PHARM Ophthalmic Disorders, Otitis Externa, Allergy

What is dry eye syndrome (DES) (keratoconjunctivitis sicca)

Compromised tear film, leading to irritation and potentially long term vision consequences

Treatment goals for DES

• Reduce symptoms and inflammation to re-establish normal ocular surface

• Restore normal tear volume and epithelial integrity

• Remove potential sources of tear film instability

• Identify and eliminate environmental factors

Nonpharmacologic Interventions for DES

• Blink regularly when reading or working on a computer

• Increase level of humidity at home and at work

• Wear sunglasses when outdoors → reduce exposure to drying winds and sun

• Remain hydrated by drinking plenty of water

• Nutritional supplements such as omega 3 supplements may be beneficial in some patients

• Local and systemic allergic reactions and inflammation usually worsen the dry eye condition

Pharm therapy for DES

First line is OTC Palliative Therapy (Lubricating drops and gels)

Drug class of Cyclosporine (Drops)

Calcineurin Inhibitor

MOA of Cyclosporine

partial immunomodulator; unknown

Before using Cyclosporine you should remove your

contacts

Drug class of Lifitegrast (Drops)

lymphocyte function-associated antigen 1 (LFA-1) antagonist

MOA of Lifitegrast

Inhibits LFA-1 from binding to intercellular adhesion molecule 1 (ICAM-1) → downregulates T lymphocyte activity

Before using Lifitegrast you should remove your

contacts

SE of Lifitegrast

may cause a change in taste

Drug class of Pilocarpine (PO)

Cholinergic agonist

MOA of Pilocarpine

binds to muscarinic (cholinergic receptors) leading to inc. in secretion of exocrine glands (lacrimal)

Pilocarpine is reserved for

severe, unresponsive dry eye; typically those with sjoren syndrome

Drug class of loteprednol (ointment) and prednisolone (ointment)

corticosteroid

MOA of loteprednol and prednisolone

inhibit inflammatory response

loteprednol and prednisolone are reserved for

moderate to severe cases of “ophthalmic inflammatory conditions”

What are ointments?

semisolid dosage forms for external use, mainly applied at night

What are solutions?

perfectly mixed homogenous solution (liquid)

What are suspensions?

only partially soluble in the solute and will separate when it settles, have to shake the bottle to mix before using

Describe the main steps for inserting eye drops

1. Wash hands

2. Remove contact lens

3. Shake drops

4. Remove the cap and do not touch dropper tip

5. Tilt head back slightly (may help to focus a point on the ceiling

6. Using one hand pull the lower eyelid back to form a pocket

7. Hold dropper over eye and squeeze gently

8. Apply gentle pressure to tear ducts (where eyelid meets the nose and hold close for a minute

9. Use a tissue to wipe any excess from eye

10. Repeat with other medication or opposite eye

11. Rewash hands

Goals of therapy for conjunctivitis

• Increase patient comfort

• Reduce the course of infection and/or inflammation

• Prevent the spread of the infection in contagious forms of conjunctivitis

Nonpharm therapy for conjunctivitis

• Avoid hand to eye contact

• Wash your hands thoroughly and frequently

• Change towel/washcloth daily

• Discard eye cosmetics

• Do not use anyone else’s personal eye care items

Mild bacterial conjunctivitis will resolve _

on their own within two weeks

Moderate to severe bacterial conjunctivitis will likely be treated with

antibiotics

Pharm Tx for mild-moderate bacterial conjunctivitis

◦ First line therapy

• Empiric (covers gram + and gram -)

  • Erythromycin ointment

  • Polymyxin B with Bacitracin

◦ Second Line Therapy

• Fluoroquinolones (may be first line in contact lens wearers)

  • (moxifloxacin, besifloxacin, gatifloxacin)

  • Polymyxin B and Trimethoprim

  • Neomycin and Polymyxin B

  • Gentamicin

  • Sulfacetamide

◦ General dosing

• Start with high frequency of administration (q2-4h) and then decrease frequency after 3-4 days

• May see symptom resolution prior to end of duration, continue treatment 3-5 days after

Pharm Tx for severe bacterial conjunctivitis

◦ Must use oral or IM 3rd generation cephalosporin

• Oral: Cefixipime

• IM: Ceftriaxone

Pharm tx for neonatal conjunctivitis

◦ Prophylaxis: Erythromycin ointment, if chlamydia trachomatis suspected

◦ Treatment: Systemic Antibiotics

• Azithromycin

Viral Conjunctivitis Tx

No FDA approved therapy to treat this typically self-limiting condition, supportive treatment only

Symptom reduction seen with use of:

• Cold compress

• Artificial tears

Tx for severe viral conjunctivitis

◦Topical corticosteroid (loteprednol, prednisolone) for symptom reduction

◦Oral antiviral medication

• Used in HSV or Varicella (VZV)

• Acyclovir, valcyclovir

What is blepharitis?

Inflammation of the eyelids/eyelid margin

Chronic disease with acute exacerbations

Types of blepharitis?

bacterial, seborrheic, and meibomian gland dysfunction (MDG)

What causes bacterial blepharitis?

staph aureus

What causes seborrheic blepharitis?

Sebaceous gland inflammation

What causes MDG blepharitis?

Blockages in the gland promote bacterial growth

Goals of therapy for blepharitis?

• Keep eyelids clean and free of foreign bodies/flaky crust

• Prevent progression to ocular lid and surface damage

• Reserve function of sight

1st line of therapy for blepharitis?

Improve ocular hygiene

• Warm compress 2-4x/day

• Vertical eyelid massage

  • Stimulates meibomian gland secretions

Cleanse eyelids daily

*Usually accompanied with baby shampoo

• OCuSOFT ® lid scrub

• OCuSOFT ® Foam scrub

Must be done regularly to assist in preventing exacerbation

Pharm therapy for blepharitis if its bacterial

Bacterial (2-4 week therapy)

◦ Topical antibiotics: Erythromycin or bacitracin ophthalmic ointment

◦ May require oral antibiotics for severe cases or MGD:

• tetracycline or azithromycin

◦ Short courses of corticosteroids may assist in reducing symptoms and inflammation

• Loteprednol (Lotemax®) 0.5% gel drops – site specific due to increased viscosity

• Fluorometholone (FML®) 0.1% ointment or suspension

  • – low ocular penetration

◦ *Do not wear contact lenses until ophthalmic therapy is complete.

goals of therapy for open-angle glaucoma

Reduce intraocular pressure (IOP) by 20-30% to decrease risk of perpetuating optic nerve damage

Preserve visual function

Nonpharm therapy for open-angle glaucoma

Surgical options (first line for pt with severe visual loss)

• Laser surgery: Laser is used to stimulate the trabecular meshwork; somewhat effective

• Conventional surgery: Trabeculectomy used if medication and laser surgery do not work; effective

  • Creates a drainage flap to allow aqueous humor to drain into the vasculature

• Drainage implants: Small silicon tube inserted to assist in draining fluid

First line of therapy for open angle glaucoma and an alternative

beta blocker of prostaglandin analog

an alternative: a-2 adrenergic agonist

If first line therapy for open-angle glaucoma is contraindicated use

carbonic anhydrase inhibitor (CAI)

patients who are unresponsive to or intolerant of a drug should be switched to

an alternative drug rather than given an additional drug

MOA prostaglandin analog

↑ aqueous Analog outflow via (Prostenoid agonist) uveoscleral and trabecular mesh

agents found in prostaglandin analog class

• Latanoprost (Xalatan) solution

• Bimatoprost (Lumigan) solution

• Travoprost (Travatan Z) solution

• Tafluprost (Zioptan) solution

SE of prostaglandin analog

• may cause iris pigmentation

• thickens/grows the eyelash

MOA of beta blocker

β-receptor antagonist at the ciliary body, causing ↓ in aqueous humor production

Agents found in beta blocker class

• timolol (Timoptic) gel

• carteolol solution

• levobunolol solution

• betaxolol solution /suspension

Cautions for beta blockers

use caution in patients with bradycardia, heart block, pulmonary disease;

Treatment may result in tachyphylaxis (drug doesn’t give as much of a response as it once did) in 20%-25% of patients

MOA of a-2 adrenergic agonist

agonist at the ciliary body, causing ↓ in aqueous humor production

Agents found in a-2 adrenergic agonist class

• brimonidine (alphagan P) solution

Contraindications of brimonidine

Infants → apneic spells/hypotensive reaction if patient on Monoamine oxidase inhibitors (MAOI- type of antidepressant)

SE of a-2 adrenergic agonist

allergic-type reaction (lid edema, foreign-object sensation, itching) occurs in 8% of patients, often leads to discontinuation

MOA of carbonic anhydrase inhibitor (CAI)

↓ in aqueous humor production

Agents found in CAI class

Topical

• Brinzolamide (Azopt®) suspension

• Dorzolamide (Trusopt®) solution

Systemic (LAST LINE)

• Acetazolamide tablets, capsules, or injection

  Methazolamide tablets

SE of Brinzolamide

brinzolamide produces more blurry vision, but less stinging than dorzolamide

MOA of cholinergic agonist

↑ in aqueous humor outflow by stimulating ciliary muscle contraction

Agents in cholinergic agonist class

Pilocarpine (Isopto Carpine®, Pilocar®) sol’n

Pilocarpine (Pilopine HS ®) gel

Carbachol (Carboptic®, Isopto Carbachol®) sol’n

cholinergic agonist are _ used

rarely

MOA of Rho kinase inhibitor

↑ in aqueous humor outflow through the trabecular meshwork

Agent found in Rho kinase inhibitor class

netarsudil ophthalmic solution (Rhopressa)

Combination products to increase patient compliance in treating open-angle glaucoma

goals of therapy in tx of closed-angle glaucoma

◦ Rapid reduction in IOP

◦ Preserve visual function

◦ Avoid surgical or laser iridectomy (a hole in iris that permits aqueous humor flow to move directly from posterior to anterior chamber)

Tx for closed-angle glaucoma

Drug therapy: A miotic (e.g. pilocarpine), secretory inhibitor (e.g. β-blocker, α2- agonist, latanoprost, or CAI), or prostaglandin agonist.

Osmotic agents: Rapidly decrease IOP (oral glycerin or IV mannitol)

◦ Increases serum osmolarity, forcing fluid outflow from the humor to plasma

Topical corticosteroids can be used to reduce ocular inflammation

Describe the steps on how to use ear drops properly

Goals of therapy for otitis externa

decreasing the accompanying pain

eradicating the causative organisms

Tx for otitis externa

Pain relief can be achieved with orally administered acetaminophen or NSAIDs given alone or in combination with an opioid for mild to moderate pain

Begin with clearing any debris from canal

Topical antibiotics preferred (ear drops)

• Helps achieve high concentration at site of infection while reducing inflammation

• Duration typically 7-10 days

Systemic antibiotics should also be considered for patients with recurrent episodes of OE or clinical signs of necrotizing OE or have underlying immunocompromised conditions

What antibiotics are used to treat otitis externa and why?

fluoroquinolone antibiotics, ciprofloxacin and ofloxacin

• antipseudomonal activity

All drops are _ in pts with perforated ear drums

contraindicated

first line agent against otitis externa

fluoroquinolone drops

fluoroquinolone drops are not recommended in

children <6 months

second line agent against otitis externa

neomycin-polymyxin B drops (usually contain steroid)

• Avoid in viral or fungal

third line agent against otitis externa

antifungals (clotrimazole)

• Consider if ear canal obstruction cannot be relieved or if infection extends beyond the ear canal

_ mastoiditis typically goes away within a month after treatment and doesn’t come back.

acute

_ mastoiditis lasts a month or longer or comes back after antibiotic treatment.

chronic

Tx for mastoiditis

Treated with IV/oral/topical antibiotics +/- steroids

◦ May require multiple rounds

Chronic may involve surgery to remove infected portion of bone

Describe a type 1 allergic reaction

immediate hypersensitivity Anaphylaxis

Give examples of a type 1 allergic reaction

asthma and allergic rhinitis

Tx for a type 1 allergic reaction

0.01 mL/kg aqueous epinephrine 1:1,000 (1 mg/mL) subcutaneously or intramuscularly; dose may be repeated every 5-15 minutes or continuous IV infusion could be necessary

Injectable antihistamine may be administered additionally if hives and itching

Nebulized albuterol can be provided for airway obstruction

Fluids (NS, colloids) as necessary to maintain hemodynamic stability

Systemic corticosteroids may be provided to prevent late-phase reactions

Goal of therapy for environmental allergies/allergic rhinitis

to alleviate the symptoms with a little to no adverse effects from medications

_ are the most potent agents available for the relief of established seasonal or perennial rhinitis

intranasal corticosteroids

MOA of intranasal corticosteroids

interfere with the antigen-antibody reaction: reduces mast cell degranulation, diminished secretion of cytokines = decreased inflammation

Drug names of intranasal corticosteroids

SE of intranasal corticosteroids

Local side effects (irritation, bleeding) rare, no significant systemic absorption

You can combine intranasal corticosteroids with _ for 2-3 days if nasal blockage present

decongestant spray

Antihistamines work by _ the pt up

drying

MOA of 1st gen antihistamines

Non-selective competitive antagonist of histamine H1 receptor

Drug names of 1st gen antihistamines

Diphenhydramine (Benadryl®)

Chlorpheniramine (ChlorTrimeton®)

SE of 1st gen antihistamines

More anticholinergic (dryness, blurry vision, urinary retention, constipation) than 2nd gen.

Causes CNS effects (may increase fall risk)

Possible paradoxical stimulation in children

Contraindications of 1st gen antihistamines

Avoid in elderly, bladder obstruction, BPH, narrow-angle glaucoma

MOA of 2nd gen antihistamines

Selective, competitive antagonist of histamine H1 receptor

Drug names of 2nd gen antihistamines (piperazines, piperidines)

Cetirizine (Zyrtec®)

Levocetirizine (Xyzal®)

Loratadine (Claritin®)

Fexofenadine (Allegra®)

Desloratadine (Clarinex®)

SE of 2nd gen antihistamines

Fewer anticholinergic effects

Do not act centrally (larger protein, thus does not cross the blood brain barrier readily)

Don’t work as quickly as 1 st gen, last MUCH longer (a day)

Decongestants work by _ congestion

reducing

Direct α- and β- agonist decongestants work by

vasoconstriction + bronchiole relaxation, respectively

Drug names for direct α- and β- agonist decongestants

Pseudoephedrine (Sudafed®) IR or ER tablets

SE of direct α- and β- agonist decongestants

Causes CV (increased BP, HR) and CNS (restlessness, insomnia, anxiety) stimulation; headaches

Contraindications of direct α- and β- agonist decongestants

Avoid in pt’s with uncontrolled HTN, narrow angle glaucoma

Direct α- agonist decongestants work by

vasoconstriction