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Summer Final: Glaucoma > Medical Management Of Glaucoma-2 > Flashcards

Medical Management Of Glaucoma-2 Flashcards

1
Q

Beta 1 receptors found where

A

Heart

Stimulation causes increase HR, cardiac contraxtiltiy and atropoventricualr conduction

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2
Q

Beta 2 receptors found where

A

Located in bronchial muscle,. Blood vessles and uterus

Stimulation causes dilation of bronchi and blood vessels

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3
Q

Beta 3 receptors found wher

A

Recently identified in mammals

Mediation of lipolysis

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4
Q

Topical ocular BBlockers (OBB)

A

B adrenergic antagonsits are competitive inhibitors

Classifications

  • selective (B1 or B2)
  • non selective (both B1 ands B2)
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5
Q

Selectivity of BBlockers

A

Selectivity is relatively at high concentrations selective B adrenergic act on all beta receptors

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6
Q

MOA of OBB

A

Reduction in aqueous formation

  • no change in outflow facility
  • aqueous formation can decrease as much as 50%
  • exact mechanisms still not clear (despite 30 years of use)
  • two hypothesis: classic and alternate
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7
Q

Classic hypothesis of OBB

A

Inhibits B adreneriv agonsits from binding its receptors, cannot act as a second messenger with cAMP, reduced production of aqueous from CB

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8
Q

Alternate mechanisms of OBBs

A
  • ciliary process are under continuous tonic stimulation to produce aqueous (medicated by epinephrine)
  • B blocker interfere with tonic stimulation
  • this is a speculative hypothesis
  • no anatomical basis identify yet
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9
Q

Indications of OBB

A
  • lowering IOP ocular hypertension and open angle glaucoma
  • may be used stand alone or in combination with other drugs
  • secondary glaucoma
  • angle closure glaucoma
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10
Q

Contraindications of OBB

A
  • relative or absolute contraindication in patients with pulmonary disease, bronchial asthma, severe COPD. Betaxolol (selective OBB is not contraindicated for above disease)
  • any pateitn with sinu bradycardia (less than 60 beats restin), overt CHF
  • any patient that develops either heart or Leung problems after starting OBBs
  • patient hypersensitivity to drug or any components
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11
Q

Any one with less than ____- beats per minute or with ______ should not be on OBB

A

60BPM

CHF

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12
Q

Treatment regimen for OBB

A
  • used once or twice daily
  • twice daily may lower IOP greater than once daily
  • more and more practictioners used qd and increase to BID if needed (to minimize side effects)
  • all OBBs twice daily
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13
Q

Exception to using OBB twice a day

A

Isatalol qam
Timoptic XE or GFS (gels) qd
Betagan qd

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14
Q

Timolol

A
  • available as timolol maleate or hemihydrate 0.25 and 0.5%
  • commonly used 0.5%
  • non selective beta adrenergic antagonist
  • no corneal anesthesia (like propranolol)
  • greater efficacy than pilocarpine
  • lowers IOP in normals, ocular hypertensive and glaucoma patients
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15
Q

Most commonly used OBB

A

Timolol maleate 0.5%

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16
Q

Selectivity of timolol

A

Non selective

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17
Q

Timolol used as an alternative

A

Good alternative for PGs

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18
Q

Onset of action for timolol

A

30m following instillation

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19
Q

Peak action of timolol

A

2 hours

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20
Q

Maximal effect of timolol persists for how long

A

12 hours

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21
Q

IOP lowering of timolol persist for

A

24 hours

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22
Q

Timolol in pateitns with systemic BBlockers

A

Don’t put them on it If they are already on an oral BBcloker

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23
Q

When should we use timolol

A

AM
-reduces IOP below baseline

Timolol PM dose foes not reduce it below baseline levels

This casts doubt on its efficacy on PM dosing

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24
Q

Short term escape: timolol

A
  • not in all pateitns
  • efficacy of timolol decreases over time (several weeks)
  • repsosne of beta receptors to constant antagonsits
  • there may be an up regulation of beta receptors in target tissue

Important-no in all patients!

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25
Q

Long term drift: timolol

A
  • over months to years
  • control of IOP not as good as once
  • washing out and re starting helps restore levels
  • lack of efficacy or poor adherence? We dont know for sure
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26
Q

Washout period of timolol

A
  • IOP lowering effects may persist for 2 weeks
  • aqueous flow up to 6 weeks
  • clinically a 4 week washout period is considered acceptable
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27
Q

Gels vs drops for timolol

A

Gels

  • improve bioavailability
  • decreases systemic absorption
  • once a day dose instead of BID-compliance/adherence may be better
  • blurs vision if left over in morning
  • timoptic XE preserved with benzododecinium bromide (not BAK)
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28
Q

Istalol

A
  • timolol maleate 0.5%
  • formulated with potassium sorbate
  • claims to enhance bioavailability so once a day
  • lower BAK concentration
  • most visits IOP difference is within 1.0mmHg between groups 95% CL
  • all visits within 1.5mmHg (compared to twice daily)
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29
Q

Why is istalol once daily

A

Formulated with potassium sorbate. Claims to enhance bioavailability, so only needed once daily

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30
Q

Betaxolol hydrochloride

A
  • selective BBlocker
  • initially 0.5% solution (1985)
  • later 0.25% suspension of resin coated beads (gradual release)-betoptic S (suspension)
  • betaxolol solution is not longer available ion USA
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31
Q

Is betaxolol solution available in US

A

No

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32
Q

Clinically a _____ wash out period is considered acceptable

A

4 week wash out

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33
Q

Why do we use betaxolol suspension (betoptic S) instead of solution

A
  • causes less ocular irritation compared to solution
  • less effective when compared to timolol
  • advantage it is selective BBlocker- can be used in patients with pulmonary disease
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34
Q

Local side effects of betaxolol

A
  • propranolol-corneal anesthesia
  • other OBBs no such effect
  • discomfort, burning stinging. Factors like active molecule, pH, preservative and vehicle
  • preservative-BAK. BAK helps with penetration fo OBBs, sensitivity not uncommon
  • ocular cicatricial pemphigoid
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35
Q

Purpose of BAK in betaxolol

A

Helps with penetration of OBBS

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36
Q

Problems with BAK in OBBs

A
  • decreased tear production
  • decreased goblet cell density
  • dry eye systmpoms
37
Q

Betaxolol and blurring

A

Transient blurring with gel form (all gels not exclusively problem with OBBS)

38
Q

Granulomatous uvetiits and meripranaolol

A

Associated with it

39
Q

Why is betaxolol suspension not well liked

A

Because you have to shake it for a long time

40
Q

Systemic side effects of OBBs

A

Enter systemic circulation via nasolacrimal system
-almost like IV dose of medication

Does not approach oral dose

41
Q

Typical oral dose of BBlockers

A

20-60mg P.O.

  • first pass hepatic metabolism
  • 50% approx 10-30mg

Peak plasma values 50-103ng/mL
Trough plasma values 0.8-7.2 Ng/mL

42
Q

Two drops of timolol plasma level ranges

A

5-9.6 ng/mL

43
Q

CNS adverse effects

A
  • detailed history is required
  • anxiety, depression, fatigue, lethargy, confusion, sleep disturbance, memory loss and dizziness
  • sexual dysfunction
  • decreased libido men and women
  • impotence in men
44
Q

CNS side effects are fewer with which OBBs

A

Betaxolol

45
Q

Cardiovascular adverse effects of OBBs

A

-blocking beta 1 receptors interferes with normal sympathetic stimulation of heart

BBlockers

  • lower HR
  • lower BP
  • decreased myocardial contractility
  • slowed conduction time
46
Q

Topical OBBs and cardiovascular side effects

A
  • decreased HR and significant bradycardia
  • reduce BP. ALWAYS CHECK BP and pulse rate on patients RXed or on OBBs
  • timoptic XE and other gels less effect;gels stay in the eye and decrease systemic absorption
47
Q

What type of OBBs if better for having less cardiovascular effects

A

Gels

-they stay in the eye and decrease systemic absorption

48
Q

Pulmonary adverse effects of BBlockers

A
  • most problems were early on due to lack of experience with OBBs
  • 12 deaths in first 8 years; 50% of these had pulmonary disease
  • pulmonary effects due to blockade to B2 receptors
  • betaxolol has been used safely in patients with pulmonary disease
49
Q

Should we give someone BBlockers if they have cardiovascular disease

A

Contraindicated

-may worsen BP-potential worsening orthostatic hypotension, cerebrovascualr disease, peripheral vascular disease

50
Q

Should we give someone BBlocker with pulmonary disease

A

Use with caution

51
Q

If someone on OBBs develop cardiovascular or pulmonary diases while on it

A

Alter medications

-may relieve symptoms/conditions

52
Q

BBlockers interaction with diabetes

A

BBclockers alter some of the symptoms of hypoglycemia- so masks effect

A true problem in insulin dependent pateitns

53
Q

Adrenergic agents

A

Clonidine
Apraclonidine
Brimonidine

54
Q

Clonidine

A

Lowers IOP well but

  • causes sedation
  • systemic hypotension
  • narrow therapeutic index
55
Q

Pharmacology apraclondine

A

More hydrophilic

  • does not penetrate eyes and BBB
  • more A2 selective
  • wide therapeutic index
56
Q

MOA of apraclonidine

A
  • decreased aqueous production
  • improves TM outflow
  • decreases EVP
57
Q

Uses of apraclonidine

A
  • FDA approved to prevent post laser treatment spikes in IOP

- adjunctive therapy-TID

58
Q

Brimonidine

A
  • highly A2 selective drug
  • MOA: reduction of aqueous flow
  • peak effectiveness in 2 hours
  • effect present at lower amount at 8 hours
  • thus TID
59
Q

Indications of brimonidine

A
  • prophylactic- to avoid postlaser IOP spike

- primary or secondary therapy glaucoma and ocular hypertension

60
Q

Contraindications of brimonidine

A
  • allergy to drug

- contraindicated in patients receiving monoamine oxidase (MAO) inhibitor therapy

61
Q

Adverse reactions to brimonidine

A
  • conkinctival follicles, ocular allergic reactions, and ocular pruritis (itching)
  • HA, blurring, FB sensation, fatigue/drowsiness
  • oral dryness
  • ocular hyperemia, burning and stinging
62
Q

Combigan

A

Brominidine and timolol-BID

63
Q

Cosopt

A

Dorzolamide and timolol-BID

64
Q

MOA of rhokinase inhibitor

A

-changes to TM-cytoskeletal modulating drugs

65
Q

Netradusil Rhopressa

A
  • another class of ROCK inhibitor-small molecule
  • alter TM cells
  • Alters NE transporter (NET). NEY inhibitor lower aqueous production
  • changes EVP
66
Q

Rhopressa vs lotanaprost

A
  • diff-IOP approx 1mmHg
  • conjunctival hyperemia 52-57%
  • conjunctival hemorrhages 5-6%
  • increased lacrimation 5-7%
67
Q

Summary of Rhopressa

A
  • shows promise as a second line drug to PGA
  • roclatan-shows IOP lowering effect better than latanaprost and Rhopressa
  • side effects conjunctival hyperemia
  • cornea issues-erosions, change in endothelium, and cornea verticillata
68
Q

How often do you take Rhopressa

A

Once a day at bedtime

69
Q

Brinzolamide + brimonidine

A

Does better than individual drugs

Simbrinza

70
Q

Cholinergic drugs for glaucoma

A

Pilocarpine

Mainly angle closure glaucoma with pupillaryblock

71
Q

MOA of pilocarpine

A

Anatomic relationship between anterior tendons of ciliary muscles and

  • scleral spur
  • peripheral cornea
  • TM
  • inner wall of Schlems canal
72
Q

Contraction of ciliary muscle in atropine causes

A

Unfolding of meshwork

Widening of sclemss canal

73
Q

How to use pilocarpine in angle closure with pupillary block

A

1-2% two-three X in 30 minutes

74
Q

Types of pilocarpine

A
  • pilocarpine nitrate (0.5% QID)
  • pilocarpine hydrochloride (0.5%)
  • preservative BAK and EDTA
  • pilocarpine gel-bed time
75
Q

Pharmacokinetics of pilocarpine

A

Absorbed by cornea
Drug binds to iris pigment
Light iris-2%
Dark iris-6% may be needed

76
Q

Dose effect varies with strength in pilocarpine

A 
1% drug 
10-30 minutes-miosis 
Max IOP reduction 75 minutes 
Mitosis lasts 4-8 hours 
IOP lowering 4-14 hours
77
Q

Side effects of pilocarpine

A

Singing
Burning
Prolonged use-raise of failure with surgery
Risk of hyphema during surgeries
Ciliary spasm, temporal, or supraoribital HA and induced myopia
-BC of drug induced contraction of ciliary muscle

Mitosis vision decreased

Intent miropsis and constant accommodation
-increase risk of pupillary block

78
Q

Long term escape of pilocarpine

A

Decreased efficacy of lowering IOP with long term use

  • mechanisms unclear
  • increasing problem in drainage mechanisms
79
Q

Systemic toxicity of pilocarpine

A

Extremely rare
If it occurs
-sweating and salivation
-GI over activity

Atropine is antagonsits for it

80
Q

Contraindications of pilocarpine

A
  • risk/Hx of RD
  • intraocualr congestion like uveitis
  • any one whom pupil size and accommodative is an issue
81
Q

CAI

A

Members of sulfonamide family

82
Q

If someone has a sulfa allergy, what drug should we not use to treat glaucoma

A

CAI

83
Q

MOA of CAI

A

Reduction of bicarbonate ions in posterior chamber

-subsequently prevents Na+ movement and hence water movement

84
Q

CAI types and dose

A

Acetazolamide max dose 250mg QID

Methazolamide max dose 150mg BID

85
Q

Contraindications of CAI

A
  • Sulpha allergies
  • DM patients susceptible to ketoacidsosis
  • patients who have hepatic insufficiency and cannot tolerate the increase in serum ammonia
  • patients with chronic obstructive pulmonary disease, in whom increased retention of carbon dioxide can cause potentially fatal narcosis from a combination of both renal and respiratory acidosis
86
Q

Side effects of CAI

A
  • many well known ocular and systemic side effects occur with administration of all the CAIs
  • these include numbness, parathesias, malaise, anorexia, nausea, flatulence, diarrhea, depression, decreased libido, poor tolerance of carbonated beverages, myopia, hirsuotims, increased serum rate, and, rarely, thrombocytopenia and idiosyncratic asplastic anemia
87
Q

Topical CAIs

A

Dorzolamide
Brinzolamide

BID or TID

Three times daily gives better reduction in IOP appx 1mmHg

88
Q

Carbonated beverages and CAIs

A

Leaves a metallic taste in the pateitns mouth. They cannot tolerate it

Summer Final: Glaucoma (15 decks)

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