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Therapeutics III > Ophthalmic Diseases - Block 4 > Flashcards

Ophthalmic Diseases - Block 4 Flashcards

1
Q

What are the types of available optic formulations?

A
  1. Solution
  2. Suspension (shake well)
  3. Ointment: applied to conjunctival sac or over lid margins -> blurred vision -> no contacts
  4. Gels: With cap on, invert and shake once to get medication to tip before instilling in the eye
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2
Q

How man mL are in 1 gtt?

A

0.05 mL

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3
Q

Are ear and eye drops interchangeable?

A

Eye drops for ear, but not ear drops for eyes

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4
Q

How should you instill eye drops?

A
  1. Clean hands
  2. Remove contacts
  3. Look up and form pocket in lower eyelid
  4. Release drop between eye and lower eyelid (don’t touch tip of bottle to eye)
  5. Close eye
  6. Nasolacrimal/punctal occlusion (NLO) x 1-3 minutes
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5
Q

What do you do if you are need to instill multiple dropps of the same med? Differnt med?

A

Same: Wait 5-10 minutees between drops

Differnet: Apply drops 5-10 minutes apart

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6
Q

What is the order of instilling solution and suspension?

A

Instill solution first then suspension

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7
Q

How can you insert contacts after drops?

A

15 minutes after

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8
Q

Right eye sig?

A

OD

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9
Q

Left eye sig?

A

OS

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10
Q

Both eyes sig?

A

OU

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11
Q

Drop sig?

A

gtt

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12
Q

What is glaucoma?

A

Optic neuropathy characterized by changes in the optic nerve head that is associated with loss of visual sensitivity and field

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13
Q

What are types primary glaucoma?

A
  1. Open angle
  2. ANgle closure:
    * with pupillary block
    * W/o pupillary block
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14
Q

What is secondary glaucoma?

A
  1. Open angle” pretrabecular, trabecular, posttrabecular
  2. Angle closure:
    * w/o pupillary block
    * With pupillary block
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15
Q

What is the aqueous humor?

A

Clear fluid and ultrafiltrate of the serum that fill the chambers of the eye

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16
Q

How is aqueous humor formed?

A

Ciliary body and epithelium through filtration (pressure) and secretion (osmosis)

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17
Q

What receptors are involved with ciliary epithelium?

A

Carbonic anahydrate, a- and b adrenergic receptors

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18
Q

What are the receptors involved with the ciliary body?

A

Increase inflow: b adrenergic agents
Decrease outflow: a2, b, dopamine blocking, carbonic anhydrase inhibitors, melatonin 1 agonist, adenylate cyclase stimulating agents

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19
Q

What is the rate of aqueous humor secretion into the posterior chamber?

A

2-3 µL/min

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20
Q

What drugs have the greatest effect in lowering IOP?

A
  1. Prostaglandin analog (nocturnal IOP)
  2. Beta blockers
  3. Carbonic anhydrase inhibitors (nocturnal IOP)
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21
Q

What is our normal IOP?

A

15.5 mmHg

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22
Q

When is IOP the highest?

A

At night after falling asleep or at awakening

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23
Q

What is ocular HTN?

A

Elevated IOP without s/s of glaucoma

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24
Q

What an advantegous way in treating glaucoma patients?

A

IOP reduction

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25
Q

What is a cup?

A

Small depression within optic disk

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26
Q

What are the alterations of the optic disk and visual fields from glaucoma?

A

Optic Disk:
1. Cup-to-disk ratio >0.5
2. Progressive increase in cup size

Visual fields:
1. Peripheral field constriction
2. Blind spots
3. Nasal visual field depression

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27
Q

Drugs that cause glaucoma?

A

Open angle: corticosteroids, anticholinergics
Closed-angle: anticholinergics, antihistamins, sympathomimetics

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28
Q

What is the difference between OAG and ACG sx?

A

OAG: none until substantial visual flied loss occurs
ACG: nonsymptomatic or prodromal sx (blurred/hazy vision with halos, HA)
* Acut sx: cloudy, pain, n/v, abdominal pain, diaphoresis

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29
Q

What are the presentations of OAG?

A

Bilateral, denetically determined

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30
Q

What are the forms of secondary OAG?

A

Pretrabecular: normal meshwork is covered and doesn’t allow aqueous humor outflow
Trabecular: alterations of meshwork or accumulation of material in intertrabecular spaces
Posttrabecular: Increased episcleral venous BP

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31
Q

What is the classification of ocular HTN?

A

IOP >22 mmHg

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32
Q

What are the RF of ocular HTN?

A
  1. IOP >25
  2. Cup:disk >0.5
  3. Central corneal thickness of < 555 μm
  4. family history of glaucoma, black, Latino/Hispanic ethnicity, severe myopia, and patients with only one eye
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33
Q

Tx for ocular htn?

A

First line: Topical PG analog or b-blocker
Alt first line: a2 agonist, CAI, netasudil

34
Q

What is the intial tx for OAB?

A

First: PG analog or beta-block
Second: CAI or Brimonidine
Last line: Dipivefrin, carbachol, topical cholinesterase inhibitors, PO CAI

CI with first: topical CAIs
Partial response: add second/thrid line or CAI

Intolerance of pharm: laser or surgical trabeculectomy

35
Q

PG analod Types?

A
  1. Latanoprost
  2. Bimatoprost
  3. Travoprost
  4. Tafluprost
  5. Latanoprostene
36
Q

PG analog ADRs?

A
  1. Iris pigmentation
  2. SUnken eyes
  3. Corneal thinning
  4. Uveitis (redness, pain, blurred vision)
37
Q

B-blocker types?

A
  1. Timolol
  2. Betaxolol
  3. Cartelol
  4. Levobunolol
  5. Metipranolol
38
Q

When would PO CAIs be used?

A

Severely high IOP that needs to be treated quickly

39
Q

How often is opthalimic therapy initiated?

A

Started in one eye to evaulate efficacy

Reassess in 2-4 weeks

40
Q

What color are your first line? second line? combo? packaging

A

PG: teal
Beta-blockers (2nd first line): yellow
CAI: orange
Combo: navy

41
Q

Omlonti

MOA, Dosing, ADR, Caution

A

MOA: selective PG E2 receptor agonist -> reducing IOP
Dosing: 1 gtt in affected eye QPM
ADR: photophobia, vision blurred, dry eye, conjuctival hyperemia
Caution: hyperpigmentation, eyelash changes, ocular inflammation, macular edema

42
Q

What are the non pharm for OAG?

A
  1. Laser trabeculoplasty
  2. Surgical trabeculectomy
43
Q

What is the tx for AACC?

A
  1. Miotics (pilocarpine)
  2. Secretory inhibitors (B-block, a2-agonist, CAI)
  3. PG analog
  4. Lack of response from topicals: mannitol or glycerin
  5. Ocular inflammation: topical corticosteroids
44
Q

What is the function of a miotic agent?

A

Pulls the peripheral irus awaw from meshwork however may worsen angle closure trough pupillary block

45
Q

What is the definitive tx for ACG?

A

Iridectomy -> hole in irus

Long-term drug therapy is only used if IOP remains high -> refer to ocular HTN

46
Q

What is the goal and monitoring paramters of ocular HTN?

A

Goal: lower IOP by 20%, or decrease 25-30% from baseline

Monitor: IOP, optic disk, visual fields, drug ADR

Unresponsive tx: switch to alternative agents
Partial: drug combo

47
Q

How often do you monitor OAG therapy?

A

IOP
Initial check: 4-6 weeks
After target: Q3-4M
Prolonged control: 6-12M

Visual fields and disk changes:
* Q6-12M

48
Q

Describe therapeutic adjustments of OAG?

A

No response: switch to alt agents
Partial: add combo (PG analog, b-blocker, brumonidine, CAI, pilocarpine)

49
Q

What is the goal for acute angle closure crisis?

A

Rapid reduction of IOP to preserve vision and avoid surgery/laser

50
Q

What is AMD?

A

Age related macular degeneration: neurodegenerative dx that produces irreversible loss of central vision due to damage to the macula

51
Q

What is the macula?

A

Responsible for all central vision and fine detail images

52
Q

What is the function of photoreceptors cells?

A

Identify light and then transfer the information to the brain to produce an image

53
Q

What is drusen?

A

Yellow deposits of lipids between the RPE (retinal pigment epithelium) and Bruch’s membrane that can develop with age

54
Q

What is the clinical presentation of AMD?

A
  1. Presence of drusen
  2. RPE abnormalities
  3. Reticular pseudodrusen
  4. RPE geographic atrophy
  5. Choroidal neovasc
  6. Retinal angiomatous proliferation
55
Q

What increased the risk of developing AMD?

A
  1. UV
  2. Tyroid dysfunction
  3. Med (Nitroglycerin, beta blockers, chloroquine, phothiazines)
  4. Pestacide
56
Q

What is the difference between non-neovascular and neovascular AMD?

A

Non-NV/atrophic dry: macula thins with age and tiny clumps of protein (drusen) grow

NV (wet): New, abnormal blood vessels grow under the retina and may leak blood or other fluids, causing scarring of the macula

57
Q

Sx of dry AMD?

A

Painless, slow, bilateral

  1. subretinal hard and soft drusen deposits
  2. THinning of macula
  3. RPE atrophy
  4. Hyperpigmentation of retina

Sx: visual distortion

58
Q

Sx of wet AMD?

A

Loss of central vision
* VEGF -> angiogenesis of BV growth

Amsler grid
Sx: dark spots in central vision, wavy lines instead of straight lines

59
Q

Non pharm for AMD?

A
  1. Smoking cessation
  2. Antioxidant vitamins and minerals
  3. Healthy diet
  4. Control cormorbities
60
Q

Tx for wet AMD only?

A
  1. VEGF inhibitors
  2. Photodynamic therapy
  3. Surgery
61
Q

Vitamins and minerals good for the eyes?

A

Vitamin E, C, beta-carotine and zinc

62
Q

VEGF inhibitors?

Types, MOA

A

Types:
* Bevacizumab
* Ranibizumab
* Afibercept
* Pegaptanib

MOA: prevents the growth of new BV into the retina from VEGF

63
Q

What is Vabysmo?

A

Treat neovascular (wet) aged-related macular degeneration and diabetic macular edema

64
Q

What is photodynamic therapy?

A

IV injection of dye (verteporfin) -> laser activates dye -> formation of thromboembolism -> seals abnormal blood vessels

ADR: light sensitivity and eye pain

65
Q

RF of dry eyes?

A
  1. Age
  2. Female
  3. Smoking
  4. Extensive computer use
  5. LASIK
  6. Med:
    * Anticholinergics
    * Hormones
    * CS
66
Q

When do you begin tx for dry eyes?

A

Moderate to severe

Nonpharm: mild

67
Q

Non-pharm for dry eyes?

A
  1. Education/environmental mods
  2. Elimination of offending meds
  3. Warm compresses, eyelid hygiene
  4. Eye drops
68
Q

Anti-inflammatory agents for dry eyes?

A
  1. Cyclosporine
  2. Lifitegrast
  3. CS
69
Q

Cyclosporine

MOA, ADR, Counselign

A

MOA: Calcineurin inhibitor -> increases eyes ability to produce tears (0.05% - Restasis)

ADR: burning, redness, watery eyes, itching
Counseling: can be used with artificial tears and shouldn’t be used with active infections or with contacts

70
Q

What are the formulations of Cyclosporine 0.05%?

A
  1. Restasis multi-dose
  2. Cequa: NCELL tech (preservative free)
71
Q

Lifitegrast

Brand, MOA, ADR

A

Xiidra 5%
MOA: Lymphocyte function-associated antigen 1 (LFA-1) antagonist
ADR: burning, dysgeusia, blurred vision, watery eyes

72
Q

What eye drops are used to treat the cause of dry eyes? which one treats the sx?

A

Cause: cyclosporine 0.05%
Sx: Lifitegrast 5%

73
Q

When can we use CS for dry eyes? ADRs?

A

Loteprednol (Lotemax): Shrot term basis up to 2 weeks

ADR: Increased IOP, cataracts

74
Q

What is blepharitis?

A

Inflammation of the eyelid margin

75
Q

What are the presentations of blepharitis?

A
  1. Swollen itchy eyelids
  2. Crusting or matting eyelashes
  3. Blurred vision
  4. Pink eye
76
Q

What is the tx for blepheritis?

A
  1. Warm compresses
  2. Eyelid cleansing
  3. Artificial tears
77
Q

Types of carbonic anhydrase inhibitors (topical>

A
  1. Brinzolamide
  2. Dorzolamide
78
Q

Types of Rho kinase inhibitors?

A

Netarsudil
ADR: cnjunctival hyperemia, hemmorhage

79
Q

Types of adrenergic agonist?

A
  1. Dipivefrin
  2. Apraclonidine
  3. Brimonidine
80
Q

Types of cholinesterase inhibitors?

A

Echothiophate

81
Q

Cholinergic agonist-direct acting?

A
  1. Carbachol
  2. pilocarpine
82
Q

Combo products?

A

Timolol/dorzolamide (Cosopt)
Timolol/brimonidine (Combigan)
Brinzolamide/brimonidine (Simbrinza)
Netarsudil/latanoprost (Rocklatan)

Therapeutics III (40 decks)

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