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Kevin's KMK Flashcards > Ocular Pharmacology (Done) > Flashcards

Ocular Pharmacology (Done) Flashcards

1
Q

Most ocular drugs are formulated as ____________ because this formulation allows better penetration and bioavailability

A

Weak bases

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2
Q

Sympathetic cell bodies are located in the ___________ regions of the CNS.

A

Thoraco-lumbar regions

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3
Q

Parasympathetic cell bodies are located in the ___________ regions of the CNS.

A

Cranio-sacral regions

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4
Q

Which outflow mechanism does Pilocarpine act on for glaucoma?

A

Pulls on scleral spur, opening up the TM for increased outflow and decreased IOP

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5
Q

What are the 4 INDIRECT acting cholinergic Agonists?

A
  1. Neostigme
  2. Pyridostigmine»treats MG
  3. Edrophonium»diagnosis of MG
  4. Echothophate
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6
Q

Aside from treating glaucoma, what else is Pilocarpine used for?

A
  1. Utilized after angle closure attack in preparation for LPI
  2. 1% pilocarpine used to differentiate 3rd nerve palsy from a sphincter tear–3rd nerve palsies will constrict with pilocarpine
  3. 0.125% pilocarpine used in diagnosis of Adie’s Tonic pupil
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7
Q

What are the main side effects of Pilocarpine?

A

> > Browaches, headaches, and myopic shifts, cataracts, retinal detachments, and secondary angle-closure glaucoma

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8
Q

What do Cholinergic Antagonists block in the nerve?

A

These drugs block Ach at muscarinic sites in the ciliary body and iris (increase sympathetic effects)

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9
Q

Why is Scopolamine more likely to have CNS toxicity?

A

Penetrates the blood brain barrier better

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10
Q

What 3 junctions make up the blood-aqueous barrier?

A
  1. Iris vessels
  2. Schlemm’s canal
  3. Tight junctions of NPCE (ciliary body)
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11
Q

Tropicamide has the fastest onset and shortest duration of mydriatic effects
»It has a much stronger ________ than ________ effect.

A

Mydriatic than cycloplegic effects

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12
Q

There are 3 classes of SYSTEMIC drugs that are cholinergic antagonists»1) Anti-psychotics 2) Anti-depressants 3) Anti-Histamines»what are they all?

A

1) Chlorpromazine, Thoridazine
2) Amimphtyline, Imipramine
3) Diphenhydramine (Benadryl), Bropheniramine, Chlorpheniramine, Promethazine

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13
Q

What symptoms will be present if a patient has Atropine toxicity?

A

Dry mouth, dry flushed skin rapid pulse, disorientation and fever due to CNS effects on hypothalamus

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14
Q

What is Atropine’s onset time and duration of cycloplegic effects?

A

60-180 minutes onset and 7-12 days duration

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15
Q

Why is cyclopentolate favored in clinic over Atropine and Homatropine?

A

better cycloplegic effects than homatropine, but similar to atropine except faster onset w/ less duration of action
»can use to treat anterior uveitis as well along with Homatropine

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16
Q

Why is Homatropine, or any cycloplegic for that matter, used to treat anterior uveitis?

A

Dilates the pupil and keeps the iris MOBILE, which decreases the likelihood of posterior synechiae formation»also reduces pain by paralyzing the ciliary and sphincter muscles

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17
Q

What role does Botox play at the neuromuscular junction?

A

Blocks the release of Ach

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18
Q

What system does Phenylephrine target? what are all of its clinical uses?

A

alpha 1 agonist w/ no effects on B receptors»dilation WITHOUT cycloplegia, palpebral widening (acts on Muller’s muscle to retract lid), diagnosing Horner’s syndrome, confirming episcleritis diagnosis, 10% used to break posterior synechiae

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19
Q

What are the 2 main non-specific adrenergic agonists?

A

Naphazoline and Tetrahydrozoline (Visine)–which acts on alpha 1

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20
Q

When is Phenylephrine contraindicated?

A

patients taking MOAI’s, TCA’s and atropine

|&raquo_space;also in patients with Grave’s disease

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21
Q

What effect does Naphazoline and tetrahydrozoline have on conjunctival blood vessels?

A

Constricts blood vessels»over time can cause dilation because of alpha effects on radial muscle.

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22
Q

What is the MAIN effect that alpha 2 agonists (apraclonide, brimonidine) have on aqueous humor outflow?

A
  1. Decreases aq. humor production

2. Increases uveoscleral outflow

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23
Q

What is the trade name of Brimonidine?

Brimonidine has show ___________ properties in rate nerve model.

A

Alphagan 0.2%, neuroprotective properties

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24
Q

In the past, Alphagan caused 30% of patients to develop _______________.

A

Follicular conjunctivitis

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25
Q

Brimonidine is contraindicated in patients taking ____________.

A

MAOI’s

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26
Q

What is the acronymn for diseases causing FOLLICLES to appear in the conjunctiva?

A

“CHAT”»chlamydia, herpes, adenovirus, and toxic

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27
Q

How can Brimonidine be effective in patients with post-refractive LASIK complaints?

A

Brimonidine causes MIOSIS and can be used to reduce glare, halos, and other night vision symptoms in these patients.

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28
Q

What is Apraclonidine used for?

A

Alpha 2 agonist with limited alpha 1 activity. used to control IOP spikes before and after ocular surgery. Also used during an acute angle closure attack, as well as in Diagnosis of Horner’s Syndrome
»Remember, Tachyphylaxis–not effective long-term

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29
Q

In what lighting setting will Horner’s syndrome be most evident?

A

Aniso will be greater in DARK, because the miotic pupil will have a dilation lag

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30
Q

What effect will Apraclonidine have on the pupil of a Horner’s syndrome patient?

A

It will cause the miotic pupil to DILATE!»in normal patients it will have no effect

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31
Q

What effect will Cocaine have on the pupil of a Horner’s syndrome patient?

A

Cocaine will have NO EFFECT on the miotic pupil in Horner’s patients
»Normal patients cocaine will DILATE

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32
Q

If a patient with Horner’s fails to dilate upon installation of Hydroxyamphetamine, what does this indicate?

A

It means it is most likely a POSTganglionic neuron that is damaged.

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33
Q

If a patient with Horner’s DILATES upon installation of Phenylephrine, what does this indicate?

A

It means the patient has a POSTganglionic lesion

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34
Q

What is the most common B-blocker used for glaucoma treatment?

A

Timolol

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35
Q

What is the main purpose of B-blockers?

A

They act primarily on B-receptors (mainly B2) in the NPCE to DECREASE aq. production

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36
Q

What is the dosing of Timolol and when should it be given?

A

Is dosed BID, but once-daily regimen is effective too. If dosed daily, MORNING dosage is recommended

37
Q

In which patients should b-blockers be used cautiously?

A

Diabetics and Hyperthyroidism because it masks symptoms and signs

38
Q

What is in the COSOPT combo drug?

A

Timolol + Dorzolamide

39
Q

What is in the COMBIGAN combo drug?

A

Timolol + Brimonidine

40
Q

What is in the SIMBRINZA combo drug?

A

Brimonidine + Brinzolamide

41
Q

Which systemic drugs are Alpha blockers (i.e. adrenergic antagonists)?

A

Prazosin, Terazosin, and Tamsulosin, which all cause Floppy Iris Syndrome

42
Q

What is a downside of long-term Timolol use?

A

Long-term drift (IOP starts to gradually rise) and Short-term escape (IOP initially lowers, but returns to normal within weeks after starting therapy)

43
Q

What makes Carteolol unique?

A

Non-selective B-blocker (NOT USED CLINICALLY cause of lack of IOP reduction)
»Has intrinsic sympathomimetic activity (causes fewer side effects)»reduces nocturnal bradycardia and less stinging

44
Q

What makes Betaxolol unique?

A

B-1 selective for people w/ COPD or asthma

|&raquo_space;not as effective as lowering IOP, limited B2 activity

45
Q

What effect do Cholinergic Agonists have on aq. outflow?

A

Increased Corneoscleral Outflow

46
Q

What effect do Alpha-Adrenergic Agonists have on aq. outflow?

A

Decrease aq. production and Increased Uveoscleral Outflow

47
Q

What effect do Prostaglandins have on aq. outflow?

A

Increased outflow via the Uveoscleral Route

48
Q

What effect do Beta-blockers have on aq. outflow?

A

Decreased Production

49
Q

What effect do CAI’s have on aq. outflow?

A

Decreased Production

50
Q

What does Carbonic Anhydrase do at the cellular level?

A

An enzyme that acts in ciliary body epithelium to catalyze the joining of CO2+ + H20 to yield bicarbonate
»Bicarbonate ions are believed to INCREASE aq. production by increasing Cl- and Na+ flux into the posterior chamber

51
Q

What are some of the adverse side effects of CAI’s?

A

metallic taste, tingling in hands, metabolic acidosis, aplastic anemia, malaise, fatigue, weight loss, myopic shifts

52
Q

What are the contraindications for CAI use?

A

Patients who have COPD, are pregnant, or Sulfa allergy

53
Q

What are the FATAL side effects of Carbonic Anhydrase Inhibitors?

A

Bone marrow suppression & Aplastic Anemia

54
Q

What is the recommended dosing? What are the contraindications for Prostaglandins?

A

Recommended Bedtime dosing; don’t use in patients with CME, Active inflammation, and pts. with previous episodes of Herpes Simplex keratitis

55
Q

What are the side effects of Prostaglandins?

A

Iris heterochromia, increased pigmentation, eyelash growth, skin darkening around the eyes, conjunctival hyperemia, pruritis

56
Q

What is the MOA of topical ocular anesthetics?

A

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

57
Q

Where are Amide anesthetics metabolized?

A

Metabolized in the LIVER»have a longer duration of action

58
Q

Where are Ester anesthetics metabolized?

A

Metabolized locally»have a shorter duration of action

59
Q

Why do we not prescribe topical anesthetics to patients?

A

Risk of Corneal melting!

60
Q

What is the MOA of Anti-histamines?

A

They BLOCK the cell receptors that Histamine acts upon»they do not prevent the release of histamine from mast cells

61
Q

What is a Summary of Type 1 Hypersensitivity Reactions beginning with 1st exposure?

A
  1. 1st exposure»IgE antibodies are produced
  2. Between exposures, IgE antibodies bind to mast cells and Basophils
  3. When antigen is re-introduced, it binds to IgE resulting in opening of Ca2+ channels
  4. Ca2+ influx depolarizes the cell»results in degranulation of mast cells»Histamine released
  5. The binding of Histamine to histamine receptors results in allergic symptoms.
62
Q

What is the main H1 Ocular Antihistamine used?

A

Emedastine»for allergic conjunctivitis (commonly prescribed in conjunction w/ Tetrahydralazine)

63
Q

What are the 4 main topical mast cell stabilizers used in clinic?

A

Cromolyn sodium, Lodoxamide, Pemirolast, and Nedocromil

|&raquo_space;not used very often because patients don’t come in until they are experiencing the symptoms!

64
Q

What are the 5 main Mast Cell-Antihistamine combos?

A

Remember BEZPOP

Bepreve, Elestat, Zaditor, Patanol, Pataday, Olopatadine

65
Q

During fight or flight conditions, ACTH is released and acts on the ________ cortex to secrete _________.

A

Adrenal cortex to secrete Cortisol

66
Q

What are the Potent steroids?

A

Prednisolone Acetate, Durezol, Dexamethasone

67
Q

What are the “Soft steroids”?

A

FML 0.1% and Lotemax (Loteprednol) 0.5%

68
Q

Which steroid is approved for year round use?

A

Alrex

69
Q

What are the approved topical NSAIDS?

A

Diclofenac sodium (withdrawn from market for corneal melting), Acular, Nepafenac, Bromfenac, Flurbiprofen

70
Q

When should topical NSAIDs be used?

A

Post-op cataract to reduce inflammation (CME), RCE, corneal abrasions, and allergic conjuntivitis

71
Q

Which topical NSAID is given prior to ocular surgery 1 drop every 30 minutes beginning 2 hours prior to surgery?

A

Ocufen (contains thimerosal

72
Q

When can Methylene blue be used?

A

to stain Corneal nerves, outline glaucoma filtering blebs, and staining the lacrimal sac prior to dacryocystorhinostomy

73
Q

What are the 2 main anti-VEGF treatments we need to know for NBEO outline?

A

Macugen (Pegaptanib) and Lucentis (Ranibizumab)

74
Q

When should Glycerine be used? Who should it be used in? what is the process by which glycerine is used to reduce IOP in acute angle closure?

A

A water-soluble compound that CANNOT cross the blood aqueous barrier»this creates osmotic gradient in which plasma in the ciliary stroma region is HYPERTONIC to the aq. humor, LOWERING IOP
»Never used in Diabetics b/c glycerine is rapidly absorbed and is metabolized into carbohydrates, which increase blood sugar levels

75
Q

What alternative hyperosmotic can be used in Diabetic patients experiencing angle closure attack?

A

Isosorbide

76
Q

Which drugs cause Whorl Keratopathy?

A

“CHAI-T”»Chloroquine, Hydroxychloroquine, Amiodarone, Indomethacin, and Tamoxifen

77
Q

Which systemic lysosomal storage disease can result in whorl keratopathy and spoke like lens opacities?

A

Fabry’s Disease

78
Q

What are the 3 main ocular side effects caused by Amiodarone (anti-arrhythmic drug)?

A
  1. Whorl Keratopathy
  2. Anterior subcapsular lens deposits
  3. NAION
79
Q

Which 2 conditions have Symblepharon as one of the ocular findings?

A

Stevens-Johnson syndrome + Cicatricial Pemphigoid

80
Q

Which drugs can cause Miosis?

A
  1. Opiates: Morphine, heroine, codeine

2. Acetylcholinesterase inhibitors

81
Q

Which drugs have anti-cholinergic effects?

A

TCA’s, Anti-histamines (systemic), Phenothiazines, B-blockers, hormone therapies, ADHD meds, and diuretics

82
Q

Which 2 drugs cause Oculogyric crisis?

A

Phenothiazines & Cetirizine (Zyrtec)
»Oculogyric crisis occurs when the extraocular muscles undergo spastic, abnormal muscle contractions that leave the eye abnormally positioned

83
Q

Which main drug according to KMK can cause secondary angle closure?

A

Topamax (Topiramate)

84
Q

What are the ocular side effects of taking Digoxin?

A

Retrobulbar optic neuritis, B/Y color defects, entoptic phenomena

85
Q

Which drugs can cause NAION?

A

Viagra, Vardenafil, Sumatriptan, and Amiodarone

86
Q

Which drugs can cause pigmentary retinopathy?

A

Thioridazine/chlorpromazine/promethazine as well as Indomethacin

87
Q

Which drugs can cause Pseudotumor Cerebri?

A

Tetracyclines, Accutane, oral contraceptives, and Nalidixic acid

88
Q

Which drugs will cause an INCREASED IOP?

A

Drugs with Anti-cholinergic activity!

ex. anti-histamines, TCA’s antipsychotics, Sudafed, Corticosteroids

89
Q

What is the physiology as to why steroids cause IOP increase?

A

Steroids interfere with phagocytosis of debris in Schlemm’s canal and increase the concentration of GAG’s within the TM; these changes result in decreased aq. humor outflow through the TM with subsequent increase in IOP.

Kevin's KMK Flashcards (13 decks)

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