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ocular disease II: glaucoma > medical therapy 2 > Flashcards

medical therapy 2 Flashcards

1
Q

” Receptors found in heart

“ Stimulation causes increase heart rate, cardiac contractility and atrioventricular conduction

A

beta 1

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2
Q

” Located in bronchial muscle, blood vessels and uterus

“ Stimulation causes dilation of bronchi and blood vessels

A

beta 2

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3
Q

” Recently identified in mammals “

Mediation of lipolysis

A

beta 3

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4
Q

Topical ocular beta blockers (OBB) are β- adrenoreceptors antagonists
! β-adrenergic antagonists are competitive inhibitors

A

beta adrenoreceptor antagonists

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5
Q

selective beta

A

either beta 1 or beta 2

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6
Q

Non-selective

A

both beta 1 and beta 2

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7
Q

Selectivity is relative at high concentrations selective β-adrenergic act on all beta receptors.

A

selectivity of beta receptors

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8
Q

Ocular beta blockers (OBBs) act by reduction in aqueous formation
! No change in outflow facility
! Aqueous formation can decrease as much as
50%
! Exact mechanism still not clear (despite 30 years of use).
! Two hypothesis ◦ Classic hypothesis
◦ Alternate hypothesis

A

moa of beta blocker

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9
Q

! Direct relationship between OBBs and cAMP not supported in all studies
! IOP can decrease in response to increase in cAMP
! Both dextro –isomer (low affinity) and levo- isomer (high affinity) of timolol decrease IOP. Which gives evidence against competitive inhibition.

A

evidence against classic hypothesis

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10
Q

Clilary process are under continuous tonic stimulation to produce aqueous (mediated by epinephrine).
! Beta- blockers interfere with tonic stimulation
! This is a speculative hypothesis ! No anatomic basis identified yet.

A

alternate mechanism of OBB

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11
Q

we have to choose a hypothesis to follow, which do we choose?

A

classic

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12
Q

! Lowering IOP ocular hypertension and open angle glaucoma
! May be used stand alone or in combination with other drugs
! Secondary glaucoma ! Angle closure glaucoma

A

indication of OBB

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13
Q

! Relative or absolute contraindication in patients with
◦ Pulmonary disease, bronchial asthma, severe COPD
◦ Betaxolol (selective OBB is not contraindicated for
above diseases)
! Any patient with sinus bradycardia (less than 60 beats resting), overt congestive heart failure
! Any patient that develops ether heart or lung problems after starting OBBs
! Patient hypersensitivity to drug or any component

A

glaucoma contrainidication

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14
Q

clinical tip: anyone we consider putting on OBB, you must measure what?

A

pulse rate and BP!

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15
Q

you put a pt on timolol, and if you notice they have lung issues they did not have before, what do u do?

A

take pt off it! this is too much of a coincidence, they didnt have this problem before

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16
Q

do beta blockers decrease heart rate?

A

yes

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17
Q

if the heart rate is

A

no! why? b/c it will further decrease heart rate

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18
Q

treatment regimen of OBB

A

OBBs used once or twice daily
! Twice daily may lower IOP greater than once
daily
! More and more practitioners use qd and increase to bid if needed (to minimize side effects)

! All OBBs twice daily

! Exception
◦ Isatalol qam
◦ Timoptic XE or GFS (gels) qd
◦ Betagan qd

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19
Q

treatment regimen of OBB

A

OBBs used once or twice daily
! Twice daily may lower IOP greater than once
daily
! More and more practitioners use qd and increase to bid if needed (to minimize side effects)

! All OBBs twice daily

! Exception
◦ Isatalol qam
◦ Timoptic XE or GFS (gels) qd
◦ Betagan qd

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20
Q

what is the most common form of timolol?

A

timolol maleate 0.5%

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21
Q

! 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

A

timolol

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22
Q

why is timolol a good alternative to pg when used appropriately?

A
  • when they dont like using PG due to its side effects

- PG is too expensive!

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23
Q

why is timolol a good alternative to pg when used appropriately?

A
  • when they dont like using PG due to its side effects

- PG is too expensive!

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24
Q

why are beta blockers prescribed bid?

A

max effect is 12 hrs

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25
Q

when does aqhu production go down?

A

night time

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26
Q

Timolol AM dose reduces IOP below baseline
! Timolol PM dose does not reduce it below baseline levels.
! This casts doubt on its efficacy on PM dosing.

A

am/pm efficacy

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27
Q

Timolol AM dose reduces IOP below baseline
! Timolol PM dose does not reduce it below baseline levels.
! This casts doubt on its efficacy on PM dosing.

A

am/pm efficacy

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28
Q

short term escape of obb

A

Not in all patients
! Efficacy of timolol decreases over time
(several weeks)
! Response of beta receptors to constant antagonist
! There may be an up regulation of beta receptors in target tissue
! Important- not in all patients!

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29
Q

long term drift of obb

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 don’t know for sure

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30
Q

what does washing out mean?

A

stopping drug completely

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31
Q

what is a good wash out period for a drug?

A

4 weeks

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32
Q

obb inhibits –> beta agonist –> activation of g protein –> membrane bound adenyl cyclase –> catalyzes ATP –> cAMP –> production of aqueous from ciliary processes

A

moa of obb

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33
Q

why would u give someone 0.25 timolol?

A

pediatric or someone that cant handle side effects of 0.5% timolol

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34
Q

its important to ask patient when they took their last dosage of medication?

A

-if they missed dosage that day, result could be high in clinic

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35
Q

what is long term drift?

A

Over months to years
! Control of IOP not as good as once.
! Washing out and re-starting helps restore levels

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36
Q

are there symptoms for poag?

A

no. not usually

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37
Q

whenever you suspect drug is not working what do u do?

A

ask pt to drop it in their eye in front of you. sometimes you will see that they aren’t good at applying it.

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38
Q

whats the washout period for drugs?

A

Clinically a 4-week wash out period is considered acceptable

IOP lowering effects may persist for 2 weeks
! Aqueous flow up to 6 weeks.

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39
Q

when would you consider washout?

A

pt is not responding to drug; or you want a clear picture of what is going on

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40
Q

pros of gels

A
  • improves bioavailability (stays where its supposed to stay)
  • decrease systemic absorption (stays in conj longer)
  • once a day dose instead of 2x a day (compliance may be better)
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41
Q

cons of gels

A

can blur vision if left over in morning

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42
Q

timoptic XE (gel) is preserved with what?

A

benzododecinium bromide (not BAK)

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43
Q

what beta blocker is applied once a day?

A

istalol

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44
Q

! Formulated with potassium sorbate
! Claims to enhance bioavailability so once daily.
! Lower BAK concentration
! Most visits IOP difference is within 1.0mmHg between groups 95% CI
! All visits within 1.5mmHg (compared to twice daily)

A

istalol

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45
Q

! Selective beta blocker
! Initially 0.5% solution (1985)
! Later 0.25% suspension of resin coated beads (gradual release) – Betoptic S (Suspension)

A

betaxolol hydrochloride

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46
Q

is betaxolol solution available in USA?

A

no (we only get suspension-coated and more comfortable)

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47
Q

! Cause less ocular irritation compared to Solution.
! Less effective when compared to Timolol
! Advantage it is selective beta blocker – can be used in patients with pulmonary disease.

A

betaxolol suspension (Betoptic S)

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48
Q

what drug can be used safely with patients with pulmonary disease due to is selectivity as a beta blocker?

A

betoptic s

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49
Q

anything that blocks calcium to cell will do what?

A

neuroprotection (calcium going to cell will cause death)

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50
Q

May possess calcium channel blocker properties
◦ Thus may have neuroprotectic effect*
◦ Highly lipid soluble, binds well with plasma
proteins
“ Significance: Lower CNS effects when compared to timolol

A

Betaxolol properties

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51
Q

if betxolol is neuroprotective, can this be our go to drug?

A

betxolol has less iop lowering than timolol and PG; it may provided neuroprotection, but it cant beat PG; iop lowering is proved to protect GC (good for glaucoma)

52
Q

local side efects?

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 of OBBs ◦ Sensitivity not uncommon
◦ Preservative free timolol is available (very expensive)

53
Q

local SE of propanolol

A

corneal anesthesia; long run can lead to keratopathy

54
Q

local SE of OBB

A

none

55
Q

local SE of any drug

A

discomfort, burning, stinging

56
Q

preservative used for obb, why?

A

breaks down corneal epithelium.

–> good for drug to pass through

57
Q

what cornea barrier is the most resistant to keep drug outside?

A

epithelium

58
Q

con of BAK

A

causes hypersensitivity
expensive
doesnt always penetrate as well as u like

59
Q

local side effect of timolol - due to preservative

A

Decreased tear production
! Decreased goblet cell density
! Dry eye symptoms
! Ocular cicatrical pemphigoid (immune rxn to drug)

60
Q

what disease can metipranolol cause?

A

granulomatous uveitis

61
Q

systemic side effects of obb?

A

OBBs enter systemic circulation via nasolacrimal system
◦ Almost like intravenous dose of medication (bypasses first pass metabolism)
! Does not approach oral dose

62
Q

typical dose of OBB?

A

20-60 mg PO

63
Q

peak plasma value of obb

A

50-103 ng/ml

64
Q

trough plasma value of obb

A

0.8-7.2 ng/ml

65
Q

two drops of timolol plasma levels range; and why is it bad?

A

5-9.6 ng/ml; this is similar to trough plasma values; can cause systemic side effects

66
Q

what do we need to make sure to do when applying timolol?

A

punctal occlusion to avoid systemic effects

67
Q 
! 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 
! CNS fewer with the use of betaxolol
A

cns adverse effects

68
Q

which obb has fewer cns adverse effects?

A

betaxolol

69
Q

what do beta blockers do?

A

◦ Lower heart rate
◦ Lower blood pressure
◦ Decreased myocardial contractility
◦ Slowed conduction time

70
Q

Blocking beta-1 receptors interferes with what?

A

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

71
Q

topical obb heart effects

A

Decreased heart rate and significant bradycardia

! Reduced blood pressure

72
Q

will topical obb have good effect on hypertension pt?

A

may not give us any further benefit; they are already taking oral obb

73
Q

what do we always check before presribing obb?

A

◦ Always check BP and pulse rate on

patients prescribed or on OBBs

74
Q

! Timoptic XE and other gels less effect-why?

A

Gels stay in eye and decreased systemic absorption.

75
Q

! 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 Beta-2 receptors.
! Betaxolol has been used safely in patients with pulmonary disease.

A

pulmonary adverse effects of obb

76
Q 
! Affects lipid metabolism
! Normal volunteers used timolol: 
◦ 12% increase in triglycerides
◦ 9% decrease in HDL
◦ Not all studies showed this effect ! Data on OBBs and lipids inconclusive.
A

metabolic adverse effects of obb

77
Q

what are low hdl levels?

A
78
Q

! Depression -1960s and 1970s
! Subsequently large scale population based studies
◦ No effect
No robust evidence for use of OBBs and depression- evaluate case by case

A

drug disease interaction-cns

79
Q

! Cardiovascular disease- contraindicated
◦ May worsen BP- potentially worsening orthostatic hypotension, cerebrovascular disease, preripheral vascular disease.
! Pulmonary disease caution
! Anyone on OBBs develops these- alter
medications
◦ May relieve symptoms/ conditions

A

drug disease interaction - cardiovascular and pulmonary disease

80
Q 
"  nervousness,
"  sweating,
"  intense hunger
 "  trembling,
"  weakness,
"  palpitations
A

symptoms of hypoglycemia

81
Q

if diabetic has hypoglycemia, what drug could mask the effects?

A

beta blockers! this is bad because its a true problem in insulin dependent patients (they wont know that they need more insulin :( )

82
Q

name 3 adrenergic agents

A

! Clonidine
! Apraclonidine
! Brimonidine

83
Q

! Lowers IOP well- but
◦ Causes sedation
◦ Systemic hypotension
◦ Narrow therapeutic index

A

clonidine

84
Q

Mechanism of action
◦ Decreased aqueous production
◦ Improves trabecular outflow
◦ Decreases episcleral venous pressure

A

moa of apraclonidine

85
Q 
More hydrophillic
◦ Does not penetrate eyes and blood brain
barrier
◦ More apha-2 selective 
◦ Wide therapeutic index
A

apraclonidine

86
Q

why is lowering episcleral venous pressure good for glaucoma?

A

aqhu can come out easier

87
Q

what is iop a function of?

A

production and outflow

88
Q

what influences outflow?

A

if episcleral venous pressure is high, aqhu cant come out

89
Q

! FDA approved to prevent post laser treatment spikes in IOP

! Adjunctive therapy- TID

A

uses of apraclonidine

90
Q

Reduction of aqueous flow

A

moa of brimonidine

91
Q

highly alpha 2 selective drug

A

brimonidine

92
Q

! Peak effectiveness in 2 hours

! Effect present at lower amount at 8 hours ! Thus TID dose

A

brimonidine

93
Q

! Prophylactic –to avoid post laser IOP spike

! Primary or secondary therapy glaucoma and ocular hypertension

A

indication of brimonidine

94
Q

contraindication of brimonidine

A

! Allergy to drug

! Contraindicated in patients receiving monoamine oxidase (MAO) inhibitor therapy (antideppresants).

95
Q

can you give antiallergy meds to someone with allergies to drugs in hopes of clearing your allergy to the drug?

A

source of allergen will continue, but you cant get out of it; anti-allergy wont solve all problems

96
Q

! Conjunctival follicles, ocular allergic reactions, and ocular pruritus (itching).
! headache, blurring, foreign body sensation, fatigue/drowsiness,
! Oral dryness,
! Ocular hyperemia, burning and stinging,

A

adverse reaction to brimonidine

97
Q

what is combigan?

A

brimonidine + timolol (BID)

98
Q

whats wrong with combigan?

A

not much logic behind this; brimonidine is supposed to be TID and timolol is BID

99
Q

cosopt

A

dorzolamide (CAI) and timolol - BID

100
Q

WHAT fixed combo drug makes sense?

A

simbrinza (brinzolamide and brimonidine) - both drugs are TID; and combined is TID; makes sense

101
Q

Any method that prevents or slows the death of neurons is considered what? therfore?

A

neuroprotective; all treatments are neuroprotective

102
Q

true neuroprotection

A

◦ Prevent destructive cellular events

◦ Enhance survival of cells after damage

103
Q

what drug is approved for use in glaucoma pts that have indication of neuroprotection

A

NONE!!!!!!!

104
Q

◦ 1) the agent must have a target in the retina;
“ Yes they are present
◦ 2) it must be neuroprotective in animal
models;
◦ 3) it must reach neuroprotective concentrations in the posterior segment after clinical dosing;
◦ 4) it must be shown to be neuroprotective in controlled clinical trials.

A

4 criteria for drug to be neuroprotective

105
Q

if drops are given topically how readily are they getting to vitreous and retina?

A

not doing a good job; its hard for it to reach retina

106
Q

cholinergic drug for glaucoma

A

pilocarpine (angle closure glaucoma with pupillary block)

107
Q

moa of pilocarpine

A 
!  Anatomic relationship between anterior tendons of ciliary muscle and
◦  Scleral spur
◦  Peripheral cornea
◦  Trabecular meshwork
◦  Inner wall of schlems canal

! Contraction of ciliary muscle causes
◦ Unfolding of meshwork
◦ Widening of Schlemm’s canal

108
Q

pilocarpine dosage?

A

1 or 2% two to 3 times in 30 minutes

109
Q

! Pilocarpine nitrate
◦ 0.5% to 4% QID (four times daily)

! Pilocarpine hydrochloride
◦ 0.5% to 6%

! Preservative BAK and EDTA
! Pilocarpine gel- bed time

A

pilocarpine

110
Q

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

A

pharmacokinetics of pilocarpine

111
Q

SE of pilocarpine

A

! Stinging
! Burning
! Prolonged use- risk of failure with surgeries ! Risk of hyphema during surgeries
! Ciliary spasm, temporal or supraorbital headace and induced myopia
◦ Because of drug induced contraction of ciliary muscle

112
Q

pilocarpine vf effect?

A

problems in dark environment - less light enters the eye; pupil should dilate in dark but with pilocarpine it stays small; glaucoma pts have periphery problems to begin with

113
Q

! 1% drug
! 10-30 minutes- miosis
! Max IOP reduction 75 minutes
! Miosis lasts 4-8 hours ! IOP lowering 4-14 hrs

A

dose effect varies with strength

114
Q

Miosis vision decrease ! Intense miosis and constant
accommodation
◦ Increase risk of pupillary block

A

SE of pilocarpine

115
Q

Decreased efficacy of lowering IOP with long term use.
◦ Mechanism unclear
◦ Increasing problems in drainage mechanism

A

long term escape of pilocarpine

116
Q

! Extremely rare
! If occurs
◦ Sweating
◦ Salivation and ◦ Gastrointestinal over activity
◦ Atropine is pharmacological antagonist for pilocarpine

A

systemic toxicity of pilocarpine

117
Q

if intraocular congestion like uveitis-why do we not give them pilocarpine?

A

if you leave iris in contracted form - chance of synechiae is increased; also we want to relieve cil muscle to decrease pain of patient

118
Q

contraindication of pilocarpine

A

! Risk/ history of retinal detachment
! Intraocular congestion like uveitis
! Any one whom pupil size and accommodation is an issue

119
Q

what can pilocarpine be combined with?

A

Can be combined with drugs that decrease aqueous humor production

120
Q

members of sulfonamide family

A

CAI

121
Q

MOA OF CAI

A

Carbonic anhydranse inhibitors causes reduction of bicarbonate ions in posterior chamber
! Subsequently prevents Na+ movement and hence water movement (LOWERS IOP)

122
Q

! Acetazolamide max dose 250mg qid

! Methazolamide max dose 150 mg bid

A

CAI

123
Q

! Sulpha allergies
! Diabetic patients susceptible to ketoacidosis
! 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

A

contraindications to CAI

124
Q

anyone with bad kidneys, livers, lungs, should not be given what drug?

A

oral CAI (b/c the drug will not be metabolized and can lead to severe systemic problems)

125
Q

SE of cai

A

numbness, paresthesias, malaise, anorexia, nausea, flatulence, diarrhea, depression, decreased libido, poor tolerance of carbonated beverages

myopia, hirsutism, increased serum urate, and, rarely, thrombocytopenia and idiosyncratic aplastic anemia

126
Q

what happens when u take cai and drink soda?

A

unpalatable metallic taste (taste change)

127
Q

Dorzolamide ! Brinzolamide
! BID or TID
! Three times daily gives better reduction in intraocular pressure approximately 1mmHg

A

topical agents cai

ocular disease II: glaucoma (6 decks)

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