Nbeo Ocular Pharm

Front 1

Mucous layer of the tears is ___ soluble.

Back 1

lipid and water

Front 2

What corneal layers are lipid soluble? Water soluble?

Back 2

Lipid = epith, endoth
Water = stroma

Front 3

The ideal ocular drug should have what kind of lipid solubility, molecular size, ionization, and pH?

Back 3

high lipid solubility, small molecular size, low ionization, and as a weak base

Front 4

T/F - Muscarinic receptors are found in smooth muscle parasymp postganglionic synapses.

Back 4

True

Nicotinic = skeletal NMJ and in both symp and parasymp preganglionic synapses

Front 5

T/F - Nicotinic receptors are found in both parasymp and symp preganglionic synapses

Back 5

True

Front 6

T/F - Postganglionic neurons are shorter in the sympathetic pathway.

Back 6

False - longer

Front 7

What ocular components have alpha adrenergic receptors? What are the actions?

Back 7

Iris dilator (A1) = dilation of pupil
CB (A2) = constriction of BVs thus reduce blood flow to CB

This relates to A2 adrenergic agonists (e.g. Iopidine, Alphagan) for IOP control

Front 8

What ocular components have beta adrenergic receptors? What are the actions?

Back 8

TM (B2) = relax TM, incr outflow
Ciliary muscle (B2) = relaxes
NPCE (B1, B2) = incr aqueous formation

Relates to B-blockers for IOP control

Front 9

What blood vessel serves as the direct source of aqueous?

Back 9

MACI (Maj Arterial Circle of the Iris), which comes off LPCA

Front 10

The NPCE allows active secretion of what molecules in order to draw water from MACI?

Back 10

Bicarb (inhibited by CAIs) and Na cross the NPCE, then water follows (thus active formation of aqueous)

Front 11

MOA of cholinergic agonists with the eye? Example of a drug?

Back 11

stimulate longitudinal muscle of CB, which pulls on scleral spur and thus opens up TM pores - results in incr outflow, decr IOP

Main example = pilo!

Front 12

Three main structures that get parasymp innervation in eye? Actions?

Back 12

sphincter muscle (miosis), ciliary muscle (incr accom), lacrimal gland (incr tears)

Front 13

What drug is used during an LPI?

Back 13

Pilo - to pull iris taut

Front 14

1% pilo is used in this diagnostic test...

Back 14

to DDx CN III palsy vs sphincter tear w/ fixed, dilated pupil or pharm block

CN III palsy will constrict, tear or pharm block won't

Front 15

0.125% pilo is used in this diagnostic test. MOA?

Back 15

Dx adie's - normal pupil won't respond, but Adie's will result in miotic pupil

Ciliary ganglion has lesion, so sphincter is starved for ACh so even a little pilo will cause miosis

Front 16

Pilo ADEs?

Back 16

Browaches, HAs, myopic shift (these apply only to pre-presbyopes since ciliary muscle still works)

Also decr vision in cataract pts (miosis exacerbates), *RDs, secondary ACG

Front 17

T/F - Cataract is a CI to pilo.

Back 17

True - smaller pupil can worsen visual problems related to cataract esp if opacity in visual axis

Front 18

What drug is used for the Tensilon Test? What Dz is involved? MOA?

Back 18

Edrophonium - for Dx MG; stimulates muscle strength

Front 19

T/F - Echothiophate is an irreversible acetylcholinesterase

Back 19

True

Front 20

Neostigmine is used to Tx...

Back 20

MG

Front 21

What cholinergic agonist has a fast onset and short mydriatic duration?

Back 21

Tropicamide

Front 22

What is the most potent ocular cholinergic agonist?

Back 22

Atropine

Front 23

How does Atropine decrease AC rxn?

Back 23

constrict blood vessels (stabilizing blood-aqueous barrier) in the CB, which contributes to aqueous formation

Front 24

Physostigmine can be used as an antidote for ___ toxicity.

Back 24

Atropine

Front 25

Botox falls in what drug class? MOA?

Back 25

Cholinergic antagonist; inhibits release of ACh at neuromuscular jxn thus inhibit muscular contraction

Front 26

Norepinephrine acts on what receptors?

Back 26

A1, A2, B1 (NOT B2, thus minimal effect on aqueous production)

Front 27

T/F - All of the adrenergic receptors in the anterior segment have B2 receptors

Back 27

True

Front 28

What percent Phenylephrine is useful for DDx Horner's? How does it work?

Back 28

1% - this is not enough to dilate normal eyes, but will give full dilation for Horner's pts

Front 29

Why is Phenylephrine not useful as a cycloplegic?

Back 29

It is an Alpha-1 agonist (which is in iris dilator). No effect on Beta receptors thus no cycloplegia

Front 30

What adrenergic agonist is useful as a Tx for reducing ptosis?

Back 30

Phenylephrine - incr sympathetic innervation to Muller's muscle, which retracts lid

Front 31

Your pt fails to dilate with cocaine and dilates with Paredrine (Hydroxyamphetamine). You suspect...

Back 31

No dilation on cocaine = (+)Horner's

Dilation with Paredrine = preganglionic lesion so must R/O Pancoast's tumor at lung apex

"Paredrine has a PreDilection to tumors"

Front 32

Epinephrine acts on what receptors?

Back 32

All adrenergic receptors (both Alphas and Betas)

Compare vs Norepi - acts on all but B2

Front 33

Naphazoline class, MOA, use, ADEs

Back 33

aka Naphcon-A (which also has antihistamine); Adrenergic agonist; used to constrict conj BVs (decr redness)

ADEs = greater alpha vs beta effects so have potential to depress CNS; excessive use can also cause dilation since affects alpha (therefore iris dilator)

Front 34

Tetrahydrazoline class, MOA, use, ADEs

Back 34

aka Visine; Adrenergic agonist; used to constrict conj BVs (decr redness)

ADEs = greater alpha vs beta effects so have potential to depress CNS; excessive use can also cause dilation since affects alpha (therefore iris dilator)

Front 35

Apraclonidine class, MOA, use

Back 35

aka Iopidine; A2 adrenergic agonist; decr aqueous production AND incr uveoscleral outflow; used to control IOP spikes after ocular surgery and for acute angle closure attack, not effective for chronic glaucoma

*Apraclonidine for Acute

Front 36

What glaucoma drug class has two IOP lowering actions in one? Name these actions.

Back 36

A2 adrenergic agonists ("onidines")- decr aqueous production and incr uveoscleral outflow

Front 37

Brimonidine class, MOA, use, ADEs

Back 37

aka Alphagan; A2 agonist; decr aqueous production AND incr uveoscleral outflow; used for long-term glaucoma Tx (compare vs Apraclonidine/Iopidine)

ADEs = follicular conjunctivitis, but Alphagan P has purite as the preservative which decr incidence of rxns

Front 38

Epinephrine MOA in lowering IOP?

Back 38

No longer used to lower IOP, but MOA = incr outflow (B2) decr aqueous production (A2)

Front 39

Contraindications for Epi?

Back 39

1) Aphakes: incr risk of CME
2) Narrow angles: slight mydriasis can lead to angle closure
3) Cardiovasc dz and hyperthyroidism: B1 effects can cause HAs, tachycardia, hypertensive crisis
4) MAOIs: incr effect

Front 40

Topical application of B-blockers can cause these ADEs...

Back 40

can be absorbed systemically, causing depression, impotence, bradycardia, bronchospasm

(hence block sympathetic)

Front 41

T/F - There is little difference in effectiveness between 0.25% and 0.50% conc in B-blockers

Back 41

True

Front 42

What type of Beta receptors are predominant in the eye? Where are these receptors exactly?

Back 42

Beta-2 ("two eyes, two lungs" - this rule applies to Beta!)

In TM, Ciliary muscle, NPCE

Front 43

Which beta blockers are cardioselective (both topical and systemic)?

Back 43

Atenolol, Betaxolol, Esmolol, Acebutol, Metoprolol

"A BEAM of B1 blockers"

Front 44

What is the only topical cardioselective beta blocker?

Back 44

Betaxolol (Betoptic-S)

Front 45

Cosopt is made of...

Back 45

Timolol (B blocker) and Dorzolamide (CAI)

Front 46

Combigan is made of...

Back 46

Timolol (B blocker) and Brimonidine (A2 agonist)

Front 47

What is the difference between Alphagan and Betagan?

Back 47

Alphagan (Brimonidine) = A2 agonist
Betagan (Levobunolol)= B blocker

Front 48

This drug intentionally induces ptosis. Why would you want to do this? MOA of this drug?

Back 48

Guanethidine; to Tx lid retraction in Grave's; causes ptosis by limiting NE through increasing release at synapse then enhance reuptake - thus decr symp response, also blocks receptors to Muller's muscle. Both contribute to ptosis

"Guanethidine Graves"

Front 49

Dapiprazole class, MOA, use

Back 49

aka Rev-Eyes; A1 antagonist; induces miosis post-dilation

Front 50

CAI MOA?

Back 50

Acts in CB epith (nonpig and pigmented), prevents carbonic anhydrase from combining CO2 + H20 into Bicarb

Bicarb normally enters into posterior chamber and draws Na and water to follow, which incr IOP.

In a nutshell: CAIs decr IOP by decr aqueous outflow

Front 51

CAI should not be used w/ pts who have a ___ allergy.

Back 51

Sulfa

Front 52

Name the topical and oral CAIs.

Back 52

Topicals = Brinzolamide (Azopt) and Dorzolamide (Trusopt)
"BRIan and DORothy"

Orals = Acetazolamide (Diamox) and Methazolamide (Neptazane)
"Ace and Meth" - you can think Ace Frehley of KISS and Method Man (yeah I know but it works for me...)

Front 53

ADEs of CAIs? How about Acetazolamide ADEs specifically?

Back 53

Metallic taste, tingling of hands, *metabolic acidosis, GI irritation

In acetazolamide = bone marrow suppression, aplastic anemia, myopic shifts

Front 54

MOA of prostaglandins?

Back 54

Incr uveoscleral outflow

Front 55

ADEs of prostaglandins?

Back 55

iris heterochromia, incr pigmentation and growth of lashes, skin darkening around eyes

Front 56

MOA of topical ocular anesthetics

Back 56

block nerve conduction by stopping influx of Na ions into nerve cytoplasm; w/o Na entry, nerve cannot depolarize (thus won't send off signal)

Front 57

This drug is used along with local anesthetics to minimize systemic absorption

Back 57

epinephrine - BV constriction

Front 58

You're having trouble remembering which anesthetic is an ester, and which is an amide, and then you remember this mnemonic...

Back 58

Amides contain an "i" somewhere before the -aine.

Esters do not (with the exception of dimethocaine).

Front 59

T/F - All topic anesthetics are amides.

Back 59

False - esters

Front 60

Which anesthetic class gets metabolized by the liver?

Back 60

Amides ("Lidocaine Longer Liver")

Front 61

Which anesthetic class is metabolized locally?

Back 61

Esters

Front 62

Cocaine causes vaso(dilation/constriction)

Back 62

constriction - thus enhances the effects of anesthesia on its own, without need for epinephrine

Front 63

Fluoress includes what anesthetic?

Back 63

Benoxinate

Front 64

Antihistamine MOA?

Back 64

Block cell receptors to histamine (H1 or H2)

DO NOT prevent histamine release from mast cells and basophils

Front 65

Naphcon-A consists of...

Back 65

Naphazoline (vasoconstrictor) + Pheniramine Maleate (H1 antihistamine)

Front 66

Topical antihistamines are (H1/H2) blockers?

Back 66

H1

Recall that H2 is in the stomach

Front 67

Mast Cell stabilizer MOA

Back 67

acts on exposed mast cells and inhibits degranulation upon re-exposure to antigen

Front 68

Mast Cell stabilizers are not effective for (acute/chronic) allergic Sx

Back 68

not effective for acute since mast cells already degranulated

Front 69

Cromolyn Sodium class, use

Back 69

Mast cell stabilizer, used for chronic allergic conjunctivitis, vernal conjunctivitis, atopic keratoconjunctivitis

Front 70

Alocril and Alomide are what class drug?

Back 70

Mast cell stabilizers

Also Alamast

Front 71

Patanol consists of...

Back 71

H1 receptor blocker and mast cell stabilizer

Front 72

VKC is almost always associated with...

Back 72

atopy (asthma, eczema, seasonal allergic rhinitis)

Front 73

VKC vs AKC?

Back 73

VKC = kids, less involved w/ outer lid & periorbital skin, *Trantas Dots (limbal papillae), *cobblestone papillae), seasonal, stringy discharge

AKC = young adults, *scaly thickened swollen ITCHY lids, all year long

Front 74

Corticosteroid MOA

Back 74

binds to receptors on target cells - steroid/receptor complex enters nucleus and makes new mRNA

Inhibits phospholipase A2, an enzyme that is in the arachidonic acid pathway; the latter pathway leads to inflammatory agents incl leukotrienes and prostaglandins

Front 75

Corticosteroids (incr/decr) capillary permeability?

Back 75

decr

Front 76

Critical corticosteroid ADEs?

Back 76

Incr risk of secondary infections (HSV!), PSCs, glaucoma (incr IOP)

Front 77

NSAID MOA?

Back 77

Blocks COX, thus stop conversion of arachidonic acid into prostaglandins and thromboxanes

Front 78

Diclofenac Sodium class, use

Back 78

aka Voltaren; ocular NSAID; for post-op inflammation/prevent CME and Tx allergic conjunctivitis

Front 79

Ketorolac Tromethamine class, use

Back 79

aka Acular; ocular NSAID; for post-op inflammation/prevent CME and Tx allergic conjunctivitis

Front 80

Trifluridine MOA

Back 80

inhibits replication of viruses by producing faulty viral DNA

Front 81

Antimetabolites are used in ophthalmic practice mostly for ___. Name two.

Back 81

trabeculectomy; 5-fluorouracil, Mitomycin C

Front 82

Rose bengal stains...

Back 82

healthy epith cells that are not covered by mucous (does not enter epith defects like NaFl or Lissamine Green)

Front 83

Lissamine green stains...

Back 83

epith cells unprotected by mucous AND epith defects

vs Rose Bengal - does not stain epith defects

Front 84

IV Fluoroscein Dye takes ___ secs for it to show up in choroidal and retinal vessels.

Back 84

10-20

Front 85

What drug class is the best to decr IOP? MOA?

Back 85

Hyperosmotic agents (draws gradient towards blood to decr outflow)

ex = Isosorbide, Glycerine

Front 86

Isosorbide class, MOA, use, ADEs

Back 86

Hyperosmotic agent; huge molecular weight compounds that draw water back into blood vessels from posterior chamber thus decr IOP; for acute angle closure attack

ADEs = vomiting if not sipped

Mixed with soft drink over crushed ice

Front 87

Glycerine class, MOA, use, ADEs

Back 87

Hyperosmotic agent; huge molecular weight compounds that draw water back into blood vessels from posterior chamber thus decr IOP; for acute angle closure attack

ADEs = vomiting if not sipped, NOT for DM b/c incr BG

Mixed with soft drink over crushed ice

Front 88

Which has more ocular contact time - methylcellulose or polyvinyl alcohol? Why?

Back 88

methylcellulose b/c more viscous

Front 89

Benzalkonium chloride MOA, use, ADEs

Back 89

aka BAK; ruptures bacterial cell memb; used as preservative

ADEs = epithelial toxicity with prolonged use

Front 90

Viroptic uses this preservative...

Back 90

Thimerosal

hence prolonged use not recommended

Front 91

Chlorhexidine use...

Back 91

preservative in Boston Simplicity and other RGP cleaners

Front 92

What causes whorl keratopathy? Although rare, this drug also causes this other ADE?

Back 92

Amiodarone; also causes optic neuritis

Front 93

T/F - Antianxiety agents tend to cause dry eyes

Back 93

True

Front 94

T/F - Antihistamines tend to cause dry eyes

Back 94

True

Front 95

Ritalin causes (miosis/mydriasis)?

Back 95

mydriasis

Front 96

Antihistamines cause (miosis/mydriasis)?

Back 96

mydriasis

Front 97

Amphetamines cause (miosis/mydriasis)?

Back 97

mydriasis

Front 98

Heroin causes (miosis/mydriasis)?

Back 98

miosis (opiate drug causes pinpoint pupils e.g Morphine, Codeine)

Front 99

Digitalis ocular ADEs...

Back 99

B/Y color defect, pain on eye movement

Front 100

Ethambutol toxicity to eye...

Back 100

optic neuritis

Front 101

Isoniazid toxicity to eye...

Back 101

optic neuritis

Front 102

Chloramphenicol toxicity to eye...

Back 102

optic neuritis

Front 103

Crystalline retinopathy is caused by toxicity from this drug...

Back 103

Tamoxifen

Front 104

These drugs cause RPE and outer retinal degeneration, pigment deposits throughout eye, and cataracts. What is this drug class?

Back 104

Phenothiazines (Chlorpromazine, Thioridazine)

Front 105

Canthaxanthin ocular toxicity?

Back 105

crystalline retinopathy, color blindness

Front 106

Oral contraceptive ocular toxicity?

Back 106

optic neuritis, papilledema, pseudotumor cerebri, dry eyes

Front 107

T/F - A drug with a aigher therapeutic index is safer

Back 107

True

TI = LD50 / ED50

Front 108

Therapeutic Index =

Back 108

LD50 / ED 50

Lethal Dose that kills 50% of experimented animals
Effective Dose = does necessary to be effective in 50% of population