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GI OP > Glaucoma E2 > Flashcards

Glaucoma E2 Flashcards

1
Q

Normal IOP Range/Elevated IOP

A

Normal: 13-21 mmHg
Elevated: 21 mmHg

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2
Q

Dx?
Glaucomataeous Changes + Normal IOP

A

Normal-Tension Glaucoma

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3
Q

Dx?
Glaucomatous Changes + Elevated IOP

A

Glaucoma

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4
Q

Dx?
No Glaucomatous Changes, but elevated IOP

A

Ocular Hypertension

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5
Q

What are the two outflow pathways for aqueous humor? Which one is IOP dependent?

A
  1. Trabecular/Schlemm’s Canal (90% of outflow) –> IOP Dependent
  2. Uveoscleral (10% of Outflow) –> IOP Independent
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6
Q

In what three situations should we treat patients with the therapies covered in this section?

A
  1. Glaucoma Diagnosis (GC and Elevated IOP)
  2. Ocular Hypertension and Risk Factors
  3. N-T Glaucoma and documentation of progression of visual field loss.
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7
Q

Goals of Glaucoma Treatment ( how much do we want to reduce IOP by in ALL patients).

A
  1. Preserve the Nerve “Stabilize the visial fields”
  2. Lower IOP (at least 25% pretreatment value) –> Reassess based on clinical progress or if the goal is not achieved.
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8
Q

Primary Open-Angle Glaucoma Risk Factors

A
  1. Elevated IOP
  2. Age >60 (40 if black)
  3. Family Hx
  4. Ethnicity (black/Hispanic)
  5. Increased cup to disc ratio
  6. Thin Central Cornea Thickness
  7. Low Ocular Perfusion Pressure (SBP/DBP minus IOP)
  8. TIIDM
  9. Myopia
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9
Q

Risk Factors of POAG Progression

A
  1. High IOP at baseline or increased at follow-up.
  2. Older age
  3. Disc hemorrhage
  4. Large Cup to Disc Ratio
  5. Thin Central Cornea
  6. Low Ocular Perfusion Pressure
  7. Low Adherence to meds
  8. Progression in fellow eye.
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10
Q

Benefits/Risks of Surgery for POAG

A

Benefits: More effective, few complications

Risk: Increased cataract risk, and increased risk of loss of visual acuity.

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11
Q

Benefits/Risks of Medical Treatment for Glaucoma

A

Benefits: Less invasive, Low cataract risk, better visual acuity stability.

Negatives: Daily for life.

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12
Q

Mechanism of Prostaglandin Analogs

A

Increase Scleral Permeability –> Reduces IOP by 25-35 %.

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13
Q

Prostaglandin Analog Contraindication

A

Existing Ocular Inflammation

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14
Q

Omnidepag Mechanism; How does it increase outflow?

A

EP2 receptor Agonist–> increases trabecular and scleral outflow.

non-inferior IOP reduction compared to latanoprost or timolol.

Similar ADE to Prostaglandin analogs but less ocular irritation.**

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15
Q

Prostaglandin Analog ADEs

A

Hyperemia
Hypertrichosis (eyelash growth)
Iris Pigmentation

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16
Q

Preferred Prostaglandins

A

Bimatoprost
OR
Latanoprost Bunod

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17
Q

Prostaglandins with the least ADEs

A
  1. Omnedepag
  2. Latanoprost Bunod
  3. Latnoprost
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18
Q

Ocular Beta-Blocker Mechanism

A

Decrease production of AH –> 20-25 % reduction in IOP.

All equally efficacious

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19
Q
  1. Preferred Beta-Blockers
  2. BB w/ least ADE
A

Preferred = Timolol or Levobunolol

Least ADEs = Betaxolol or Cartelol

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20
Q

BB ADE

A
  1. Local Irritation
  2. Systemic Symptoms ( Cardiac/Pulmonary/CNS)–> Minimized w/ proper administration.
  3. Tachyphylaxis (diminishing effect)
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21
Q

Ocular BB Contraindications

A
  1. Sinus Bradycardia
  2. Heart Block
  3. Heart Failure
  4. Pulmonary Disease
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22
Q

Brimonidine Mechanism; How does this lead to a reduction of IOP.

A

Alpha-2-agonist
*Decreases AH production –> Leads to 20-25% IOP reduction.
*May have a neuroprotective effect

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23
Q

Brimonidine ADEs

A
  1. Local Irritation
  2. Systemic (Drowsiness, Xerostomia)
  3. Tachyphylaxis

Precaution = CVD

24
Q

Which is preferred and why:
Brimonidine/Timolol or Latanoprost

A

Latanoprost Preferred due to price

25
Q

Carbonic Anhydrase Inhibitor Mechanism
How are topical agents different

A

Inhibit Carbonic Anhydrase leading to a decrease in AH production by the ciliary body by decreasing bicarbonate secretion.

Topical Agents = Specific for CA-2

26
Q

CAI Oral vs Topical Efficacy

A

Oral Agents = 20-30% IOP reduction

Topical = 15-20% reduction

27
Q

Oral CAIs

A

Acetazolamide
Metazolamide

28
Q

Topical CAIs

A

Brinzolamide
Dorzolamide

29
Q

Preferred CAI combination product

A

Preferred = Dorzolamide/Timolol (similar efficacy to latanoprost, better diurnal control than brimonidine)

Alternatives = Brinzolamide/Brimonidine

30
Q

Rhopressa [Netarsudil] Mechanism. Explain how this reduces IOP.

A

Rho Kinase Inhibitor –> Decrease actin-myosin contractions which leads to an increase in trabecular outflow.

*20% IOP reduction if <27 mmHg. However, more pronounced effect at higher IOPs.

31
Q

Rhopressa ADEs

A

HIGH INCIDENCE
*53% hyperemia
*20% Conjunctival Hemorrhage

32
Q

Open-Angle Glaucoma First Line Agents

A

Preferred = Prostaglandins
Alternative = Beta-Blocker

Use as few drugs as possible at the lowest effective dose

educate on lacrimal occlusion to prevent systemic side effects

33
Q

Open-Angle Glaucoma Second Line Agents

A
  1. Brimonidine
  2. Dorzolamide/Timolol
  3. CAIs
  4. Netarsudil/Omnidenepag
34
Q

How frequent should you schedule follow up for open-angle glaucoma patients under the following situations:

  1. Disease Progression?
  2. No progression, IOP met for 6 + months
  3. No progression, IOP met <6 months
  4. No progression, IOP goal not met.
A
  1. 1-2 months
  2. 6-12 months
  3. 6 months
  4. 3-6 months
35
Q

When should you treat Ocular Hypertension?

A

If they have risk factors including:
ethnicity, family history, thin central cornea, large cup to disc ratio, IOP >25.

36
Q

When should you treat a patient with normal-tension glaucoma?

A

If they have documented the progression of visual field loss.

37
Q

What is the main pathophysiology of Primary-Angle Closure Glaucoma

A
  1. Pupillary Block –> Lens contact iris at the pupillary margin. or “Iris bombe” where the iris bows and contacts the trabecular meshwork.
  2. Plateau Iris –> “Less Common”
    *Anatomical Defect of the ciliary body

*Typically Unilateral

38
Q

Primary Angle-Closure Glaucoma Clinical Presentation

A

*Unilateral
*Rapid IOP Fluctuations (up to 80 mmHg)
*Rapid Vision Damage

39
Q

PACG RF

A
  1. Shallow Anterior Chamber Depth
  2. Eastern Asian Ancestry
  3. Family History
  4. Hyperopia
  5. Age
40
Q

Subacute vs Acute PACG Attacks

A
  1. Subacute–> Self Limiting (vary by pain threshold of the patient. Relieved by sleep or miosis.
  2. Acute “AACC”
    Signaled by prodrome
    Caused by rapid mydriasis
    Halo around light
    Edematous Cornea
    Pain, HA, N/V
    Ophthalmic Emergency
41
Q

PACG Treatment Goals

A
  1. Preserve Vision (Decrease optic nerve damage)
  2. Prep Eye for Laser Peripheral Iridotomy (decrease IOP, inflammation, and open the angle)
42
Q

Agents used to reduce IOP in PACG

A
  1. Carbonic Anhydrase Inhibitors (IV Preferred) –> Acetazolamide 500 mg IR
  2. Topical Beta-Blocker
  3. Topical Alpha Agonist –> Apraclonidine Preferred

No prostaglandins–> Take too long

43
Q

What CAI is preferred in PACG?

A

Acetazolamide 500 mg IR IV

44
Q

What alpha agonist is preferred in PACG to reduce IOP?

A

Apraclonidine

45
Q

What agent is used in acute PACG to open the angle?

A

Pilocarpine

46
Q

How does Pilocarpine work?

A

It induces myosis, pulling the iris away from the trabecular network.

This prevents ciliary body thickening.
It also can cause vascular congestion, cholinergic crisis, spasm, brow ache, headache, and lid twitch.

47
Q

What agent is used in acute PACG to address inflammation?

A

Ophthalmic Steroids.

48
Q

In acute PACG, when are hyperosmotics used?

A

When anti-secretagogues and pilocarpine have no effect after 1 hour.

These cause the quickest and largest reduction in IOP.

49
Q

How do hyperosmotics work?

A

They reduce vitreous volume significantly leading to a quick and large IOP decrease.

50
Q

What are the oral hyperosmotics?

A
  1. Glycerin (1-2 g/kg)
  2. Isosorbide (1-2g/kg)
51
Q

What is a risk of using glycerin?

A

Ketoacidosis in TIIDM

52
Q

What is an IV hyperosmotic?

A

Mannitol (1.5-2 g/kg)

53
Q

What is the risk of using mannitol?

A

Circulatory overload risk

54
Q

What is the goal of PACG treatment? What three things are we targetting?

A

Lower IOP, Open the Angle, Maintain a miotic Pupil.

55
Q

After initial treatment for PACG, when should clinicians follow up on the patient?

A
  1. Check IOP q 15-30 minutes
  2. Check angle when IOP drops into normal range.
56
Q

In the management of acute PACG, what should be done 1 hour after initial treatment?

A
  1. Give hyperosmotic if needed for high IOP
  2. Repeat First Line Medications
  3. Add steroid as needed for inflammation
57
Q

How is chronic PACG managed?

A

Keep the angle open to reduce the risk of attack

Managed similar to Primary Open-Angle Glaucoma.

First Line = Prostaglandin Analogs or Beta-Blockers

May also perform Iridotomy

GI OP (18 decks)

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