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Sensory Changes Flashcards

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1
Q

What is the triad of glaucoma sx and how is it related to treatment?

A

Blurred vision
Increased intraocular pressure
Optic nerve degeneration

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2
Q

What are the characteristics of glaucoma?

A

IOP
Degeneration of the optic nerve head
Restriction of visual field

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3
Q

When might patients with open-angle glaucoma who are untreated may have increased IOP when taking what?

A

Systemic medications with anticholinergic properties

Vasodilators

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4
Q

All ll patients taking glucocorticoids may have increased what?

A

IOP

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5
Q

What is the most common symptom of glaucoma?

A

Asymptomatic

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6
Q

When do symptoms present in glaucoma?

A

After substantial loss of retinal ganglion occurs

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7
Q

What are the physiologic causes of glaucoma?

A

Primary optic neuropathy

Axonal injury, retinal ganglion cells, apoptosis

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8
Q

Are symptoms usually unilateral or bilateral?

A

Bilateral

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9
Q

How is diagnosis of glaucoma done?

A

Inspecting the optic
disk
Retinal nerve fiber layer
Visual fields

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10
Q

What can happen to the IOP in glaucoma?

A

May be normal or elevated

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11
Q

What are optic disk changes in glaucoma?

A

Enlarged cup
Asymmetric cup
Splinter hemorrhages
Optic cupping

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12
Q

What are visual field changes in glaucoma?

A

Peripheral is most common

Central vision is typically maintained, even in later stages

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13
Q

What is the textbook presentation of glaucoma?

A

Elevated IOP along with disk and visual field changes

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14
Q

What are atypical presentations of glaucoma?

A

Normal tension glaucoma - disk changes and visual field loss but IOP less than 21 mmHg

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15
Q

What is ocular hypertension?

A

Elevated IOP w/o disk or visual field changes

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16
Q

Is ocular hypertension glaucoma?

A

No, may be glaucoma suspects

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17
Q

What are first line therapies in glaucoma?

A

PGs (some say BB as well)

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18
Q

What are the treatment goals of glaucoma?

A

Stabilize optic nerve/retinal fiber layer
Control IOP
Stabilize visual fields

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19
Q

What are the initial goals of glaucoma?

A

Based on baselines IOP and amount of vision loss

30% lowering from baseline is typically the goal

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20
Q

What lowering % of IOP do guidelines suggest?

A

At least 20-30%

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21
Q

What IOP pressure goal do professional aim for?

A

Less than or equal to 24 mmHg

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22
Q

What factors does the ultimate goal depend on?

A

Extent of ocular damage
Whether recent disease progression has occurred
Stability of IOP
Patient adherence

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23
Q

What is the prognosis for patients with glaucoma and high IOP?

A

Generally excellent when discovered early and treated adequately

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24
Q

What are the agents that are second line for glaucoma?

A

Most other agents

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25
What agents are third line for glaucoma and why?
Pilocarpine Dipivefrin d/t high frequency of dosing, AE, reduced efficacy
26
What do we do if monotherapy is not effective in glaucoma?
Switch to another monotherapy
27
What do we do if monotherapy is somewhat effective in glaucoma?
Add another agent
28
Which agents are PG analogs?
Bimatoprost Latanoprost Travoprost Tafluprost
29
What is the MOA of PG analogs?
Increases uveoscleral outflow which reduces IOP
30
What is the usual dosing of PG?
1QHS
31
What are the BBs for glaucoma?
Betaxolol (Betoptic) Levobunolol (Betagan) Timolol (Timoptic XE)
32
What is the MOA of BB for glaucoma?
Reduces aqueous humor production
33
What is the dosing of BB for glaucoma?
1 drop BID for all | Timolol can be BID or QD
34
What is the alpha antagonist for glaucoma?
Brimonidine (Alphagan)
35
What is the dosing for alpha agonists in glaucoma?
1TID
36
What are the carbonic anhydrase inhibitors for glaucoma?
Brinzolamide (Azopt) | Dorzolamide (Trusopt)
37
What is the dose for carbonic anhydrase inhibitors for glaucoma?
1TID
38
What are the cholinergic agents for glaucoma?
Carbachol (Isopto carbachol) | Pilocarpine (Isopto Carpine)
39
What is the dosing for cholinergics?
1-2 drops 3-6x/day (gel = QHS)
40
What are the combination glaucoma products?
Timolol-dorzolamide (Cosopt BID) Timolol-Brimonidine (Combigan BID) Brinzolamide-Brimonidine (Simbrinza TID)
41
What are the CI/warnings for PG analogs?
Hypersensitivty Use with caution in patients with blue, green, gray eye color d/t long term changes in iris Caution in pregnancy
42
What are the local SE for PG analogs?
Hyperemia Iris pigmentation (become brown over 3-12 months) Hypertrichosis (increased eyelash pigmentation) Punctuate corneal erosiosn Enopthalmos Local irritation may be d/t preservative
43
What are the systemic SE for PG analogs?
``` URTI Flu syndrome Myalgia Arthralgia HA Asthenia Chest pain ```
44
What is the MOA of BB agents?
Decrease the production of aqueous humor by the ciliary body via beta-1 receptor blockade
45
What are the CI/warnings of BB agents?
Related to systemic absorption of BB | Selective vs Nonselective
46
What are the local SE of BB agents in glaucoma?
``` Stinging Dry eyes Corneal anesthesia Blepharitis Blurred vision Rare = conjunctivitis, uveitis, and keratitis ```
47
What are the systemic SE of BB agents in glaucoma?
Bradycardia Hypotension Negative inotropy Bronchospasm
48
What are the alpha-2 agonists MOA in glaucoma?
Structurally similar to clonidine Reduce IOP by decreasing the rate of aqueous humor production "Stimulate presynaptic feedback inhibition of NE and reduce aqueous humor formation"
49
What are the CI/warnings for alpha-2 agonists in glaucoma?
Patients taking MAOIs Caution in patients with severe CV or cerebrovascular disease, depression, Raynaud's disease, orthostasis, hepatic/renal impairment
50
What are the local SE of alpha-2 agonists in glaucoma?
Blurred vision Burning Ocular itching Conjunctival blanching
51
What are the systemic SE of alpha-2 agonists in glaucoma?
``` Dizziness Fatigue Somnolence Dry mouth Possible reduced BP and pulse ```
52
What are the allergic type reactions of alpha-2 agonists in glaucoma?
Lid edema Eye discomfort Foreign-object sensation Itching
53
What is the MOA of carbonic anhydrase inhibitors?
Reduce IOP by decreasing ciliary body aqueous humor secretion Blocks secretion of sodium and bicarbonate ions from the ciliary body to the aqueous humor
54
What are the CI/warnings for carbonic anhydrase inhibitors?
Sulfonamide allergy | Warning in renal impairment
55
What are the local SE of carbonic anhyrase inihibitors?
``` Transient burning and stinging Transient blurred vision Tearing Conjunctivitis (rare) Superficial punctuate keratitis ```
56
What are the systemic SE of carbonic anhydrase inhibitors in glaucoma?
``` Dry mouth Sedation Hypotension HA Fatigue Abnormal taste Depression ```
57
When is oral carbonic anhydrous inhibitors for glaucoma?
Those who have failed to respond to maximized topical therapy
58
What are the oral carbonic anhydrous inhibitors for glaucoma?
Acetazolamide (1-4 times daily) | Methazolamide (2-3 times daily)
59
Can you use both an oral and topical carbonic anhydrous inhibitor?
No, lack of evidence of safety
60
How long should you wait between drops?
5-10 minutes
61
Should solutions or suspensions be used first and why?
Solutions prior to suspensions as this has a longer retention time
62
If ointment is being applied in combination with drops, how should they be separated?
Drops 10 minutes prior to use of any ointment
63
How do you use drops if the patient is wearing contacts?
Remove contact lenses prior to instillation, wait 15 minutes for reinsertion
64
How long should eyes stayed closed after instilling medication?
3 minutes
65
In what direction do we lean our head after instillation?
Towards floor so drops coat cornea
66
How do we improve ocular bioavailability and to reduce systemic absorption?
Nasolacrimal occlusions
67
How do we perform nasolacrimal occlusions?
for 1-3 minutes, by closing the eyes and placing the index finger over the nasolacrimal drainage system in the corner of the eye.
68
What is the leading cause of blindness in adults in industrialized countries?
Age-related Macular degeneration (AMD)
69
What is drusen?
Yellow/white accumulations of material under retinal pigment epithelium
70
What is dry type AMD?
Formation of drusen, which may increase in size and number over time. This may lead to retinal pigment epithelial detachment and atrophy, causing vision loss
71
What are the types of AMD?
Dry type | Wet type
72
What is wet type AMD?
Characterized by choroidal neovascularization (CNV) under retinal pigment epithelium or retina. May cause exudate and hemorrhage, leading to damage to photoreceptors and vision loss
73
What are the clinical presentation for dry type AMD?
Gradual vision loss in one or both eyes | Partial vision loss
74
What are the clinical presentation for wet type AMD?
May present as acute vision distortion or loss of central vision Usually symptoms appear in one eye, though disease is present in both eyes
75
How can AMD be prevented?
Smoking cessation | Diet of fruit, green leafy vegetables, fish and nuts can still be encouraged
76
What are the treatments for dry type AMD for non-smokers?
Vitamins complex: | Including A, C, and beta carotene plus zinc
77
What are the treatments for dry type AMD for smokers?
Smoking cessation Vitamin complex w/o beta-carotene (which can increase risk for lung cancer, especially in smokers) Typically add in lutein and zeaxanthin as a substitute
78
What are the non pharmacologic treatment options for wet type AMD?
Possibly laser photocoagulation Photodynamic therapy Supplementation with zinc and vitamins
79
What are the pharmacologic treatment options for wet type AMD?
Vascular endothelial growth factor (VEGF) inhibitors
80
What do VEGF inhibitors do?
Decrease angiogenesis
81
What are some VEGF inhibitors?
Pegaptanib Bevacizumab (no injection, must be compounded for injection) Ranibizumab Aflibercept
82
How are VEGFi agents administered?
Intravitreously
83
When is there greater likelihood of treatment success with VEGFi?
Recent, smaller lesions
84
When is VEGFi recommended ASAP?
Those with active disease (leaky fluid, hemorrhage, recent vision loss)
85
How do we treat well-defined extrafoveal lesions?
Laser photocoagulation +/- VEGFi
86
What is the definition of cataracts?
Opacity of the lens causing partial or total blindness
87
What is the leading cause of blindness in the world?
Cataracts
88
What causes cataracts?
Lenses of the eye do not shed nonviable cells as other epithelium do Eye is more susceptible to cell damage if it occurs
89
What is the clinical presentation of cataracts?
Painless Progressive Bilateral visual loss affecting night driving, reading fine print, reading road signs
90
What is the treatment option for cataracts?
Surgical removal of lens
91
What is the most common causes of blindness in those aged 25-74?
Diabetic retinopathy
92
What is the pathophysiology of diabetic retinopathy?
Retinal damage secondary to elevated glucose Vision loss typically secondary to the development of macular edema (retinal thickening and edema of the macular), hemorrhage, retinal detachment, or neovascular glaucoma
93
What are the clinical presentation types of diabetic retinopathy?
``` Nonproliferative DR (NPDR) Proliferative DR (PDR) ```
94
Which DR type does not involve neovascularization?
NPDR
95
What is an indication for therapy in DR?
Clinically significant macular edema (CSME)
96
What is the primary prevention of DR?
Control of blood glucose | Treating HTN has also shown to help
97
What are the nonpharmacologic treatment of DR?
Photocoagulation
98
What are the treatment options for severe cases of CSME?
Photocoagulation therapy may be combined with VEGFi | If no improvement, steroids may be added (intravitreal triamcinolone)
99
What is a severe case of CSME?
Central involvement or vision loss

Geriatrics (15 decks)

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