <7 years— better outcome
65
Q

Strabismus
* What is it?
* Imbalance of what?
* Described by what?

A
  • Misalignment of eyes
  • Imbalance of eye muscles
  • Described by position of eye
66
Q

Strabismus:

A
67
Q

What is the txt of strabismus?

A
  • Patch the strong eye – encourages use of a weak eye
  • Alternative- atropine eye drops (consider if poor compliance with patching)
68
Q

Glaucoma
* What is it?

A

Damage to the optic nerve– typically with increased intraocular pressure

69
Q

Glaucoma:
* Second most leading cause?
* What are the risk factors?

A
70
Q

What is present in glaucoma?

A
71
Q

Normal Eye Physiology
* What is aqueous humor?
* What determines IOP?
* What is trabecular meshwork?

A
  • Aqueous humor is produced by the ciliary body in the posterior chamber, flows through pupil, reaches anterior chamber angle, exits the eye
  • Balance between fluid production and drainage determines intraocular pressure (IOP)
  • Trabecular meshwork is the tissue in the angle that acts as a sieve when the fluid drains
72
Q

What is the pathophysiology of Primary angle-closure?

A
73
Q

Glaucoma Pathophysiology
* in short what happens?

A

impaired aqueous humor drainage causes increased pressure in the eye

74
Q

Primary Angle Glaucoma- Open vs Acute
* What is the difference?

A
75
Q

What is this?

A
76
Q

Open angle Glaucoma (Gradual)
* What happens to vision?
* What is the presentation?

A
  • Progressive peripheral visual field loss followed by central field loss due to optic nerve damage
  • Presentation- Usually asymptomatic, often found incidentally on screening (recommended for age >40)
77
Q

Open angle Glaucoma (Gradual)
* How do you dx?
* How do you txt is?

A
78
Q

Acute Angle-Closure Glaucoma
* What happens?
* What is blocked and what happens?
* What happens without treatment?
* What is ti?
* What are the sxs?

A
  • Entire angle is blocked suddenly
  • Complete pupillary block-> Rapid rise in IOPs
  • Without treatment->vision loss and blindness can occur (over hours to days)
  • Ophthalmic emergency!
  • Symptoms: Halos around lights, HA, N/V, severe eye pain
79
Q

Acute Angle-Closure Glaucoma
* Patients with anatomically narrow angles are at risk for what?
* What is the classic story?

A
  • Patients with anatomically narrow angles are at risk for future angle-closure. The width of their anterior chamber angles is smaller than in normal eyes, and their peripheral iris is closer to their anterior chamber angle than normal.
  • Classic story-Asian in movie theater or planetarium
80
Q

Acute Angle-Closure Glaucoma- Dx and Txt
* What is shown on the exam?
* How do you dx it?

A
  • Exam: conjunctival redness, corneal edema/cloudiness, dilated, non-reactive pupil, elevated IOPs with tonometry
  • Diagnosis: Suggested by presentation, exam, tonometry. Confirmed by ophtho. Avoid pupil dilation.

Pupillary dilation should be deferred in untreated cases of suspected angle-closure glaucoma, as this may exacerbate the condition.

81
Q

Acute Angle-Closure Glaucoma- Dx and Txt
* How do you tx it?

A

Treatment- emergency care by an ophthalmologist
* Topical eye drops to reduce IOPs (ex: Timolol)
* Oral or IV meds (acetazolamide or mannitol)
* Definitive- laser peripheral iridotomy

This procedure creates a tiny hole in the peripheral iris through which aqueous humor can flow and reach the angle [23]. Once the iridotomy is patent, pupillary block is bypassed. A peripheral iridotomy is usually created with a laser

82
Q
A
83
Q

Cataract
* What is it?

A

Clouding of the normally clear lens of the eye.
* Lens disorder?
* Absense of red reflect?

84
Q

Cataract- Epidemiology & Risk Factors
* Opacity of what?
* May progress to what?
* May occur when?
* What are risk factors?

A
  • Opacity of the lens causing blurred vision
  • May progress to blindness (leading cause worldwide!)
  • May occur as a normal process of aging
  • Risk factors include; age, smoking, ETOH, sunlight exposure, malnutrition, DM, lack of physical exercise, HIV/AIDS, corticosteroids – oral and inhaled, lead exposure
85
Q

Cataract
* pain or painless?
* Highly what?
* Loss of what?
* Increase in what?

A
  • Painless
  • Highly variable, often bilateral
  • Loss of night vision
  • Increase in near sightedness
86
Q

Cataract- Clinical Presentation
* Frequent updates of what?
* Problems with what?
* Suspect if what?
* Most commonly in who?

A
  • Frequent updates of corrective lenses
  • Problems with night driving, reading road signs, fine print
  • Suspect if painless progressive decline in vision
  • Most commonly patients >60 years, or younger individuals with risk factors
87
Q

Cataract- Diagnosis and Progression
* Dx by what? What is shown?
* Dilated what?

A
88
Q

Cataract
* A “mature” cataract degrades what?
* What is a hypermature cataract?
* Cataract may block what?

A
  • A “mature” cataract degrades vision to 20/400 or worse
  • A “hypermature” cataract – the cortex of the lens liquifies.
  • Cataract may block retinal exam
89
Q
A
90
Q

Cataracts-
* What is the Treatment?

A

  • New lens deployed
  • Pseudophakia -term refers to the implanting of an intraocular lens to replace a natural lens, the lens being the clear part of the eye that focuses light and images, enabling a person to see, often occurs during cataract surgery.
91
Q

Eye Malignancies/Neoplasms
* What is rare?
* What are the signs?
* If concerned, refer?

A
92
Q

Ruth is a 70 y/o female who presents with complaint of sudden onset of vision in her right eye that resolved in 5 minutes. She describes it as a curtain descending over her vision. She has a hx of HTN and tobacco use. Her exam is completely normal, visual acuity is currently 20/20 OD, OS, OU. The most likely diagnosis is…
* A. Glaucoma
* B. Optic neuritis
* C. Amaurosis fugax
* D Amblyopia
* E. Central retinal artery occlusion

A
  • C.Amaurosis fugax
93
Q

Ruth is a 70 y/o female who presents with complaint of sudden onset of vision in her right eye that resolved in 5 minutes. She describes it as a curtain descending over her vision. She has a hx of HTN and tobacco use. Her exam is completely normal, visual acuity is currently 20/20 OD, OS, OU. Your management is:
* A. Reassurance and discharge
* B. Ischemic workup
* C. Refer to optho for tonometry
* D. VEGF injections

A
  • B. Ischemic workup
94
Q

Joe is a 90 y/o male who presents complaining of diminishing central vision for the last several months. His fundoscopic exam shows subretinal hemorrhages and drusen spots. Most likely cause of his symptoms is:
* A. Dry macular degeneration
* B. Wet macular degeneration
* C. Glaucoma
* D. Retinal detachment

A
  • A. Dry macular degeneration
95
Q

Mr. Bob presents with bilateral eye redness, inflammation of his sclera, and severe boring eye pain that worsens at night. You suspect a diagnosis of scleritis. He most likely has what other condition:
* A. Leukemia
* B. Hx of prior CVA
* C. Diabetes
* D. Rheumatoid arthritis

A
  • D. Rheumatoid arthritis
96
Q

Jane is a 35-year-old otherwise healthy female who presents with right eye vision loss and pain that started today. She also notes decrease in her ability to see color in the right eye. Exam shows pain with EOM. OD 20/200, OS 20/20. Most likely diagnosis is
* A. Strabismus
* B. Amaurosis fugax
* C. Optic neuritis
* D. Central retinal artery occlusion

A
  • C. Optic neuritis
97
Q

Jane is a 35-year-old otherwise healthy female who presents with right eye vision loss and pain that started today. She also notes decrease in her ability to see color in the right eye. Exam shows pain with EOM. OD 20/200, OS 20/20. How would you confirm the diagnosis?
* A. MRI with gadolinium contrast
* B. ESR
* C. fundoscopic exam
* D. elevated IOPs on tonometry

A
  • A. MRI with gadolinium contrast
98
Q

Jane is a 35 year old otherwise healthy female who presents with right eye vision loss and pain that started today. She also notes decrease in her ability to see color in the right eye. After confirming her diagnosis, what would be a reasonable treatment?
* A. po aspirin
* B. IV acetazolamide
* C. po prednisone
* D. IV methylprednisolone

A
  • D. IV methylprednisolone

Clinical Medicine 2 (16 decks)

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