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Clinical Neuro > OPTH Lec07 and 08 > Flashcards

OPTH Lec07 and 08 Flashcards

1
Q

Bioavailability

A

% of unchanged drug that is absorbed in the circulation; want to increase bioavailability of eye drops

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1
Q

Surfactants

A

increase solubility of hydrophilic drugs; Improves penetration through the cornea Benzalkonium Chloride = MC Emulsifies cell walls – improves penetration, but can cause ocular surface damage

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2
Q

How can we improve bioavailability

A

Osmotics – adjust tonicity of drops to prevent reflex tearing Non-ionized forms of drugs = lipid soluble, thus better penetration

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3
Q

How are eye drop measurements expressed

A

Parts per 100 1% = 1 gram per 100 cc How many mg of atropine in 5cc of a 1% solution? (1 gram/100 cc ) * 5 cc = .05 grams = 50 mg

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4
Q

Administration of Eye Drops

A

Drugs to Nasolacrimal duct to Mucosa No first pass effect through GI tract and liver

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5
Q

Anesthetic Eye Drops do what?

A

Prevents generation and conduction of nerve impulse Anesthesia impedes sodium access to the axon by blocking transmembrane sodium channels

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6
Q

Name the Anesthetic Eye Drops:

A

tetracycline, proparacaine

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7
Q

What does tetracaine do?

A

Onset: 15-20 seconds Duration: 15 – 20 minutes Corneal Toxicity, Never prescribe for home use

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8
Q

What does proparacrine do?

A

Better tolerated than tetacaine Onset: 12.9 seconds Duration: 20 minutes Allergic Dermatitis

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9
Q

What kind of neurons are there in the symp nervous system?

A

1st order - from in hypothalamus, descend to IML horn of lower cervical and upper thoracic spinal cord 2nd order - Pass through sympathetic chain and synapse in superior cervical ganglion 3rd order - Travel to the eye with branches of carotid artery to innervate smooth muscles and glands

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10
Q

What kind of receptors are there in the symp nervous system and where are they?

A

Alpha 1 – most vascular smooth muscle, pupillary dilator, heart Alpha 2 - adrenergic and cholinergic nerve terminals Beta 1 – heart, fat cells Beta 2 – respiratory and vascular smooth muscle, skeletal muscle

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11
Q

Name the alpha drugs that act on autonomics:

A

norepinephrine, epinephrine

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12
Q

Naem the beta drugs that act on autonomics:

A

epinephrine, isoproterenol

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13
Q

What are alpha blocking drugs?

A

thymoxamine

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14
Q

Which drugs do you use for Galucoma?

A

Beta blocking – timolol, betaxolol, levobunalol, etc. Alpha agonist – clonidine, apraclonidine, brimonidine

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15
Q

What does Epinephrine do?

A

Increases trabecular outflow; Small increase in aqueous production; Vasoconstriction; Mydriasis; Mostly alpha, slight beta effect

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16
Q

Describe Epinephrine Toxicity:

A

o Nervousness, anxiety, tachycardia, headache o May exacerbate CAD, HTN, Thyrotoxicosis o Corneal pigmentation, madarosis, turns contact lenses black o Rebound Hyperemia o Conjunctival Pigment Deposits

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17
Q

What does Phenylephrine do?

A

Direct acting, alpha agonist; Alpha-1 selective, little effect on Beta; Used for mydriasis; Onset 15-60 mins, duration 3.7 hours; No effect on ciliary muscle

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18
Q

What is the toxicity of phenylephedrine?

A

Acute Hypertension Seen with 10% solution Never use 10% in infants Hypersensitivity in patients with diabetic neuropathy Pulmonary Edema, arrhythmia

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19
Q

What does clonidine do?

A

– Central acting, even topically – Alpha 2, some alpha 1 agonist – Decreases aqueous production by vasoconstricting the ciliary body – Little effect on pupil. Accommodation, or vision – Multiple cardiovascular effects

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20
Q

What is apraclonidine?

A

– Alpha agonist, mostly alpha 2 – Lowers IOP by suppressing aqueous production – Vasoconstriction of the ciliary body may also play a role – Does not cross blood brain barrier in adults – Can cause somnolence in children – No effect on BP, almost no cardiac effects

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21
Q

What are the side effects of apraclonidine?

A

Transient dry nose, mouth (30-40%) Eye lid retraction Mydriasis Conjunctival blanching Do not use in kids!

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22
Q

What is brimonidine and what is it used for?

A

– Alpha agonist, primarily alpha-2 – Decreases aqueous production – Increases uveoscleral outflow – Less allergy than apraclonidine – No heart rate/BP effects – Can cause sedation by stimulating central alpha-2 receptors

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23
Q

What are the side effects of Brimonidine?

A

10-30% dry mouth, burning, fatigue, redness Visual Disturbance Contraindicated in young children due to somnolence

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24
Q

What is Thymoxamine (0.5%)

A

– Alpha blocker – Inhibits pupillary dilator muscle of the eye – Competes against NE – Constricts Pupil – No effect on IOP, Aqueous production – No effect on accommodation

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25
Q

What are clinical uses for Thymoxamine?

A

Reverse phenylephrine dilation Treatment of angle closure glaucoma Treatment of lid retraction from thyroid disease (sympathetic innv to Muller’s muscle) Maintain position of IOL

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26
Q

What are the side effects of Thymoxamine?

A

Burning, Conjunctival Hyperemia

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27
Q

What is Timolol?

A

– Nonspecific Beta Blocker (β -1 and β -2 receptors) – Antagonizes circulating catecholamines at the β -1 and β -2 receptors at the ciliary epithelium – Decreases aqueous production/ No influence on outflow – No change in vision, pupil, or accommodation – IOP decrease seen in 30-60 minutes – Short term increase in weeks with upregulation of beta receptors – No effect on optic nerve blood flow

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28
Q

What are the contraindications of Timolol?

A

Asthma, COPD, Bradycardia, Arrhythmias

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29
Q

What is the toxicity/side effects of Timolol?

A

Depression, decreased pulse, GI irritation Anxiety, confusion, decreased sexual function, hair loss Exacerbation of Myasthenia Gravis Decreased response to hypoglycemic episodes

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30
Q

What is Betaxolol?

A

– β -1 selective blocker – Decreases aqueous production by 32-47%/No effect on outflow or pupil – Less potent than timolol, but safer to use in lung disease

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31
Q

What are the side effects fo Betaxolol?

A

Local: Burning, spk, conjunctivitis Systemic: Less than timolol, Decrease pulse, BP, arrhythmia

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32
Q

What is Carteolol?

A

– Non selective Beta Blocker – Intrinsic Sympathomimetic activity = Transient beta agonist activity – Similar efficacy in IOP lowering – Less ocular irritation – Similar Side Effect Profile to Timolol

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33
Q

Describe the effect of Beta blockers on Lipids:

A

– Beta Blockers inhibit lipoprotein lipase and lecithin cholesterol acetyltransferase – Timolol decreases HDL by 8-11% – Carteolol decreases HDL by 3% – Oral nonselective Beta Blockers decrease HDL by 19%

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34
Q

Where do cholinergic medications act?

A

– Muscarinic- affect smooth muscle and glands; Blocked by Atropine; found in the eye; Iris sphincter muscle – Nicotinic – affect skeletal muscle and autonomic ganglia; found outside the globe; Extra Ocular muscles

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35
Q

How is acetylcholine administered?

A

– Cannot use topically bc corneal cholinesterase destroys it – Injected intracamerally (into anterior chamber) during cataract surgery to cause miosis

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36
Q

What is methacholine?

A

– More resistant to cholinesterase – Can administer topically – 2.5% used to diagnose Adie’s tonic pupil

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37
Q

What is Carbachol?

A

– Combination of acetylcholine and physostigmine – Can administer topically, more effective intracamerally – Causes Miosis – Increases trabecular outflow

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38
Q

What are the side effects of Carbachol?

A

Accommodative spasms, conjunctival hyperemia

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39
Q

What is physostigmine?

A

cholinesterase inhibitor

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40
Q

What is pilocarpine?

A

– Direct acting; ONLY on muscarinic receptors – Effective even on denervated structures – Penetrates cornea well

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41
Q

What are the side effects of pilocarpine?

A

Salivation; Lacrimation; Sweating; N/V/D; Bronchiolar spasm/ pulmonary edema

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42
Q

What are the uses of pilocarpine?

A

Angle Closure Glaucoma; Reversal of pupillary dilation

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43
Q

What are the effects of pilocarpine?

A

Miosis; Pupillary block in high concentrations; Induces myopia; Increase trabecular outflow; Decrease uveoscleral outflow

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44
Q

What type of medication is physiostigmine?

A

– Indirect parasympathomimetic – Temporarily inactivates cholinesterase – Improves ciliary contraction – Miosis Lasts 12-36 hours – Antidote for anticholinergic overdose (atropine, scopolamine, cyclopentolate) – Careful with use, very potent, high doses dangerous

45
Q

What are the toxic effects of physiostigmine?

A

death

46
Q

What are the cholinergic side effects?

A

Diarrhea, salivation, bradycardia, diaphoresis, bronchial constriction, nausea, vomiting, coma, loss of reflexes

47
Q

What are the anticholinergic drugs?

A

Atropine, Homatropine, Scolpolamine, Cyclopentolate, Tropicamide

48
Q

What is atropine?

A

Competitive antagonist of acetylcholine Causes: Mydriasis and cycloplegia

49
Q

What are the uses of atropine?

A

Iritis – relaxes the ciliary body; mblyopia – alternative to patching; hyphema; Reverses oculocardiac reflex

50
Q

What is the toxicity of atropine?

A

100 mg fatal in adults, 50 mg fatal in children Hot as a hare, red as a beet, dry as a bone, blind as a bat, mad as a hatter

51
Q

What is the duration of use for atropine, homatropine, scolpolamine, cyclopenotolate, and tropicamide?

A

Atropine = 14 days, Homatropine = 2-4 days, Scolpolamine = 6 dasy, Cyclopentolate = 24 hours, Tropicamide = 4-6 hours

52
Q

What are the signs of anticholinergic toxicity?

A

Decrease GI motility, increase gastric secretion; Dry mouth; Urinary retention; Decreased sweating; Tachycardia; Bronchial dilation; Confusion; Treat toxicity with Physostigmine; Mydriasis; Cycloplegia

53
Q

What is glaucoma?

A

Death of the optic nerve; Elevated IOP is a risk factor

54
Q

What causes glaucoma?

A

Decreased Production of Aqueous Humor; Increase Outflow of Aqueous Humor via Trabecular Outflow or Uveoscleral Outflow -treatment by decreasing IOP

55
Q

How do you treat galucoma?

A

Decrease aqueous production using Beta blockings, alpha agonists, Carbonic Anhydrase Inhibitors; or; Increase outflow via Adrenergics, Prostaglandin Analogues, Cholinergics

56
Q

Name the medications that are Beta Blockers:

A

Timolol, Betaxolo, Carteolol

57
Q

Name the medications that are alpha agonists:

A

Apraclonidine, Brimonidine

58
Q

Name the medications that are Carbonic Anhydrase Inhibitors:

A

– Topical: Dorzolamide, Brinzolamide – Systemic: Acetazolamide

59
Q

How do Carbonic Anhydrase Inhibitors work?

A

– HCO3 + H- à H2CO3 à Co2 + H20 – Carbonic anhydrase catalyzes this reaction in the ciliary process to make aqueous – CAIs are sulfonamide derivatives – avoid in sulfa allergies – CAI’s reduce Aqueous production by 32% – Must inhibit 90% of carbonic anhydrase before you see a decrease in IOP

60
Q

Describe CAI Toxicity:

A

GI side effects; Malaise; Depression; Weight Loss; Kidney Stones; Metabolic Acidosis; Do not use in sickle cell pts

61
Q

What is Diamox?

A

– Can also be used to decrease elevated ICP in pseudotumor cerebri – Increases rate of subretinal fluid absorption between retina and pigment epithelium (Used to treat CME) – Coadministration of ASA and Diamox may lead to acid base abnormalities

62
Q

What are contraindications to administering CAIs?

A

– Adrenal Insufficiency – Kidney and Liver Disease – Addison’s Disease – Hyperchloremic acidosis – Severe Pulmonary Obstruction

63
Q

How do prostaglandin analogs work?

A

– Increase uveoscleral outflow – Causes relaxation of the ciliary muscle and changes in the extracellular matrix between muscle fiber bundles – Upregulates matrix-metalloproteinases – Lowers IOP 33%, no effect on aqueous production

64
Q

Name the prostaglandin analogs:

A

– Latanoprost (Xalatan) – Travoprost (Travatan) – Bimatoprost (Lumigan / Latisse)

65
Q

What are the side effects of prostaglandin analogs?

A

– Hyperemia – Irreversible darkening of irides – Periorbital skin hyperpigmentation – Hypertrichosis/ eyelash growth (Bimatoprost marketed as Latisse) – Reversible CME cystoid macular edema (Use controversial with patient undergoing cataract surgery)

66
Q

What are the anti-inflammatory corticosteroids?

A

o Hydrocortisone o Cortisone o Prednisone o Prednisolone o Dexamethasone o Betamethasone o Triamcinolone o Flucinolone

67
Q

What are the anti-inflammatory NSAIDS?

A

o Diclofenac o Bromfenac o Nepafanac

68
Q

How do corticosteroids work?

A

– Inhibition of degranulation of mast cells, basophils, neutrophils – Inhibits release of inflammatory mediators - histamines, bradykinins, platelet activating factor – Stabilization of intracellular and lysosomal membranes – Suppresses lymphocyte proliferation – Inhibits phospholipase A synthesis à decreased synthesis of prostagladins and leukotrienes – Inhibits cell mediated immune response – Prolonged use decreases antibody production

69
Q

What are the uses for corticosteroids?

A

Uveitis, Corneal Edema, Hyperemia, Conjunctivitis, Macular Edema

70
Q

What are the contraindications of corticosteroids?

A

Acute epithelial HSV, fungal eye disease; prevent’s healing after removal of superficial corneal foreign body; Acute, untreated eye infections

71
Q

What are the ocular side effects of corticosteroids?

A

Cataracts (Posterior Subcapsular Cataract); Ptosis/mydriasis; Delayed wound healing; Enhanced microbial proliferation; Ischemia; Punctate keratopathy; Elevation in IOP

72
Q

What are the systemic side effects of corticosteroids?

A

Peptic Ulcer; Bone resorption/Calcium loss; Immunosuppression; Growth suppression/muscle atrophy; Euphoria/psychosis; Pseudotumor cerebri; Aggravates DM/HTN; Edema/weight gain/hirsutism

73
Q

What are the formulations of corticopsteroids?

A

Phosphates, Acetates, Alcohols; Acetate and Alcohol are biphasic and have better corneal penetration

74
Q

How do NSAIDS work and when are they used?

A

– Inhibition of cyclooxygeenase à inhibit synthesis of prostaglandins – Unlike corticosteroids, leukotriene synthesis unaffected – Uses: Post-Op CME

75
Q

What are the side effects of NSAIDS?

A

– Stinging/burning, No increase in IOP seen – Inhibit platelet aggregation - caution in patient with bleeding tendency or on ASA therapy – Increased incidence of corneal melting in generic NSAIDS

76
Q

What is the treatment for Allergic Conjunctivitis?

A

– Mast Cell Stabilizers – H-1 Receptor Antagonists – Combo drugs – NSAIDS – Hallmark of Allergic Conjunctivitis = “Itching”

77
Q

Name the Mast Cell Stabilizers:

A

– Cromolyn sodium – Lodoxamide – Nedocromil – Pemirolast

78
Q

What is Cromolyn Sodium?

A

– Blocks cellular influx of calcium, therefore stabilizing mast cell membrane – Almost no side effects

79
Q

What is Lodoxamide Tromehtamide?

A

– Blocks degranulation of mast cells – Inhibits type I hypersensitivity – Indirectly prevents antigen stimulated release of Histamine – Takes several days to work

80
Q

Name the H-1 Receptor Antagonists?

A

– Bepotastine – Emedastine – Levocabastine – Pheniramine

81
Q

What is Levocabastine?

A

– Blocks H1 receptor sites – Not for use with Contact Lenses – Works in minutes

82
Q

Name the Mast Cell Stabilizers with H1 antagonist combination use:

A

– Ketotifen – Olopatidine – Azelastine – Epinastine

83
Q

What are the categories of antibiotic eye drops?

A

– Fluoroquinolones – Aminoglycosides – Macrolides – Others

84
Q

Name the Fluoroquinolones:

A

– Ciprofloxacin – Ofloxacin – Levofloxacin – Gatifloxacin – Moxifloxacin – Besifloxacin

85
Q

What do fluoroquinolones do?

A

– Inhibit DNA Gyrase – Broad Spectrum – effective against gram positive and negative, including Pseudomonas – Not effective against anaerobes

86
Q

What are fluoroquinolones used for?

A

– Used to treat bacterial conjunctivitis, corneal ulcer – Useful in CL wearers due to increased Psuedomonas coverag

87
Q

Name the aminoglycosides:

A

– Gentamicin – Tobramycin – Amikacin – Neomycin

88
Q

What do the aminoglycosides do?

A

– Bind to 30-S ribosome unit to disrupt protein synthesis – Bactericidal – Treatment of gram negative ocular aerobic bacteria (including Pseudomonas) – Not effective alone vs. Gram positive

89
Q

Where do aminoglycosides have an effect on toxicity?

A

– Vestibular – Auditory – Renal – Neuromuscular blockade – Skin Rashes – Retinal infarction with intravitreal use

90
Q

Name the macrolides:

A

– Erythromycin – Azithromycin – Clrithromycin

91
Q

How do the macrolides work and what are they effective for?

A

– Binds to 50S Ribosome to inhibit protein synthesis – Effective against most gram + cocci and gram – bacilli – Not effective against pseduomonas – Low serious side effects/allergies – Useful in treatment of blepharitis and bacterial conjunctivitis

92
Q

How does vancomycin work?

A

– Interferes with cell wall synthesis – Fortified solution used topically in serious corneal ulcers – Used intravitreally in treatment of endophthalmitis

93
Q

How do penicillins work?

A

– Act through inhibition of peptidoglycan (mucopeptide) synthesis in the bacterial cell wall – Bactericidal – Rarely used topically – Concern over allergic reaction – Increasing resistance

94
Q

How does bacitracin work?

A

inhibits the synthesis of the cell wall

95
Q

How does polymyxin work?

A

alters the bacterial cytoplasmic membrane permeability

96
Q

How do sulfonamides work?

A

inhibit the nucleic acid synthesis

97
Q

How is Bacterial Conjunctivitis treated?

A

– Caused by Staph Aureus – Choose antibiotics with gram positive coverage – Gentamicin commonly prescribed, but has poor gram positive coverage – Need Pseudomonas coverage in Contact Lens wearers

98
Q

How is endophthalmitis treated?

A

– Endophthalmitis Vitrectomy Study – Treated with intravitreal antibiotics – 60% are coagulase negative staph – 10% gram negative – Vancomycin + Amikacin or Caftazidime

99
Q

Name the antivirals and what they are used for:

A

– Trifluridine - Fluorinated pyrimidine nucleoside analog; Treatment of HSV Keratitis (Dendritic lesion of cornea); 1 drop 9x/day for 10-14 days

100
Q

What are the side effects of tirfluridine?

A

burning, spk, hypersensitivity, hyperemia, epithelial erosions, scarring of puncta

101
Q

What is a Cyclosporine used for and what are the side effects?

A

– Topical immunomodulator with anti-inflammatory effects – Treatment of Keratoconjunctivitis Sicca – Improves tear production – Takes 3-6 months before see effects – SE: burning

102
Q

What are ocular side effects of Phenothiazines (systemic medications)?

A

(Chlorpromazine, Thioridazine): Binds to Melanin -> Pigmentary changes in retina – Deposits on lens, then cornea – Digitalis - Changes in visual perception; Snowy, green, white yellow

103
Q

What are the side effects of estrogen/progesterone?

A

Optic Neuritis, papilledema, contact lens intolerance

104
Q

What are the side effects of tamsulosin?

A

floppy iris syndrome; Caution during cataract surgery; take once = lifelong ris

105
Q

What are the side effects of amiodarone?

A

Accumulates in cornea; Vortex Keratopathy after 1 month

106
Q

What are the side effects of tamoxifen?

A

Whorl like subepithelial opacities; White refractile intraretinal deposits

107
Q

What are the side effects of hydroxychloroquine?

A

Corneal deposits (verticillata); Retinal Toxicity; Bilateral Pigmentary Retinopathy; Drug binds to melanin; Bulls Eye Maculopathy

108
Q

What are the side effects of topamax?

A

Acute myopia; Bilateral acute angle closure; Ciliary body swelling and choroidal effusions

109
Q

What are the side effects of sidenafil?

A

Blue Haze in vision; Light sensitivity; Pupil sparing 3rd nerve palsy

Clinical Neuro (6 decks)

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