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BOARDS > OCular PHarm > Flashcards

OCular PHarm Flashcards

1
Q

How much topical drug is lost to evaporation

A

25%

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2
Q

Three fates of a topical drug (other than evaporation)

A
  1. Drainage into the NL
  2. Absorption into the systemic circulation bu the conjucunvtival and old vasculature
    3 penetration into the cornea
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3
Q

Percent of unchanged drug delivered to the desired site

A

Bioavailability

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4
Q

What drugs get through more, lipid or warmer?

A

Lipid

Small, non-ionized (uncharged), lipid soluble is best

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5
Q

Tear layers: lipid vs water

A

Lipid layer: lipid soluble
Aqueous layer: water soluble
Mucous layer: combo

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6
Q

Corneal layers: Walter vs lipid soluble

A

Epithelium and endothelium: lipid soluble

Stroma: water soluble

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7
Q

Maximize bioavailability

A

Drugs must have a combo of lipid and non lipid soluble components to maximize bioavailability

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8
Q

Most ocualr drugs are formulated as

A

Weak bases

Allows better penetration and bioavailability due to presence of more non-ionized (lipid soluble) portions of the drug reaching the aqueous humor

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9
Q

Pros of topical administration

A

At site of desired effect

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10
Q

Cons of topical administration

A

Site irritation, systemic side effects (BBlockers)

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11
Q

Oral administration pros

A

Simple dosage, easily administered, time released

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12
Q

Cons of oral administration

A

GI probs, drug degradation (1st pass metabolism in liver), absorption problems

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13
Q

Pros of subconjunctival administration

A

Rapid, effective absorbed

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14
Q

Cons of subconjunctival administration

A

Fear. Pain, inflammation

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15
Q

What route of administration has the highest bioavailability

A

IV

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16
Q

Pros of IV administration

A

Very rapid, dose accuracy, bypass digestive tract

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17
Q

Cons of IV administration

A

Danger of cardiotoxicity (bolus), sterility

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18
Q

IM administration pros

A

Rapid, controlled absorption

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19
Q

Cons of IM administration

A

Pain, necrosis

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20
Q

Involuntary motor systemic

A

Autonomic drugs

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21
Q

Efferent nerves can be either

A

Somatic (voluntary) or autonomic (involuntary)

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22
Q

Two major divisions of the autonomic pathway

A

Parasympathetic (cholinergic)

Sympathetic (adrenergic)

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23
Q

Where does parasympathetic begin

A

Cranio sacral

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24
Q

Which is longer in parasympathetic, pre or post ganglionic neuron

A

Preganglionic

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25
Q

What NT is released at the junction of the pre and post ganglion in parasympathetic

A

Ach

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26
Q

What NT is released at the junction of the post ganglion neuron and the target organ/gland

A

ACH

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27
Q

What receptors are found at the SOA in parasympathetic

A

M1, M2, M3

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28
Q

Functions of the parasympathetic

A

Rest/digest
Bronchoconstriction/miosis
SLUD (wet)

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29
Q

Where does sympathetic pathway start

A

Thoraco-lumbar

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30
Q

Which is longer in sympathetic, pre or postganglionc neurons

A

Postganglionic

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31
Q

What NT is released at the junction of the pre and post ganglionic neuron in sympathetic

A

Ach

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32
Q

What NT is released as the junction of the postganglionic neuron and the SOA in sympathetic

A

NE and epi

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33
Q

What receptors are on the SOA in sympathetic

A

A1,a2,b1,b2

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34
Q

Functions of sympathetic

A

Fight/flight
Bhronchodilate/ mydriasis
Dry

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35
Q

Iris sphincter receptors

A

M3

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36
Q

Ciliary muscel receptors

A

M2, M3

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37
Q

Lacrimal gland receptors

A

M2, M3

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38
Q

Iris dilator receptor (radial muscle)

A

A1

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39
Q

TM receptor

A

B2

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40
Q

Ciliary muscle adrenergic receptor

A

B2

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41
Q

NPCE adrenergic receptor

A

B2 (little B1)

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42
Q

CB vasculature adrenergic receptr

A

A2

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43
Q

What do cholinergic agonists promote

A

Parasympathetic

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44
Q

Three main structure of the eye that receive parasympathetic innervation

A

Sphincter muscle
Ciliary muscle
Lacrimal gland

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45
Q

What are chilinergic agonists used for in the eye

A

Glaucoma

accomodative ET

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46
Q

What are cholinergic agonists used to treat accomodative ET

A

The amount of acommodative convergence is based on the central nerves system stimulus to the ciliary muscle for accommodation. By directly stimulating the cholinergic receptors of the CM, cholinergic agonsits decrease the amount of central nervous system stimulation to the CM, which resutls in decreased convergence

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47
Q

What are the direct cholinergic agonsits for the eye

A

Pilocarpine

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48
Q

What are the indirect cholinergic agonists for the eye

A
  1. Neostigmine
  2. Pyridostigmine
  3. Edrophonium
  4. Echothiphate
  5. Donepizil
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49
Q

What happens to IOP if you increased ACH

A

Decreases

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50
Q

Pilocarpine wIOP reduction

A

30%

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51
Q

Design of pilocarpine

A

QID because short half-life

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52
Q

Concentrations of pilo

A

0.5-12%

1,2,4% used most

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53
Q

MOA of pilocarpine

A

Stimulate the longitudinal muscle of the ciliary body, which pulls posteriorly on the scleral spur and secondarily opens up the TM spaces for increased outflow and decreased IOP

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54
Q

When do we use IP

A

AFTER angle closure attack in prep for LPI. The miotic action of the drug pulls the iris taut and allows the LPI to be more effective and to equilibrate pressure

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55
Q

1% pilo

A

Used to differentiate CN III palsy from a sphincter tear in a patient with a fixed, dilated pupil-3rd nerve palsies will constrict with Phil

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56
Q

0.125% pilo

A

Diagnosis of ADie’s tonic pupil. The iris sphincter is supersensitized and will repsond with miosis to a diluted form of pilo

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57
Q

Main side effects of pilo

A 
Browache, HA, myopic shift (prolonged accommodation)
Miosis
Cataracts 
RD
Secondary angle closure 
Pupillary block
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58
Q

What type of aqueous outflow does pilo work on

A

Corneoscleral

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59
Q

Indirect cholinergic agonists

A

Anticholinesterse inhibitors

  • edrophonium
  • neostigmine
  • Echothiophate
  • pyridostigmine
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60
Q

Edrophonium

A

Indirect cholinergic agonist: antocholinesterase agent

  • diagnosis of MG
  • If ptosis improves in 1-2m, the test is positive for MG
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61
Q

Neostigmine

A

Indirect cholinergic agonist

  • anticholinesterase agent
  • treats MG
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62
Q

Echothiphate

A
  • indirect cholinergic agonist
  • anticholinesterase agent
  • pesticide
  • Dx/Rx of accommodative ET and rarely for glaucoma
  • irreversible side effects
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63
Q

Pyridostigmine

A
  • indirect cholinergic agonsit
  • anticholinesterase agent
  • Tx MG
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64
Q

Pralidoxime

A

Given IV to reverse the effects of IRREVERSIBLE ACH inhibitors. It binds to Ach inhibitors, thereby freeing ACHase to break down Ach in the synaptic cleft. Often give to reverse the systemic side effects of pesticide poisoning. Can also be given as an antidote for overtreatment of MG. NOT effective against reversible ACHase inhibitors. Although atropine is typically used to reverse muscarinic side effects, it will not reverse the weakness that resutls from ACHase toxicity, as atropine does not act at nicotinic ACHreceptrs in the NMJ

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65
Q

What are the cholinergic antagonists for the eye

A

STop ACH

  • scopolamine
  • tropicamide
  • Atropine
  • Cyclopentolate
  • Homatropine
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66
Q

What does anticholinergic antagonist promote

A

ANTI parasympathetic=sympathetic

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67
Q

What are cholinergic antagonists use for in the eye

A

Cycloplegic refractions, pupillary dilation, and management of uveitis

Block Ach at the M receptors in the ciliary body and iris

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68
Q

MOA of cholinergic antagonists

A

Block Ach at the M receptors in the CB and iris

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69
Q

Order of the cholinergic antagonists from strongest/longest lasting to weakest/shortest acting

A

ASH CiTy

  • atropine
  • scopolamine
  • homatropine
  • cyclopentolate
  • tropicamide
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70
Q

What do anticholinergics in the eye generally cause

A

Dry eye
Mydriasis
Increased IOP

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71
Q

Scopolamine

A

Anticholinergic

  • rarely used in topical bc side effects
  • CNS toxicity (penetrates BBB)
  • hallucinations, amnesia, unconsciousness, confusion, restlessness, incoherence, vomiting, and urinary incontinence
  • usually used as a patch for motion sickness
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72
Q

What is the safest anticholinergic used for dialtion

A

Tropicamide

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73
Q

Tropicamide

A
  • anticholinergic
  • fastest onset and shortest duration of mydriatic effects
  • much stronger mydriatic than cycloplegic effect
  • standard drug used for dilation
  • max mydriatic effect in 35m
  • lasts for 6 hours
  • max cyclo effect 20-45m
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74
Q

Side effects of tropicamide

A

NONE DONT PICK THIS IF THERE IS A SIDE EFFECT QUSTION

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75
Q

Atropine

A

Anticholinergic

  • onset: 1 hour
  • duration: 7-12 days
  • too prolonged for routine cyclo refractions
  • can be used for treatment of uveitits, but homatropine is the standard
  • amblyopia treatment: good eye treated with atropine (penalization)
  • systemic side effects: dont give to kids under 3, incorrect dosage, sick, DOWN SYNDROME
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76
Q

Atropine toxicity

A 
Dry mouth 
Dry flushed skin
Rapid pulse 
Disorientation 
Fever

Due to CNS effects on the hypothalamus

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77
Q

Cyclopentolate

A

Anticholinergic

  • fastest onset and shortest duration of cycloplegic effects. Standard cyclo agent in clinic
  • cycloplegic effect
  • max effect: 45m
  • routine cyclo refraction for all ages, esp kids
  • treatment of anterior uveitits
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78
Q

What is the best anticholinergic to treat uveitis with

A

Homatropine

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79
Q

BAB tight junctions

A

NPCE
Iris vessels
Schlemms canal

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80
Q

Homatropine

A
  • standard for treating anterior uveitis
  • keeps iris mobile, which decreases PS formation
  • reduces pain by paralyzing CB and sphincter muscle
  • stabilizes the BAB
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81
Q

Anticholinergic toxicity

A 
Hot has a hare
Red as a beet 
Dry as a bone 
Mad as a hatter 
Blind as a bat
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82
Q

Botox

A
  • anticholinergic
  • blacks the release of Ach at the NMJ (nicotinic), inhibiting muscle contraction
  • when utilized for blepharospasm, orb oculi function returns quickly, not permanent
  • single injections for strabismus=premanent correction
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83
Q

Main uses for Botox

A

Wrinkles
Blepharospasm
Strab

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84
Q

What are the ocular adrenergic agents

A

Phenylephrine (a1)
Naphzoline/tetrahydrolazine (a1)
Brimonidine (a2)
Apraclonidine (a2)

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85
Q

What do adrenergic agonists stimulate

A

Sympathetic activity

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86
Q

Uses of adrenergic agonists

A

Dilation, conjunctival constriction, minor allergic conditions, temporary IOP control, POAG

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87
Q

Difference between NE and epi

A

NE does not act on B2 receptors

epi: a1 a2 b1 b2
NE: a1 a2 b1

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88
Q

Phenylephrine

A
  • adrenergic agonist
  • a1
  • 2.5% routinely used with tropicamide for dilation
  • cannot provide a fixed dilated pupil by itself (miosis still happens)
  • MOA: a1 agonist, no effects on B receptors. Allows it to cause dilation without cycloplegia
  • used for dilation without cycloplegia
  • palpebral widening (good for BIO): mullers
  • scerlitis from episcleitits (epi blanches)
  • horners syndrome (1% for diagnosis)
  • 10% for breaking PS
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89
Q

Phenyl 10%

A

Limited to break PS formation because of side effects

-contraindicated in: MAOI, TCAs, atropine, graves

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90
Q

Naphzoline and tetrahydrolazine

A

Adrenergic agonists

  • a1
  • ocular decongestants to constrict the conjunctival blood vessels
  • greater alpha than beta effects, potential to depress the CNS
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91
Q

Visine and fixed dilated pupil

A

If a patient presents with a fixed dilated pupil, ask about visine use, excessive use can cause dilation because of the alpha effects of tetrhydrolazine on the radial muscle (a1)

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92
Q

Naphcon A

A

OTC drug that combines naphzoline (Reduce redness), and antihistamine for relief of eye itching

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93
Q

A2 agonsits for glaucoma MAO

A

Decreases aqueous humor production and increase uveoscleral outflow

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94
Q

Brimonidine

A

Adrenergic agonsits

  • a2
  • highly selective a2 agonist (30x more than apraclonidine), allowing effective IOP lowering and long term treatemtn of glaucoma
  • neuroprotective properties in a crushed rat nerve model
  • can cause follicular conjunctivitis.
  • Alphagan P: contains purite as preservative and reduces allergy
  • TID dosing
  • brimonidine causes MIOSIS and can be used to reduce glare, haloes, and other night vision problems for LASIK patients
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95
Q

Pupil with brimonidine

A

Causes MIOSIS

  • no a1!! A2=CNS sympathetic off switch
  • good for LASIK patietns and those with night vision problems
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96
Q

Systemic side effects of brimonidine and apraclonidine

A

Dry mouth

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97
Q

Brimonidine is contraindicated in those taking

A

MAOI

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98
Q

A2 and sympathetic

A

A2 is the sympathetic off switch

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99
Q

Apraclonidine

A

Adrenergic agonist

  • A2
  • limited a1 activity
  • control IOP SPIKES
  • used during acute angle closure attacke
  • 30-40% IOP reduction, not used for chronic therapy because of tachyphylaxis
  • onset 1 hour
  • can be used for diagnosis of horners
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100
Q

Horners syndrome: Dx without pharmacological testing

A

Anisocoria will be greater in the dark. Turn the lights off and observe the miotic pupil; a delayed dilation will exist due to abnormal sympathetic innervation to the dilator muscle; if this “dilation lag” exists along with ptosis, horners syndrome can be Dx without pharmacological testing

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101
Q

Step 1 of horners syndrome pharm dx

A

cocaine or apraclonidine

  • cocaine: dilation in healthy eye, no effect on horners eye
  • apraclonidine: no effect on healthy eye. In horners it will cause a dilation (hypersensitized a1)
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102
Q

After step one of horners pharm testing, and before step two, what must you do

A

Wait 24-48 hours

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103
Q

Step two of horners pharm testing

A

Hydroxyamphetamine or phenyl 1%

  • hydroxy: if patient fails to dilate, postganglionic neuron damaged
  • phenyl: full dilation in postganglionc horners syndrome
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104
Q

Horners dilates with phenyl 1%

A

Postganglionic damage

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105
Q

Horners patietns does not dilate with hydroxyamphetamine

A

Postganglioic damage

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106
Q

Adrenergic antagonists promote what

A

Parasympathetic

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107
Q

What are the adrenergic antagonsits for the eye

A

BBlockers

  • timolol
  • carteolol
  • betaxolol
  • levobunolol
  • metipranolol
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108
Q

What is the most common BBlocker for the eye

A

Timolol

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109
Q

CNS effects of BBlockers

A

Disorientation, depression, fatigue

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110
Q

Cardio effects of BBlockers

A

Bradycardia, arrhythmias, syncope

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111
Q

Pulmonary effects of BBlockers

A

Dyspnea, wheezing, bronchospasms

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112
Q

GI problems with BBlockers

A

Nausea, vomiting, diarrhea, pain

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113
Q

Reproductive problems with BBlockers

A

erectile dysfunction

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114
Q

Which ocular drug is assocaited with erectile dysfunction

A

BBlockers

115
Q

Contraindication of BBlockers

A

Respiratory problems, cardio problems

They are formulated with specificity towards B1 and B2 receptors

116
Q

MOA of BBlockers

A

Block B receptors throughout the body. Topically, they act primarily on B receptors (mainly B2) in the NPCE to decreased aqueous production

117
Q

What is the only B1 selective topical drug

A

Betaxolol

118
Q

Timolol

A
  • 0.25%, once daily AM
  • non selective BBlocker.
  • most effective at lowering IOP (25%)
  • unilateral use of timolol causes a crossover effect
  • long term and short term drift
  • use with caution in: DM, hyperthyroidism, and MG
119
Q

Who should not take BBlockers

A

Diabetics
Hyperthyroidism
MG

120
Q

cosopt

A

Timolol + dorolamide

121
Q

Combigan

A

Timolol + brimonidine

122
Q

What glaucoma drugs offer neuroprotection

A

Betaxolol

Brimonidine

123
Q

Carteolol

A
  • non selective BBlocker
  • intrinsic sympathomimetic activity, reduces nocturnal bradycardia and more comfortable
  • less side effects
  • modest reduction in cholesterol
124
Q

Normal cholesterol levels

A

<200

125
Q

How much do statins reduced cholesterol

A

40%

400->240

126
Q

Betaxolol

A
  • cardioselective B1 blocker, 0.25%
  • limited B2 activity, minimizes respiratory effects
  • not as effective as timolol
  • neuroprotective
  • can worsen CHF
127
Q

Levobunolol

A

Non selective Bblocker

Similar to timolol in efficacy

128
Q

Metipranolol

A

Non selective BBlocker

No used anymore because not effective

129
Q

MOA of cholinergic agonsits for glaucoma

A

Increased corneoscleral outflow

Pilo is the only one

130
Q

A agonist MOA for glaucoma

A

Decrease production and increase uveoscleral outflow

131
Q

Drugs that increase outflow

A

Pilo (corneoscleral, TM)
A2 agonists
PGs

132
Q

Drugs that decrease aqueous production

A

CAI
A2 agonsits
BBlocker

133
Q

Carbonic anhydrase

A

An enzyme that acts on the CB (NPCE and PCE) to catalyze the joining of CO2 + H20 to yield bicarbonate

134
Q

Bicarbonate ions

A

Believed to increase aqueous production by increasing Cl- andNa+ flux into the posterior chamber

135
Q

Who should you not give topical CAIs to

A

Sulfa allergies

136
Q

Topical CAIs

A

Brinzolamide, Dorzolamide

137
Q

Oral CAIs

A

Acetazolamide

Methazolamide

138
Q

Topical side effects of CAIs

A

Bad taste

Sting

139
Q

CAI RXing

A

Usually not given as a primary medication but in combo (cospot)

140
Q

Acetazolamide and methazolamide

A

-acetazolamide given with liquid during acute angle closure
-quickly absorbed into GI
-potent decrease in IOP
-can be used for POAG, but used as last resort because of side effects
-

141
Q

Oral CAI side effects

A

-metallic taste, tingling hands and feet, metabolic acidosis
-thrombocytopenia, agranulocytosis, aplastic anemia
-malaise, fatigue, weight loss, anorexia, impotence, depression, diarrhea, and myopic shifts
-

142
Q

Contraindications of CAIs

A

COPD, sulfa allergies, liver and renal disease

143
Q

What drugs cause aplastic anemia

A

Chloramphenicol
Acetazolamide
Methazolamide

144
Q

Drugs that cause myopic shifts

A

Topamax
Pilo
CAI

145
Q

Drugs not to give DM

A

oral CAI
Osmotic
BBlockers

146
Q

Fatal side effects of oral CAIs

A

Bone marrow suppression

Aplastic anemia

147
Q

First line drugs for POAG

A

PGs

148
Q

PGs cause a ____ IOP decrease

A

30%

149
Q

What glaucoma drug has the highest IOP lowering capabilities

A

PG at 30%

150
Q

Travatan Z is differnet how

A

PG

Has sofzia as a preservative instead of BAK

151
Q

MOA of PGs

A

Act on PF receptors (PGF2a receptors) on the ciliary muscle, which causes reduction of neighboring collagen (via MMPS), decreasing resistance within the uveoscleral meshwork for increased outflow. Also acts on the skin receptors (activating phospholipids C) to alter hair follicles, contributing to some of the side effects

  1. FP receptors
  2. Skin receptors
152
Q

Dosing of PGs

A

Bedtime dosing

  • better diurnal control
  • has a daytime peak effect
153
Q

Contraindications of PGs

A

-patients who are at risk of CME, cases of active inflammation (uveitis), and patients with previous episodes of HSK

154
Q

Side effects of PGs

A

Iris heterochromia (permanent), increased pigmentation of the skin and growth of eyelashes and skin darkening around the eyes (not best for monocular glaucoma)

  • conjunctival hyperemia can occur with all three drugs, but is worse with luminance and least common with xalatan
  • Pruritis is also mor enoted with luminance
155
Q

What are the PGs

A

Latanaprost
Bimatoprost
Travoprost

156
Q

PG IOP decrease

A

33%

157
Q

BBlocker IOP decrease

A

25%

158
Q

Brimonidine and dorzolamide IOP decrease

A

18%

159
Q

Pilo IOP decrease

A

30%

160
Q

MOA of topical ocular anesthetics

A

Local anesthetics block nerve conduction and change membrane permeability by stopping the influx of Na+ into the nerve cytoplasm. Without Na+ entry, the nerve can no longer be depolarized

161
Q

Why A.R. injected anesthetics given with epinephrine

A

So that blood vessels are constricted and systemic absorption is minimal. This keeps the drug localized, allowing more potent affects

162
Q

Structure of anesthetics

A 
Aromatic residue (lipophilic)
Intermediate chain
Amino group (hydrophilic)

The bond between the intermediate chain and the amino group tells us if its an ester or amide

163
Q

Anesthetics: amides

A

Longer duration of action
Metabolized by liver
Less toxic

164
Q

Example of an amide

A

LIDOCAINE

165
Q

Esters

A

Shorter duration of action
Metabolized locally
ALL TOPICAL ANESTHETICS ARE ESTERS

166
Q

All topical anesthetics are

A

Esters

167
Q

Things that can cause corneal melt

A

Topical NSAIDS

Topical anesthetics

168
Q

Proparacaine/benoxinate

A

Esters
10-20s onset
10-20m duration

169
Q

Fluoress

A

Combination of fluorescein and benoxinate.

170
Q

First topcai lanesthetic used

A

Cocaine

171
Q

Why do we not RX topical anesthetics for pain

A

Corneal melt

172
Q

MOA of antihistamines

A

Block type I HS reactions

-do not prevent the release of histamine, they block the cell receptors that histamine acts upon

173
Q

Type I HS

A
  • first exposure: IgE antibodies formed, no symptoms
  • between exposures, IgE ab bind to mast cells and basophils
  • when antigen reintroduces, binds to IgE/mast cell complex resulting in opening of Ca2+ channels
  • Ca+ influx depolarizes the cells, resulting in degranualtion of mas cells, causing the release of histamine and other inflammtory mediators into the blood
  • the binding of histamine to receptors resutls in allergic stymptoms
174
Q

H1 antihistamines

A

Emedastine

175
Q

Emedastine

A

H1 antihistamine

  • mild to moderate cases of allergic conjunctivitis
  • more commonly Rxed in combo with a vasoconstriction game agent,
  • not common
176
Q

Mast cell stabilizers

A

Cromolyn
Lodoxamide
Pemirolast
Nedocromil

177
Q

Use of mast cell stabilizers for eye

A
  • not effective in acute allergic symptoms
  • acts on exposed mast cells and inhibits their degranualtion upon re-exposure.
  • stabilizes mast cell membrane, PREVENTING CA2+ INFLUX and degranualtion
  • effects begin days to weeks after starting therapy
  • chronic allergic conjunctivitis, VKC, and AKC
178
Q

Mast cell-antihistamine combo

A

BEZPOP

  • bepreve
  • elestat
  • Zaditor
  • patanol
  • optivar
  • pataday
179
Q

MOA of mast cell stabilizer-antihistamine combo

A

The dual mechanism of action for these drugs allows effectiveness in long term management of ocualr related itching and allergic conjunctivitis, as well as relief of acute symptoms

Prevent Ca2+ influx
Block H receptors

180
Q

Overall actions of corticosteroids

A

Anti-inflammatory and immunosuppressive

Inhibits phospholipase A2 and thus the arachidonic acid pathway

Decrease inflammatory mediators and decrease cap permiability=significant decrease in immune system response

Decrease fibroblast and collagen formation=decreased healing

181
Q

Side effects of corticosteroids

A

Increased risk of secondary infections (immunosuppresive), PSC cataracts, and glaucoma (increased IOP)

182
Q

PSC cataracts and coritcosteroids

A

Irreversible and dose dependent

183
Q

How can corticosteroids cause glaucoma

A

Increased IOP

Decreased outflow at hte corneal scleral (TM)

184
Q

HSV keratitis and steroids

A

Decreased immune repsosne, allows virus to proliferate. Do cotton swab Tess

185
Q

Where does ACTH come from

A

Ant pituitary

186
Q

Potent steroids

A

Prednisone 1% acetate, rimexalone, difluprednate, and dexamethasone

187
Q

Soft steroids

A

Flurometholone (FML) 0.1%, and loteprednol (lotemax)

188
Q

What is the safest steroid and why

A

Loteprdnol because ester based

189
Q

Soft steroids and IOP repsosne

A

Less likely to cause a spike in IOP

190
Q

Normal patietns and steroids repsonse

A

5% are high steroid responders

191
Q

POAG and steroid responders

A

90% of POAG pateints are steroid responders

-try to avoid steroids in glaucoma patients

192
Q

What do NSAIDs block

A

COX I and II

193
Q

Drugs that block phosphlipase A 2

A

Steroids
Chloroquine
Hydroxychloroquine

194
Q

NSAIDs list

A

“Nac, lac, profen”

  • diclofenac
  • ketorolac
  • nepafenac
  • bromfenac
  • flurbiprofen
195
Q

MOA of NSAIDs

A

Block Cox I and II which decreased inflammation by inhibiting the conversion of arachidonic acid into PGs and thromboxanes

196
Q

Dosing of NAIDS

A

Diclofenac and Ketorolac are dosed QID

Nepafenac TID

Bromfenac is BID

197
Q

Only topical NSAID formulated for Qday dosing

A

Bromday

198
Q

NSAID before ocular surgery

A

Flurbiprofen

199
Q

Clinical use of topical NSAIDs

A

Post op cataract patients, decreases the risk of post op inflammation, particularly that of the macula (CME), RCE, corneal abrasions, and allergic conjunctivitis

200
Q

Only NSAID approved for topical treatment of seasonal allergic conjunctivits

A

Ketorolac

Use something else if they have corneal involvement

201
Q

Side effects of topical NSAIDs

A 
Corneal toxicity (corneal melt)
Stinging upon instillation
202
Q

What NSAID should not be RXed in someone with sulfa allergies

A

Xibrom (bromfenac)

BAK and sodium sulfate preservatives

203
Q

What NSAID has thimerosol as preservative

A

Flurbiprofen

204
Q

Which NSAID causes corneal melt

A

Generic Voltaire’s (diclofenac)

205
Q

Best dye for TBUT

A

NaFL

206
Q

Fluorescein

A

Water soluble, quickly dissolved in the aqueous portion of the tears

Eval of

  1. Tear film quality
  2. Epithelial defects
207
Q

Rose bengal

A

Stains dead and devitalized cells as wel las cells that have lost their mucous coating

  • stains Boarders of of simplex dendrites
  • stains the whole dendrite in zoster
208
Q

Lissamine and rose bengal: virus

A

Both have mild antiviral properties, whereas methylene blue is bacteriostatic. If cell culturing is indicated, do not instill these drops prior to culture if the organisms you are suspecting are going to be altered by the agent

209
Q

Lissamine green

A

Less sting
Similar use as rose bengal
-more commonly utilized for dry eye

210
Q

Methylene blue dry

A

Staining properties similar to rose bengal, it also stains corneal nerves. Outlines filtering bleb and for staining the lac sac before DCR

211
Q

FL dye

A

IV for FA

  • takes 10-20 seconds to occur
  • macular degeneration to determine if CNVM present

Nausea, anaphylaxis, yellow pee

212
Q

Agents for exudative ARMD

A

Pegaptanib (macugen)

Ranibizumab (lucentis)

213
Q

Pegaptanib (macugen)

A

Exudative ARMD

Antineoplastic agent=decreased VEGF

214
Q

Ranibizumab (lucentis)

A

Exudative ARMD

Monoclonal Ab=decreased VEGF

215
Q

What does anti VEGF do

A

Decrease neo

Decrease vascular permeability (prevent CME)

216
Q

What hyperosmotic agent can be given to DM

A

Isosorbide

217
Q

Hyperosmotic agents

A 
Glycerine 
Muro 128 (NaCl)
218
Q

Glycerine

A

Hyeprosmotic

  • Hight molecular weight that is unable to cross the BAB; this creates an osmotic gradient in which the plasma in the ciliary stroma region is hypertonic to they aqueous humor, lowering IOP
  • used to lower fluid volume during an acute angle attack. Mixed with a drink to prevent vomitting (sip)
  • rapidly absorbed, increases blood glucose. Do not give to diabetics (isosorbide instead)
219
Q

What is the best of ANYTHING to reduce IOP

A

Glycerine

220
Q

Tear osmolarity

A

308
Main: Na+
Other: lots of K+

221
Q

Muro 128

A

Hyperosmotic
NaCl
Hypertonic solution used for reduction of corneal edema. Eye drops and ointment

Fuchs endothelial dystrophy

222
Q

Tear substitutes are RXed how often

A

QID

223
Q

Tear substitutes

A

Water beaded solutions that are used to lubricate the eye and replace the aqueous portion fo the tears.
Cellulose esters and PVA

224
Q

Of someone needs artificial tears more than QID

A

Go preservative free

225
Q

Disadvantage of artificial tears

A

90% of the drop volume is enlisted from the eye within the first minute or two. Methylcellulose increases the viscosity of solutions, allowing more contact time on the cornea. PVA is also commonly incorpated , although it is less viscous

226
Q

Ointments

A

High viscosity solutions they provide longer duration of action with minimal irritation

  • obstruct vision
  • bed time use
  • increased risk of infection
  • helpful in kids
227
Q

Restasis

A

Inhibits IL2
Stops formation of T cells
-takes 3 months to work, lifespan of a T cell

228
Q

Preservatives in CL soltksuon

A

Prevent and kill bacterial, viruses, and other contaminates.

  • BAK: very common=SPK
  • thimerosol=mercury
  • EDTA=Ca2+ (band K)
  • purite=favored
229
Q

Diffuse SPK and follicles and preservatives

A

Common if a patient has a toxic reaction to a preservative

230
Q

Drugs that cause Whorl Keratopathy

A

CHAI-T

  • chloroquine
  • hydroxychloroquine
  • amiodarone
  • tamoxifen
  • indomethacin
231
Q

Fabrys disease

A

Lysosomal storage disease that can result in corneal verticillata (whorl K) and spoke like lens opacities
-pain in extremeites and abdomen

Fabry likes to WHORL his CHAI-T

232
Q

Drugs that cause dry eye

A

All drugs with BAK, including topical ophthalmic glaucoma meds

233
Q

Drugs that case SPK

A

Isotretinoin (Accutane), topical aminoglycosides

234
Q

Drugs that cause endothelial/descemets membrane pigmentation

A

Chlorpromazine
Thioridazine
Promethazine

235
Q

What do -zine drugs cause to the eye

A

Lens
Cornea
Retina

Pigment on all of these

236
Q

Stromal gold deposits: what drugs

A

Gold salts

237
Q

Drugs that cause delayed corneal healing

A

Topical and oral corticosteroids

238
Q

Eye side effects of amiodarone

A

-anti-arrhythmic drug

Work K
Anterior subcapsular lens deposits
NAION

239
Q

Drugs causing anterior subcapsular effects

A

Chlorpromazine
Thioridazine
Amiodarone
Miotics

May Trigger Anterior Cataracts

240
Q

Drugs that cause PSC

A

Any steroids

241
Q

PSC from steroids

A

Dose dependent
Irreversible
Hispanics more common

242
Q

Drugs affecting the conjunctiva and lids

A 
Isoretinoin (accutane)
NSAIDs and other blood thinners 
Sulfonamide 
Tetracyclines 
SIldenafil
PGs
Tamiflu
243
Q

Isotrtinoin and conjunctiva and lids

A

Blepharoconjunctivitis, dryness, lid edema

Sebaceous glands (meibomian and zeiss)

244
Q

NSAIDs and blood thinners and lids/conj

A

Subconjunctival hemorrhage

245
Q

Sulfa drugs and lids/conj

A

SJS

246
Q

Tetracyclines and lids/conj

A

Pigmented cysts on the conjunctiva

247
Q

SIldenafil and lids/conj

A

Subconjunctival hemorrhage, conjunctival hyperemia

PDE-5 inhibitor
Vasodilates

248
Q

Tamiflu and lids/conj

A

Conjunctivitis in 1%

249
Q

PGs and lids/conj

A

Conjunctival hyperemia, increased growth of lashes, increased pigmentation of the skin and eyelashes

250
Q

Things that can cause a subconjunevtial hemorrhage

A

Valsalva
Clotting diease
NSAIDs (aspirin)

251
Q

Drugs that decrease tear production (cause mydriasis and increase IOP too)

A

Anticholinergic effects
-anticholinergics
-tricyclic ANTI depressants (amytriptiline, imipramine)
-ANTIhistamines: chlorpehiramine, bropheniramine, diphenhydramine, promethazine
-ANTIpsychs: phenothiazines (chlorpromazine, thioridazine)
Isotetinoin
BBclockers (doesnt make sense)
Hormone therapies (BC, HRT)
ADHD meds (Ritalin, Dexedrine)
Diuretics: HCTZ, chlorothiazide, furosemide, triamteren

252
Q

Drugs that cause mydriasis

A
  • anticholinergics
  • antihistamines
  • SSRIs
  • SNRIs
  • TCAs
  • Phenothiazines (antipsychotic)
  • benzodiazepine
  • dopamine agonists
253
Q

Drugs that resutls in mydriasis can

A

Cause angle closure in patietns with narrow anterior chamber angles

254
Q

Drugs that can cause miosis

A

Opiates
ACHase inhibitors
Pilocarpine

255
Q

Drugs that can cause nystagmus

A

Phenytoin, phenobarbital, salicylates (NSAIDs)

256
Q

Drugs that can cause diplopia

A

Antidepressants, antianxiety, phenytoin

257
Q

Drugs that affect smooth pursuits

A

Alcohol

258
Q

Drugs that cause oculogyric crisis

A

Phenothiazines

Cetirizine

259
Q

Oculogyric crisis

A

EOMS undergo spastic, abnormal muscle contractions that leave th eye abnormally postioned (usually elevated)

260
Q

Drugs that affect sclera and uvea

A
  • A1 blockers: floppy iris

- blue sclera: corticosteroids, minocyline

261
Q

Topiramate and the eyes

A

May lead to secondary angle closure glaucoma by causing choroidal swelling, which moves the iris forward into apposition with the TM
-can cause myopia too

262
Q

Drugs affecting the ON

A 
Digoxin
Ethambutol 
Chloramphenicol
Streptomycin
Sulfonamide 
Isoniazid 
Methotrexate 
SIldenafil 
Vardenafil
sumatriptan
Amiodarone 
Oral contraceptives
263
Q

Digoxin and the ON

A

Retrobulbar optic neuritis, BY color defects entropic phenomenon (snowy vision)

264
Q

Ethambutol and ON

A

Optic neuritis

265
Q

Isoniazid and methotrexate and ON

A

Unlikely culprits of optic neuritis

266
Q

Drugs that cause NAION

A

Sildenfil
Vardenafil
Sumatriptan
Amiodarone

267
Q

Oral contraceptives and ON

A

Optic neuritis
Papilledema
Pseudotumor cerebri

268
Q

Drugs that can affect the retina

A 
Chloroquine 
Epinephrine 
Tamoxifen 
Thioridazine/chlorpromazine/ promethazine 
indomethacin 
Talc
Isotrtinoin
NSAIDs
Oral BC
Zidovudine
269
Q

Chloroquine and the retina

A

Mottled RPE first

Bulls eye maculoapthy next

270
Q

Epinephrine and retina

A

CME

271
Q

Tamoxifen and retina

A

Yellow or white crystalline depots with or without macular edema

272
Q

Thioridazine/chlorpromazine/ promethazine and retina

A

Pigmentary retinopathy that looks like bulls eye maculopathy

273
Q

Indomethacin and retina

A

Retinal hemorrhage, pigmentary changes (mottling)

Can also cause whorl K

274
Q

Oral BP can cause

A

ON
Dry eye
CRVO/BRVO

275
Q

Isotretinoin and retina

A

Loss of color vision, nyctalopia

276
Q

NSAIDs and retina

A

Hemorrhage

277
Q

BC and retina

A

Vasculopathy, retinal hemorrhage

278
Q

Zidovudine and retina

A

Macualr edema

279
Q

Drugs that cause ICP

A 
CATS
Contraceptive 
Accutane/Vit A
Tetracyclines 
Synthroid/steroids
280
Q

Drugs increasing IOP

A

Anticholinergic activists

  • atropine/scopolamine
  • antihistamines
  • antidepressants
  • antipsychotics
  • short acting B2 agonists
  • pseudoephedrine
  • corticosteroids
281
Q

Drugs that decrease IOP

A

Systemic BBlockers
Cardiac glycosides (digoxin)
Alcohol
Ccannabinoids

282
Q

Marijuana

A

Max effect on IOP occurs 60-90m after inhalation and lasts about 4 hours

283
Q

How do steroids increase IOP

A

Decreasing TM outflow

BOARDS (14 decks)

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