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
What NT is released at the junction of the pre and post ganglion in parasympathetic
Ach
26
What NT is released at the junction of the post ganglion neuron and the target organ/gland
ACH
27
What receptors are found at the SOA in parasympathetic
M1, M2, M3
28
Functions of the parasympathetic
Rest/digest Bronchoconstriction/miosis SLUD (wet)
29
Where does sympathetic pathway start
Thoraco-lumbar
30
Which is longer in sympathetic, pre or postganglionc neurons
Postganglionic
31
What NT is released at the junction of the pre and post ganglionic neuron in sympathetic
Ach
32
What NT is released as the junction of the postganglionic neuron and the SOA in sympathetic
NE and epi
33
What receptors are on the SOA in sympathetic
A1,a2,b1,b2
34
Functions of sympathetic
Fight/flight Bhronchodilate/ mydriasis Dry
35
Iris sphincter receptors
M3
36
Ciliary muscel receptors
M2, M3
37
Lacrimal gland receptors
M2, M3
38
Iris dilator receptor (radial muscle)
A1
39
TM receptor
B2
40
Ciliary muscle adrenergic receptor
B2
41
NPCE adrenergic receptor
B2 (little B1)
42
CB vasculature adrenergic receptr
A2
43
What do cholinergic agonists promote
Parasympathetic
44
Three main structure of the eye that receive parasympathetic innervation
Sphincter muscle Ciliary muscle Lacrimal gland
45
What are chilinergic agonists used for in the eye
Glaucoma | accomodative ET
46
What are cholinergic agonists used to treat accomodative ET
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
47
What are the direct cholinergic agonsits for the eye
Pilocarpine
48
What are the indirect cholinergic agonists for the eye
1. Neostigmine 2. Pyridostigmine 3. Edrophonium 4. Echothiphate 5. Donepizil
49
What happens to IOP if you increased ACH
Decreases
50
Pilocarpine wIOP reduction
30%
51
Design of pilocarpine
QID because short half-life
52
Concentrations of pilo
0.5-12% | 1,2,4% used most
53
MOA of pilocarpine
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
54
When do we use IP
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
55
1% pilo
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
56
0.125% pilo
Diagnosis of ADie’s tonic pupil. The iris sphincter is supersensitized and will repsond with miosis to a diluted form of pilo
57
Main side effects of pilo
``` Browache, HA, myopic shift (prolonged accommodation) Miosis Cataracts RD Secondary angle closure Pupillary block ```
58
What type of aqueous outflow does pilo work on
Corneoscleral
59
Indirect cholinergic agonists
Anticholinesterse inhibitors - edrophonium - neostigmine - Echothiophate - pyridostigmine
60
Edrophonium
Indirect cholinergic agonist: antocholinesterase agent - diagnosis of MG - If ptosis improves in 1-2m, the test is positive for MG
61
Neostigmine
Indirect cholinergic agonist - anticholinesterase agent - treats MG
62
Echothiphate
- indirect cholinergic agonist - anticholinesterase agent - pesticide - Dx/Rx of accommodative ET and rarely for glaucoma - irreversible side effects
63
Pyridostigmine
- indirect cholinergic agonsit - anticholinesterase agent - Tx MG
64
Pralidoxime
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
65
What are the cholinergic antagonists for the eye
STop ACH - scopolamine - tropicamide - Atropine - Cyclopentolate - Homatropine
66
What does anticholinergic antagonist promote
ANTI parasympathetic=sympathetic
67
What are cholinergic antagonists use for in the eye
Cycloplegic refractions, pupillary dilation, and management of uveitis Block Ach at the M receptors in the ciliary body and iris
68
MOA of cholinergic antagonists
Block Ach at the M receptors in the CB and iris
69
Order of the cholinergic antagonists from strongest/longest lasting to weakest/shortest acting
ASH CiTy - atropine - scopolamine - homatropine - cyclopentolate - tropicamide
70
What do anticholinergics in the eye generally cause
Dry eye Mydriasis Increased IOP
71
Scopolamine
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
72
What is the safest anticholinergic used for dialtion
Tropicamide
73
Tropicamide
- 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
74
Side effects of tropicamide
NONE DONT PICK THIS IF THERE IS A SIDE EFFECT QUSTION
75
Atropine
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
76
Atropine toxicity
``` Dry mouth Dry flushed skin Rapid pulse Disorientation Fever ``` Due to CNS effects on the hypothalamus
77
Cyclopentolate
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
78
What is the best anticholinergic to treat uveitis with
Homatropine
79
BAB tight junctions
NPCE Iris vessels Schlemms canal
80
Homatropine
- standard for treating anterior uveitis - keeps iris mobile, which decreases PS formation - reduces pain by paralyzing CB and sphincter muscle - stabilizes the BAB
81
Anticholinergic toxicity
``` Hot has a hare Red as a beet Dry as a bone Mad as a hatter Blind as a bat ```
82
Botox
- 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
83
Main uses for Botox
Wrinkles Blepharospasm Strab
84
What are the ocular adrenergic agents
Phenylephrine (a1) Naphzoline/tetrahydrolazine (a1) Brimonidine (a2) Apraclonidine (a2)
85
What do adrenergic agonists stimulate
Sympathetic activity
86
Uses of adrenergic agonists
Dilation, conjunctival constriction, minor allergic conditions, temporary IOP control, POAG
87
Difference between NE and epi
NE does not act on B2 receptors epi: a1 a2 b1 b2 NE: a1 a2 b1
88
Phenylephrine
- 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
89
Phenyl 10%
Limited to break PS formation because of side effects | -contraindicated in: MAOI, TCAs, atropine, graves
90
Naphzoline and tetrahydrolazine
Adrenergic agonists - a1 - ocular decongestants to constrict the conjunctival blood vessels - greater alpha than beta effects, potential to depress the CNS
91
Visine and fixed dilated pupil
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)
92
Naphcon A
OTC drug that combines naphzoline (Reduce redness), and antihistamine for relief of eye itching
93
A2 agonsits for glaucoma MAO
Decreases aqueous humor production and increase uveoscleral outflow
94
Brimonidine
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
95
Pupil with brimonidine
Causes MIOSIS - no a1!! A2=CNS sympathetic off switch - good for LASIK patietns and those with night vision problems
96
Systemic side effects of brimonidine and apraclonidine
Dry mouth
97
Brimonidine is contraindicated in those taking
MAOI
98
A2 and sympathetic
A2 is the sympathetic off switch
99
Apraclonidine
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
100
Horners syndrome: Dx without pharmacological testing
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
101
Step 1 of horners syndrome pharm dx
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)
102
After step one of horners pharm testing, and before step two, what must you do
Wait 24-48 hours
103
Step two of horners pharm testing
Hydroxyamphetamine or phenyl 1% - hydroxy: if patient fails to dilate, postganglionic neuron damaged - phenyl: full dilation in postganglionc horners syndrome
104
Horners dilates with phenyl 1%
Postganglionic damage
105
Horners patietns does not dilate with hydroxyamphetamine
Postganglioic damage
106
Adrenergic antagonists promote what
Parasympathetic
107
What are the adrenergic antagonsits for the eye
BBlockers - timolol - carteolol - betaxolol - levobunolol - metipranolol
108
What is the most common BBlocker for the eye
Timolol
109
CNS effects of BBlockers
Disorientation, depression, fatigue
110
Cardio effects of BBlockers
Bradycardia, arrhythmias, syncope
111
Pulmonary effects of BBlockers
Dyspnea, wheezing, bronchospasms
112
GI problems with BBlockers
Nausea, vomiting, diarrhea, pain
113
Reproductive problems with BBlockers
erectile dysfunction
114
Which ocular drug is assocaited with erectile dysfunction
BBlockers
115
Contraindication of BBlockers
Respiratory problems, cardio problems They are formulated with specificity towards B1 and B2 receptors
116
MOA of BBlockers
Block B receptors throughout the body. Topically, they act primarily on B receptors (mainly B2) in the NPCE to decreased aqueous production
117
What is the only B1 selective topical drug
Betaxolol
118
Timolol
- 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
Who should not take BBlockers
Diabetics Hyperthyroidism MG
120
cosopt
Timolol + dorolamide
121
Combigan
Timolol + brimonidine
122
What glaucoma drugs offer neuroprotection
Betaxolol | Brimonidine
123
Carteolol
- non selective BBlocker - intrinsic sympathomimetic activity, reduces nocturnal bradycardia and more comfortable - less side effects - modest reduction in cholesterol
124
Normal cholesterol levels
<200
125
How much do statins reduced cholesterol
40% | 400->240
126
Betaxolol
- cardioselective B1 blocker, 0.25% - limited B2 activity, minimizes respiratory effects - not as effective as timolol - neuroprotective - can worsen CHF
127
Levobunolol
Non selective Bblocker | Similar to timolol in efficacy
128
Metipranolol
Non selective BBlocker | No used anymore because not effective
129
MOA of cholinergic agonsits for glaucoma
Increased corneoscleral outflow | Pilo is the only one
130
A agonist MOA for glaucoma
Decrease production and increase uveoscleral outflow
131
Drugs that increase outflow
Pilo (corneoscleral, TM) A2 agonists PGs
132
Drugs that decrease aqueous production
CAI A2 agonsits BBlocker
133
Carbonic anhydrase
An enzyme that acts on the CB (NPCE and PCE) to catalyze the joining of CO2 + H20 to yield bicarbonate
134
Bicarbonate ions
Believed to increase aqueous production by increasing Cl- andNa+ flux into the posterior chamber
135
Who should you not give topical CAIs to
Sulfa allergies
136
Topical CAIs
Brinzolamide, Dorzolamide
137
Oral CAIs
Acetazolamide | Methazolamide
138
Topical side effects of CAIs
Bad taste | Sting
139
CAI RXing
Usually not given as a primary medication but in combo (cospot)
140
Acetazolamide and methazolamide
-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
Oral CAI side effects
-metallic taste, tingling hands and feet, metabolic acidosis -thrombocytopenia, agranulocytosis, aplastic anemia -malaise, fatigue, weight loss, anorexia, impotence, depression, diarrhea, and myopic shifts -
142
Contraindications of CAIs
COPD, sulfa allergies, liver and renal disease
143
What drugs cause aplastic anemia
Chloramphenicol Acetazolamide Methazolamide
144
Drugs that cause myopic shifts
Topamax Pilo CAI
145
Drugs not to give DM
oral CAI Osmotic BBlockers
146
Fatal side effects of oral CAIs
Bone marrow suppression | Aplastic anemia
147
First line drugs for POAG
PGs
148
PGs cause a ____ IOP decrease
30%
149
What glaucoma drug has the highest IOP lowering capabilities
PG at 30%
150
Travatan Z is differnet how
PG | Has sofzia as a preservative instead of BAK
151
MOA of PGs
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
Dosing of PGs
Bedtime dosing - better diurnal control - has a daytime peak effect
153
Contraindications of PGs
-patients who are at risk of CME, cases of active inflammation (uveitis), and patients with previous episodes of HSK
154
Side effects of PGs
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
What are the PGs
Latanaprost Bimatoprost Travoprost
156
PG IOP decrease
33%
157
BBlocker IOP decrease
25%
158
Brimonidine and dorzolamide IOP decrease
18%
159
Pilo IOP decrease
30%
160
MOA of topical ocular anesthetics
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
Why A.R. injected anesthetics given with epinephrine
So that blood vessels are constricted and systemic absorption is minimal. This keeps the drug localized, allowing more potent affects
162
Structure of anesthetics
``` 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
Anesthetics: amides
Longer duration of action Metabolized by liver Less toxic
164
Example of an amide
LIDOCAINE
165
Esters
Shorter duration of action Metabolized locally ALL TOPICAL ANESTHETICS ARE ESTERS
166
All topical anesthetics are
Esters
167
Things that can cause corneal melt
Topical NSAIDS | Topical anesthetics
168
Proparacaine/benoxinate
Esters 10-20s onset 10-20m duration
169
Fluoress
Combination of fluorescein and benoxinate.
170
First topcai lanesthetic used
Cocaine
171
Why do we not RX topical anesthetics for pain
Corneal melt
172
MOA of antihistamines
Block type I HS reactions | -do not prevent the release of histamine, they block the cell receptors that histamine acts upon
173
Type I HS
- 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
H1 antihistamines
Emedastine
175
Emedastine
H1 antihistamine - mild to moderate cases of allergic conjunctivitis - more commonly Rxed in combo with a vasoconstriction game agent, - not common
176
Mast cell stabilizers
Cromolyn Lodoxamide Pemirolast Nedocromil
177
Use of mast cell stabilizers for eye
- 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
Mast cell-antihistamine combo
BEZPOP - bepreve - elestat - Zaditor - patanol - optivar - pataday
179
MOA of mast cell stabilizer-antihistamine combo
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
Overall actions of corticosteroids
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
Side effects of corticosteroids
Increased risk of secondary infections (immunosuppresive), PSC cataracts, and glaucoma (increased IOP)
182
PSC cataracts and coritcosteroids
Irreversible and dose dependent
183
How can corticosteroids cause glaucoma
Increased IOP | Decreased outflow at hte corneal scleral (TM)
184
HSV keratitis and steroids
Decreased immune repsosne, allows virus to proliferate. Do cotton swab Tess
185
Where does ACTH come from
Ant pituitary
186
Potent steroids
Prednisone 1% acetate, rimexalone, difluprednate, and dexamethasone
187
Soft steroids
Flurometholone (FML) 0.1%, and loteprednol (lotemax)
188
What is the safest steroid and why
Loteprdnol because ester based
189
Soft steroids and IOP repsosne
Less likely to cause a spike in IOP
190
Normal patietns and steroids repsonse
5% are high steroid responders
191
POAG and steroid responders
90% of POAG pateints are steroid responders | -try to avoid steroids in glaucoma patients
192
What do NSAIDs block
COX I and II
193
Drugs that block phosphlipase A 2
Steroids Chloroquine Hydroxychloroquine
194
NSAIDs list
“Nac, lac, profen” - diclofenac - ketorolac - nepafenac - bromfenac - flurbiprofen
195
MOA of NSAIDs
Block Cox I and II which decreased inflammation by inhibiting the conversion of arachidonic acid into PGs and thromboxanes
196
Dosing of NAIDS
Diclofenac and Ketorolac are dosed QID Nepafenac TID Bromfenac is BID
197
Only topical NSAID formulated for Qday dosing
Bromday
198
NSAID before ocular surgery
Flurbiprofen
199
Clinical use of topical NSAIDs
Post op cataract patients, decreases the risk of post op inflammation, particularly that of the macula (CME), RCE, corneal abrasions, and allergic conjunctivitis
200
Only NSAID approved for topical treatment of seasonal allergic conjunctivits
Ketorolac Use something else if they have corneal involvement
201
Side effects of topical NSAIDs
``` Corneal toxicity (corneal melt) Stinging upon instillation ```
202
What NSAID should not be RXed in someone with sulfa allergies
Xibrom (bromfenac) | BAK and sodium sulfate preservatives
203
What NSAID has thimerosol as preservative
Flurbiprofen
204
Which NSAID causes corneal melt
Generic Voltaire’s (diclofenac)
205
Best dye for TBUT
NaFL
206
Fluorescein
Water soluble, quickly dissolved in the aqueous portion of the tears Eval of 1. Tear film quality 2. Epithelial defects
207
Rose bengal
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
Lissamine and rose bengal: virus
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
Lissamine green
Less sting Similar use as rose bengal -more commonly utilized for dry eye
210
Methylene blue dry
Staining properties similar to rose bengal, it also stains corneal nerves. Outlines filtering bleb and for staining the lac sac before DCR
211
FL dye
IV for FA - takes 10-20 seconds to occur - macular degeneration to determine if CNVM present Nausea, anaphylaxis, yellow pee
212
Agents for exudative ARMD
Pegaptanib (macugen) | Ranibizumab (lucentis)
213
Pegaptanib (macugen)
Exudative ARMD | Antineoplastic agent=decreased VEGF
214
Ranibizumab (lucentis)
Exudative ARMD | Monoclonal Ab=decreased VEGF
215
What does anti VEGF do
Decrease neo | Decrease vascular permeability (prevent CME)
216
What hyperosmotic agent can be given to DM
Isosorbide
217
Hyperosmotic agents
``` Glycerine Muro 128 (NaCl) ```
218
Glycerine
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)
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What is the best of ANYTHING to reduce IOP
Glycerine
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Tear osmolarity
308 Main: Na+ Other: lots of K+
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Muro 128
Hyperosmotic NaCl Hypertonic solution used for reduction of corneal edema. Eye drops and ointment Fuchs endothelial dystrophy
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Tear substitutes are RXed how often
QID
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Tear substitutes
Water beaded solutions that are used to lubricate the eye and replace the aqueous portion fo the tears. Cellulose esters and PVA
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Of someone needs artificial tears more than QID
Go preservative free
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Disadvantage of artificial tears
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
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Ointments
High viscosity solutions they provide longer duration of action with minimal irritation - obstruct vision - bed time use - increased risk of infection - helpful in kids
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Restasis
Inhibits IL2 Stops formation of T cells -takes 3 months to work, lifespan of a T cell
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Preservatives in CL soltksuon
Prevent and kill bacterial, viruses, and other contaminates. - BAK: very common=SPK - thimerosol=mercury - EDTA=Ca2+ (band K) - purite=favored
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Diffuse SPK and follicles and preservatives
Common if a patient has a toxic reaction to a preservative
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Drugs that cause Whorl Keratopathy
CHAI-T - chloroquine - hydroxychloroquine - amiodarone - tamoxifen - indomethacin
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Fabrys disease
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
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Drugs that cause dry eye
All drugs with BAK, including topical ophthalmic glaucoma meds
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Drugs that case SPK
Isotretinoin (Accutane), topical aminoglycosides
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Drugs that cause endothelial/descemets membrane pigmentation
Chlorpromazine Thioridazine Promethazine
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What do -zine drugs cause to the eye
Lens Cornea Retina Pigment on all of these
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Stromal gold deposits: what drugs
Gold salts
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Drugs that cause delayed corneal healing
Topical and oral corticosteroids
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Eye side effects of amiodarone
-anti-arrhythmic drug Work K Anterior subcapsular lens deposits NAION
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Drugs causing anterior subcapsular effects
Chlorpromazine Thioridazine Amiodarone Miotics May Trigger Anterior Cataracts
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Drugs that cause PSC
Any steroids
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PSC from steroids
Dose dependent Irreversible Hispanics more common
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Drugs affecting the conjunctiva and lids
``` Isoretinoin (accutane) NSAIDs and other blood thinners Sulfonamide Tetracyclines SIldenafil PGs Tamiflu ```
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Isotrtinoin and conjunctiva and lids
Blepharoconjunctivitis, dryness, lid edema Sebaceous glands (meibomian and zeiss)
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NSAIDs and blood thinners and lids/conj
Subconjunctival hemorrhage
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Sulfa drugs and lids/conj
SJS
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Tetracyclines and lids/conj
Pigmented cysts on the conjunctiva
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SIldenafil and lids/conj
Subconjunctival hemorrhage, conjunctival hyperemia PDE-5 inhibitor Vasodilates
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Tamiflu and lids/conj
Conjunctivitis in 1%
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PGs and lids/conj
Conjunctival hyperemia, increased growth of lashes, increased pigmentation of the skin and eyelashes
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Things that can cause a subconjunevtial hemorrhage
Valsalva Clotting diease NSAIDs (aspirin)
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Drugs that decrease tear production (cause mydriasis and increase IOP too)
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
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Drugs that cause mydriasis
- anticholinergics - antihistamines - SSRIs - SNRIs - TCAs - Phenothiazines (antipsychotic) - benzodiazepine - dopamine agonists
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Drugs that resutls in mydriasis can
Cause angle closure in patietns with narrow anterior chamber angles
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Drugs that can cause miosis
Opiates ACHase inhibitors Pilocarpine
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Drugs that can cause nystagmus
Phenytoin, phenobarbital, salicylates (NSAIDs)
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Drugs that can cause diplopia
Antidepressants, antianxiety, phenytoin
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Drugs that affect smooth pursuits
Alcohol
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Drugs that cause oculogyric crisis
Phenothiazines | Cetirizine
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Oculogyric crisis
EOMS undergo spastic, abnormal muscle contractions that leave th eye abnormally postioned (usually elevated)
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Drugs that affect sclera and uvea
- A1 blockers: floppy iris | - blue sclera: corticosteroids, minocyline
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Topiramate and the eyes
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
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Drugs affecting the ON
``` Digoxin Ethambutol Chloramphenicol Streptomycin Sulfonamide Isoniazid Methotrexate SIldenafil Vardenafil sumatriptan Amiodarone Oral contraceptives ```
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Digoxin and the ON
Retrobulbar optic neuritis, BY color defects entropic phenomenon (snowy vision)
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Ethambutol and ON
Optic neuritis
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Isoniazid and methotrexate and ON
Unlikely culprits of optic neuritis
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Drugs that cause NAION
Sildenfil Vardenafil Sumatriptan Amiodarone
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Oral contraceptives and ON
Optic neuritis Papilledema Pseudotumor cerebri
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Drugs that can affect the retina
``` Chloroquine Epinephrine Tamoxifen Thioridazine/chlorpromazine/ promethazine indomethacin Talc Isotrtinoin NSAIDs Oral BC Zidovudine ```
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Chloroquine and the retina
Mottled RPE first | Bulls eye maculoapthy next
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Epinephrine and retina
CME
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Tamoxifen and retina
Yellow or white crystalline depots with or without macular edema
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Thioridazine/chlorpromazine/ promethazine and retina
Pigmentary retinopathy that looks like bulls eye maculopathy
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Indomethacin and retina
Retinal hemorrhage, pigmentary changes (mottling) Can also cause whorl K
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Oral BP can cause
ON Dry eye CRVO/BRVO
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Isotretinoin and retina
Loss of color vision, nyctalopia
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NSAIDs and retina
Hemorrhage
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BC and retina
Vasculopathy, retinal hemorrhage
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Zidovudine and retina
Macualr edema
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Drugs that cause ICP
``` CATS Contraceptive Accutane/Vit A Tetracyclines Synthroid/steroids ```
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Drugs increasing IOP
Anticholinergic activists - atropine/scopolamine - antihistamines - antidepressants - antipsychotics - short acting B2 agonists - pseudoephedrine - corticosteroids
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Drugs that decrease IOP
Systemic BBlockers Cardiac glycosides (digoxin) Alcohol Ccannabinoids
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Marijuana
Max effect on IOP occurs 60-90m after inhalation and lasts about 4 hours
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How do steroids increase IOP
Decreasing TM outflow