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Geriatrics > Sensory Changes > Flashcards

Sensory Changes Flashcards

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
Q

What agents are third line for glaucoma and why?

A

Pilocarpine
Dipivefrin
d/t high frequency of dosing, AE, reduced efficacy

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26
Q

What do we do if monotherapy is not effective in glaucoma?

A

Switch to another monotherapy

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27
Q

What do we do if monotherapy is somewhat effective in glaucoma?

A

Add another agent

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28
Q

Which agents are PG analogs?

A

Bimatoprost
Latanoprost
Travoprost
Tafluprost

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29
Q

What is the MOA of PG analogs?

A

Increases uveoscleral outflow which reduces IOP

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30
Q

What is the usual dosing of PG?

A

1QHS

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31
Q

What are the BBs for glaucoma?

A

Betaxolol (Betoptic)
Levobunolol (Betagan)
Timolol (Timoptic XE)

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32
Q

What is the MOA of BB for glaucoma?

A

Reduces aqueous humor production

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33
Q

What is the dosing of BB for glaucoma?

A

1 drop BID for all

Timolol can be BID or QD

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34
Q

What is the alpha antagonist for glaucoma?

A

Brimonidine (Alphagan)

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35
Q

What is the dosing for alpha agonists in glaucoma?

A

1TID

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36
Q

What are the carbonic anhydrase inhibitors for glaucoma?

A

Brinzolamide (Azopt)

Dorzolamide (Trusopt)

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37
Q

What is the dose for carbonic anhydrase inhibitors for glaucoma?

A

1TID

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38
Q

What are the cholinergic agents for glaucoma?

A

Carbachol (Isopto carbachol)

Pilocarpine (Isopto Carpine)

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39
Q

What is the dosing for cholinergics?

A

1-2 drops 3-6x/day (gel = QHS)

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40
Q

What are the combination glaucoma products?

A

Timolol-dorzolamide (Cosopt BID)
Timolol-Brimonidine (Combigan BID)
Brinzolamide-Brimonidine (Simbrinza TID)

41
Q

What are the CI/warnings for PG analogs?

A

Hypersensitivty
Use with caution in patients with blue, green, gray eye color d/t long term changes in iris
Caution in pregnancy

42
Q

What are the local SE for PG analogs?

A

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
Q

What are the systemic SE for PG analogs?

A 
URTI
Flu syndrome
Myalgia
Arthralgia
HA
Asthenia
Chest pain
44
Q

What is the MOA of BB agents?

A

Decrease the production of aqueous humor by the ciliary body via beta-1 receptor blockade

45
Q

What are the CI/warnings of BB agents?

A

Related to systemic absorption of BB

Selective vs Nonselective

46
Q

What are the local SE of BB agents in glaucoma?

A 
Stinging
Dry eyes
Corneal anesthesia
Blepharitis
Blurred vision
Rare = conjunctivitis, uveitis, and keratitis
47
Q

What are the systemic SE of BB agents in glaucoma?

A

Bradycardia
Hypotension
Negative inotropy
Bronchospasm

48
Q

What are the alpha-2 agonists MOA in glaucoma?

A

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
Q

What are the CI/warnings for alpha-2 agonists in glaucoma?

A

Patients taking MAOIs
Caution in patients with severe CV or cerebrovascular disease, depression, Raynaud’s disease, orthostasis, hepatic/renal impairment

50
Q

What are the local SE of alpha-2 agonists in glaucoma?

A

Blurred vision
Burning
Ocular itching
Conjunctival blanching

51
Q

What are the systemic SE of alpha-2 agonists in glaucoma?

A 
Dizziness
Fatigue
Somnolence
Dry mouth
Possible reduced BP and pulse
52
Q

What are the allergic type reactions of alpha-2 agonists in glaucoma?

A

Lid edema
Eye discomfort
Foreign-object sensation
Itching

53
Q

What is the MOA of carbonic anhydrase inhibitors?

A

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
Q

What are the CI/warnings for carbonic anhydrase inhibitors?

A

Sulfonamide allergy

Warning in renal impairment

55
Q

What are the local SE of carbonic anhyrase inihibitors?

A 
Transient burning and stinging
Transient blurred vision
Tearing
Conjunctivitis (rare)
Superficial punctuate keratitis
56
Q

What are the systemic SE of carbonic anhydrase inhibitors in glaucoma?

A 
Dry mouth
Sedation
Hypotension
HA
Fatigue
Abnormal taste
Depression
57
Q

When is oral carbonic anhydrous inhibitors for glaucoma?

A

Those who have failed to respond to maximized topical therapy

58
Q

What are the oral carbonic anhydrous inhibitors for glaucoma?

A

Acetazolamide (1-4 times daily)

Methazolamide (2-3 times daily)

59
Q

Can you use both an oral and topical carbonic anhydrous inhibitor?

A

No, lack of evidence of safety

60
Q

How long should you wait between drops?

A

5-10 minutes

61
Q

Should solutions or suspensions be used first and why?

A

Solutions prior to suspensions as this has a longer retention time

62
Q

If ointment is being applied in combination with drops, how should they be separated?

A

Drops 10 minutes prior to use of any ointment

63
Q

How do you use drops if the patient is wearing contacts?

A

Remove contact lenses prior to instillation, wait 15 minutes for reinsertion

64
Q

How long should eyes stayed closed after instilling medication?

A

3 minutes

65
Q

In what direction do we lean our head after instillation?

A

Towards floor so drops coat cornea

66
Q

How do we improve ocular bioavailability and to reduce systemic absorption?

A

Nasolacrimal occlusions

67
Q

How do we perform nasolacrimal occlusions?

A

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
Q

What is the leading cause of blindness in adults in industrialized countries?

A

Age-related Macular degeneration (AMD)

69
Q

What is drusen?

A

Yellow/white accumulations of material under retinal pigment epithelium

70
Q

What is dry type AMD?

A

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
Q

What are the types of AMD?

A

Dry type

Wet type

72
Q

What is wet type AMD?

A

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
Q

What are the clinical presentation for dry type AMD?

A

Gradual vision loss in one or both eyes

Partial vision loss

74
Q

What are the clinical presentation for wet type AMD?

A

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
Q

How can AMD be prevented?

A

Smoking cessation

Diet of fruit, green leafy vegetables, fish and nuts can still be encouraged

76
Q

What are the treatments for dry type AMD for non-smokers?

A

Vitamins complex:

Including A, C, and beta carotene plus zinc

77
Q

What are the treatments for dry type AMD for smokers?

A

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
Q

What are the non pharmacologic treatment options for wet type AMD?

A

Possibly laser photocoagulation
Photodynamic therapy
Supplementation with zinc and vitamins

79
Q

What are the pharmacologic treatment options for wet type AMD?

A

Vascular endothelial growth factor (VEGF) inhibitors

80
Q

What do VEGF inhibitors do?

A

Decrease angiogenesis

81
Q

What are some VEGF inhibitors?

A

Pegaptanib
Bevacizumab (no injection, must be compounded for injection)
Ranibizumab
Aflibercept

82
Q

How are VEGFi agents administered?

A

Intravitreously

83
Q

When is there greater likelihood of treatment success with VEGFi?

A

Recent, smaller lesions

84
Q

When is VEGFi recommended ASAP?

A

Those with active disease (leaky fluid, hemorrhage, recent vision loss)

85
Q

How do we treat well-defined extrafoveal lesions?

A

Laser photocoagulation +/- VEGFi

86
Q

What is the definition of cataracts?

A

Opacity of the lens causing partial or total blindness

87
Q

What is the leading cause of blindness in the world?

A

Cataracts

88
Q

What causes cataracts?

A

Lenses of the eye do not shed nonviable cells as other epithelium do
Eye is more susceptible to cell damage if it occurs

89
Q

What is the clinical presentation of cataracts?

A

Painless
Progressive
Bilateral visual loss affecting night driving, reading fine print, reading road signs

90
Q

What is the treatment option for cataracts?

A

Surgical removal of lens

91
Q

What is the most common causes of blindness in those aged 25-74?

A

Diabetic retinopathy

92
Q

What is the pathophysiology of diabetic retinopathy?

A

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
Q

What are the clinical presentation types of diabetic retinopathy?

A 
Nonproliferative DR (NPDR)
Proliferative DR (PDR)
94
Q

Which DR type does not involve neovascularization?

A

NPDR

95
Q

What is an indication for therapy in DR?

A

Clinically significant macular edema (CSME)

96
Q

What is the primary prevention of DR?

A

Control of blood glucose

Treating HTN has also shown to help

97
Q

What are the nonpharmacologic treatment of DR?

A

Photocoagulation

98
Q

What are the treatment options for severe cases of CSME?

A

Photocoagulation therapy may be combined with VEGFi

If no improvement, steroids may be added (intravitreal triamcinolone)

99
Q

What is a severe case of CSME?

A

Central involvement or vision loss

Geriatrics (15 decks)

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