Pharmacology chapter 42(p-3)

Lecture Notes for 2nd year students

Digitalis Glycosides
inhibit the sodium potassium pump; causing increased intracellular sodium and increase influx of
calcium; result in muscle fibers contracting more efficiently.

Digitalis has three effects on heart muscle what are they>

1. Positive Inotropic action; increased myocardial contraction stroke volume. 2. Negative chronotropic
action; decreases heart rate. 3. Negative Dromotropic; decreases conduction of heart cells.

IV Inotropic agents for HF

IV inotropic agents (dopamine and dobutamine);

Cardiac glycosides can treat which dysrhythmias? How?

Afib and Aflutter; by using negative chronotropic effects (decreased heart rate) and negative
dromotropic effects (decrease conduction through AV node).

When digoxin does not convert Afib which medication/s are used?
CCBs (verapamil) with warfarin; this is to slow heart rate down and decreasing chance of
thromboemboli.

ANP lab range? Why is it excreted? What does it represent? What does it do?
20-77 pg/mL; excreted because of over expansion of atria; vasodilation and increases GFR causing
large amounts of urine to decrease blood volume and pressure; if high indicated HF

BNP lab range? What is the purpose of the lab when identifying HF? What age related consideration
should be considered?
<100 pg/mL; it helps identify if a person is experiencing dyspnea from lung conditions or HF; it is more
accurate than ANP for Dx of HF. It can be higher in women over 65 years old.

Protein binding for digoxin is? rate of absorption for digoxin?

30%; 70-90%.

Half life of digoxin? Where is it excreted?

30-40 years; 30% metabloized by liver and the rest is from kidneys unchanged.

Therapeutic serum level for digoxin? For HF what therapeutic level should be maintained and also
for dysrhythmias.
0.8-2.0 ng/mL; HF should have lower end of therapeutic level; dysrhythmias should have higher level
of therapeutic serum.

Major symptoms of digoxin toxicity

Bradycardia, PVCs, dysrhythmias, visual illusions

Three reasons why ventricular dysrhytmias are induced with digoxin toxicity
1; suppression of AV conduction. 2. increased automaticity. 3. decreased refractory period in
ventricular muscle

Which drugs are effective for treating digoxin toxicity? What is the antidote for Cardiac/Digitalis
Glycosidees
Licocaine (ST) and phenytoin; Digoxin immune Fab (ovine, Digibind; for severe toxicity)

Digitalis toxicity can cause ______ degree, _______ degree, or ________ heart block.
first; second; complete

Which medications have interactions with digitalis? How are these interactions avoided?
Cortisone/potassium wasting diuretics (due to causing hypokalemia); Antacids (which cause
decreased absorption)...Eat foods high in potassium or potassium supplements; stagger antacid
doses with digoxin.

Phosphodiesterase Inhibitors; what is the name of one of these meds; how does it work; how is it
administered and how long; what are important considerations?
Positive inotropics; milrinone lactate; increases stroke volume, caridac output, and vasodilation.
Works by inhibiting phsophodiesterase. It is administered IV no longer than 48-72 hours. Important
nursing considerations are close cardiac/ECG monitoring for dysrhythmias.

What are the three ways Arteriolar dilators work?

Reduce after load and increase cardiac output; dilate arterioles of kidneys for fluid loss; improve
circulation to skeletal muscles.

Nursing interventions digoxin

Check apical pulse for one minute and make sure it is above >60 bpm before admin; determine signs
for pulmonary and peripheral edema (HF); monitor serum digoxin (0.8-2) and serum potassium (3.5-
5).

Diet for Digoxin

high in potassium; fresh/dried fruits, fruit juices, vegetables (potatoes)

Herbal interactions with Digoxin (8)

Ginseng ↑ false digoxin levels; St. Johns Wart ↓ absorption of digoxin; Psyllium ↓ digoxin
absorption; Hawthrom ↑ effect of digoxin; Licorice ↑ potasssium loss; Aloe ↑ potassium loss; Ma-
huang or ephedra ↑ toxicity; Goldenseal ↓ effects of digoxin and antidysrhythmics

ACE inhibitors for HF; how do they work; what major drug interactions and side effects can cause
problems
Usually prescribed; dilate venules and arterioles, moderately reduce aldosterone (↓ sodium and fluid
retention); Can increase serum potassium levels especially with potassium sparing diuretics.

Angiotensin II receptor blockeres (ARBs); name main drugs; why are they used
valsartan (Diovan) and candesartan (Atacand); approved for HF; used when ACE inhibitors are
contraindicated.
Potassium sparing diuretic; name of drug;how does it work; recommended dose; nursing
considerations; what does it treat
spironolactone (Aldactone); blocks the production of aldosterone (↑ sodium/water excretion and ↓
potassium excretion). Decreases myocardial fibrosis; RDA 12.5-25 mg/day; hyperkalemia occurs with
>50 mg/day, but levels should still be monitored.

Beta Blockers HF
Should be started very low doses and gradually increased; improve cardiac performance; one to three
months for therapeutic effect to develop.

Nesirtide (Natrecor)
Natriuretic peptide hormone; inhibits ADH and increases sodium loss. Causes vasodilation, natiuresis,
and diuresis. Usesful for acute decompensated HF with dyspnea.

BiDil
Combo of hydralazing (BP) and isosorbide dinitrate (dilator for heart pain); uses specifically for African
Americans.

Nonpharmacologic ways to avoid angina attacks

avoid heavy meals, smoking, extreme weather changes, stenuous exercise, emotional upset

Antianginal Drugs for Variant angina

Use CCBs and/or nitrates; BBs can affravate.

Antianginal Drugs for Unstable Angina

Medical emergency; nitrates given sublingually or IV; if the pain is not relieve then give BBs IV; if
patient cannot tolerate give CCBs.

How do Calcium channel blockers work to help angina

Dilate arterioles to decrease afterload and O2 demand. Only Verapamil and diltiazem decrease HR
and contractility

How do Beta Blockers work to help angina

Decrease HR and contractility

Sublingual Nitroglycerin
Absorbed into the internal jugular vein; 40-50% of nitrates inactivated by liver if administered via GI.

Nitroglycerin Pharmacodynamics
Acts directly on smooth muscle; decreases preload (amount of blood in ventricle at the end of
diastole); and decreases afterload (peripheral vascular resistance); and reduces myocardial O2
demand.

Onset of action of Nitro; Sublingual; transdermal.

SL (1-3) minutes; transdermal (30-60 minutes)
Duration of action of nitro ointment?
6-8 hours.

What happens with abrupt withdrawal of nitro? What happens with rapid admin of nitro?
Myocardial ischemia; reflex tachycardia (HR increases because of overcompensation of cardiovascular
system)

Drug interactions of Nitro

BBs, CCBs, Vasodilators, and Alcohol enhance nitro effect; IV nitro antagonize effects of heparin

BBs are best for what kind of angina

Stable

Abrupt discontinuation of BBs

reflex tachycardia and angina

Conditions that are contraindication to use BBs

Decreased HR or BP, and second or third degree AV block

Nonselective BBs; name some medications; what do they do

pindolol, nadolol, propanolol; decrease HR and cause bronchoconstriction act strongly on beta 1.

Selective BBs; name some meds; what angina do they control best
metoprolol, atenolol; best for controlling angina pectoris

Half life of propanolol? Half life of atenolol? Half life of Metprolol?

3-6 h; 6-7h; 3-7

Propanol and metprolol are excreted where? Where is atenolol excreted from? IV BBs are excreted
where?
Metabolized and excreted by liver; 50% excreted unchanged in feces; 85% excreted in urine within 24
hours.

Onset,Peak and duration of non selective BBs? Of cardioselective? Of selective metoprolol

NS; 30 min, 1-1.5 h, 4-12 h; CS; 60 m, 2-4 h, 24 h. SM; 15 m, duration 6-12 h

Side effects/adverse reactions of BBs? Any nursing considerations

Nonselective can cause bronchospasm, psychotic response, taper off for 1 to 2 weeks and monitor
vitals closely.

CCVs used for long term treatment of angina

verapamil, nifedipine, diltiazema
Absorption of CCBs and bioavailability if they are metabolized
80-90% absorbed through GI; first pass decreases the availability to; 20% (Verapamil), 45-65%
(diltiazem), 35-40% (nifedipine).

Are CCBs protein bound? What is the half life of main LT drugs
Highly protein bound; 2-9 hours.

The most potent CCB is and which CCB causes bradycardia as the most common problem
Nifedipine; Verapamil

Onset of action and duration of; verapamil, nifedipine, and diltiazem.

verapamil; 10 m, 3-7h. nifedipine and diltiazem; 30 m, 6-8 h

Nursing considerations CCBs

Assess for peripheral edema, assess serum liver enzymes.

Drug alert Nifedipine (immediate release capsules)

SCD; only used in hospital

Nitroglycerin not used for marked __________ or ____________ __________- ___________

hypotension; acute myocardial infarction

Nursing interventions nitro

give sips of water before SL (dry mouth can ↓ absorption), place patient in supine position with legs
elevated if hypotension from SL results.

Constipation facts
-it's a symptom, not a disease
-can be caused by a variety of diseases or drugs
-it's about consistency not quantity

Constipation causes
-ignore urge
-low residue diet
-decreased activity
-stress
-excessive laxative use
-decreased fluids

Ideal laxative function

-non irritant
-non toxic
-rapid action with normal stool
-one stool with no residue
-work in lower GI tract - descending colon
-not interfere with nutrient absorption
Laxative therapy
-bowel prep
-cardiovascular disease (decrease strain)
-parasites
-poisoning
-constipation
-any condition where straining is to be avoided

Actions of Drugs Used to Affect Motor Activity of the GI Tract

-speed up or improve movement
-increase the tone of the GI tract
-decrease movement along the GI tract

three ways laxatives work

-chemical stimulation
-bulk or increased fluid in the lumen
-lubrication of the intestinal bolus

Laxatives indications
-short term relief of constipation
-diagnostic procedures

Types of laxatives
Stimulants
Bulk forming
saline cathartics (Osmotic)
lubricants

Stimulant laxatives
-chemical irritation
-selective action on wall of intestine
-effects whole tract
-decreases absorption of digoxin, nitofuration, salicylates, tetracycline, oral anticoagulants
-laxative dependence
-often produce a watery, diarrheal stool

Most common stimulant laxative

bisacodyl (Dulcolax) (OTC)

Bulk laxatives MOA

bulk forming; absorbs water, distends bowel to initiate reflex bowel activity

Bulk forming laxatives

-safest laxative
-large volume of fluids needed, ALWAYS
-decreases absorption of digoxin, nitofuration, salicylates, tetracycline
-more likely to produce "normal" stool
Saline (osmotic) laxatives
-draw water through cell walls
-systemic effect
-used for rapid bowel evacuation
-toxicity, renal insufficiency CV disease, dehydration

GoLYTELY
-used for bowel preps
-moves large amount of H2O into colon
-complete cleanse in 4 hours
-GI procedures

Lactulose
-water drawn into colon
-ammonia from blood passes to colon

Lubricants
lubricate the fecal material and intestinal walls

Example of lubricant
mineral oil

Stool softeners
-promote more water and fat in the stools
-non irritant
-do not stimulate peristalsis
-non dependent

common stool softener

colace (Surfak)

Side effects of laxatives

all laxatives can cause electrolyte imbalances

Laxatives: Nursing Implications

-fluid intake should be encouraged
-long term use of laxatives often results in decreased bowel tone and may lead to dependency
-all laxative tablets should be swallowed whole with 8oz of water

Enemas
-may cause laxative/enema dependence

Suppositories
usually contain stimulant drugs
-common suppository is bisacodyl
Role of the nurse: laxative therapy for bowel evacuation
-peristalsis must be restored prior to laxative therapy
-assess for colon cancer, esophageal obstruction, intestinal obstruction, fecal impaction, undiagnosed
abdominal pain
-if diarrhea occurs, discontinue laxative use
-take with 1-2 glasses of water
-educate patients about proper use

Gastrointestinal stimulant
metoclopramide (Reglan) (leads to increased GI activity and rapid movement of food through the
upper GI tract PO, IV, IM) (prokinetic agent)

contraindications of GI stimulants
increased GI activity can cause GI obstruction

Diarrhea
-it's a symptom
-abnormal passage of frequent watery stools
-untreated diarrhea may cause malnutrition, fluid and electrolyte imbalance and exhaustion

Acute Diarrhea
-sudden onset
-lasts from 3 days to 2 weeks

Chronic Diarrhea
lasts for more than 3 weeks

Pharmacotherapy for severe diarrhea

opioids

Medications for mild diarrhea

loperamide (Imodium)
Probiotic supplements (lactobacillus)

Antidiarrheal therapy
-assess fluid and electrolyte status
-assess patient's ability to get out of bed safely

Actions and indications of antidiarrheal therapy

slow the motility of the GI tract
relief of symptoms

Antidiarrheals; opioids prototype drug

Lomotil
Adverse effects of Lomotil
dizziness and drowsiness

antidiarrheal drug
loperamide (Imodium)

Antidiarrheals MOA
Adsorbents: coat the walls of the GI tract
Anticholinergics: decrease intestinal muscle tone and peristalsis of GI tract
Intestinal flora modifiers (NIB): restores normal GI flora

Adsorbents
may prevent absorption of medications and nutrients

Antidiarrheal anticholinergic drugs

-reduce intestinal motility
-can have dangerous side effects

Antidiarrheals: opiates: MOA

-decrease bowel motility and relieve rectal spasms
-decrease transit time through the bowel, allowing more time for water and electrolytes to be
absorbed
-examples: paregoric, opium tincture, codeine, loperamide, diphenoxylate

Antidiarrheal agents; nursing implications

Do not give bismuth subsalicylate to children younger than age 16 or teenagers with chickenpox
because of risk of Reye's syndrome

Nausea and vomiting

most common and most uncomfortable complaints
vomiting is complex and is a defense mechanism

Nausea
unpleasant feeling that often precedes vomiting. Often accompanied with weakness, diaphoresis and
increased saliva

Emesis (vomiting)
forcible emptying of gastric, and occasionally, intestinal contents
-associated with many conditions

Antiemetic agents
used to relieve nausea and vomiting
centrally acting or locally acting
varying degrees of effectiveness

Emetics
Cause vomiting
No longer recommended for at-home poison control

VC
vomiting center

CTZ
Chemoreceptor trigger zone
-not protected

Treatment of N/V (antiemetics)

moderate to severe nausea treated

5-HT3 receptor blockers (serotonin blockers)

Ondansetron (Zofran)
-given prophylactically

What are 5-HT3 blockers (Serotonin blockers) primarily used for

N/V for patients receiving chemo, radiation and postoperative nausea and vomiting.

Anticholinergics/Antihistamines
diphenhydramine, scopolamine

anticholinergics/antihistamines recommended uses

for n/v associated with motion sickness or inner ear problems.
Take before travel

Antimetics, phenothiazines and phenothiazide-like drugs prototype drug

prochloperazine (Compazine)

Phenothiazines
prochlorperazine (Compazine)
promethazine (Phenergan)
-also used for intractable hiccups

Phenothiazines recommended uses

treatment of N/V, esp assoc with anesthesia and severe vomiting

Nonphenothiazine
metoclopramide (Reglan)
-stimulates peristalsis in the GI tract
-also used for GERD, delayed gastric emptying

scopolamine (Transderm-Scop)
used to treat motion sickness; prophylaxis
-patch

Substance P/Neurokinin 1 receptor antagonists

newest class of drugs for N/V
-approved for highly emetogenic antineoplastic chemotherapy

Emetics (inducing vomiting)

should only be used in emergency situations only when directed

Nursing implications
-assess complete nausea and vomiting history, including precipitating factors
-assess current medications
-assess for contraindications and potential drug interactions
**most are more effective when given prophylactically

Role of the nurse: antiemetic therapy

-patient safety is a concern because of drowsiness
-assess risk for falls
-prevent aspiration

Antiemetics education
-many agents cause severe drowsiness; warn patients about driving or performing any hazardous
tasks
-Taking with alcohol may cause severe CNS depression
-Teach patients to change position slowly to avoid hypotensive effects
-many agents should be administered 30 minutes prior to meals or treatments (for chemo, often
given 30 minutes to 3 hours prior to chemo treatment)
-incorporate nonpharmacological measures also

Cornea
The clear tissue that covers the front of the eye

Watch for scratches

Pupil Dilation
Sympathethic motor nerve fiber

Caused by dim lights

Mydriatic Agents

Pupil Constriction
Parasympathetic motor nerve fibers

Caused by bright lights

Miotic agents

Glaucoma
Abnormal elevation of intraocular pressure (IOP) caused by:
1. Excessive production of aqueous humor
OR
2. Diminished ocular fluid outflow

Increased pressure → compresses retina & optic nerve → BLINDNESS

Eye Exam Recommendations

Ages 40 to 64: every 2 to 4 years

After age 65: every 1 to 2 years

For African-Americans: increased frequency

Tonometry
Procedure eye care professionals perform to determine the intraocular pressure (IOP), the fluid
pressure inside the eye.

Norms: 10-23 mm Hg

(average ~ 16 mm Hg)

3 Types of Glaucoma
1. Primary
-Open angle
-Closed angle

2. Secondary
-eye surgery
-disease

3. Congenital

Open Angle Glaucoma

Drains are blocked, gradual, build up of pressure.

Most common type (90%)

Usually bilateral

S/S:
Decreased peripheral vision
Frontal headache
Eye pain, brow pain
Tunnel vision with white halos

3Ps of Blindness due to Open Angle Glaucoma

Preventable
Painless
Permanent
Closed Angle Glaucoma
This condition involves sudden blockage of the outflow of aqueous humor (sudden increase in IOP)

10% of cases

S/S: Severe eye pain (bulging iris)

Severe headache

Nausea & vomiting

Tunnel vision with white halos

EMERGENCY

Treatment for Glaucoma

Goal: ↓ IOP & prevent blindness

Surgical: lasers; trabeculoplasty; shunts

Medical: Medications
-Miotics
-Meds that inhibit production of aqueous humor

Drug Class: Carbonic Anhydrase Inhibitors

Action: inhibition of carbonic anhydrase results in decreased production of aqueous humor & ↓IOP

Examples:
acetozolamide (Diamox) po
dorzolamide (Tusopt) ophthalmic sol'n.

Use: Closed and open angle glaucoma

Side Effects: gastric irritation, electrolyte imbalance (↓Na, K, Cl)

Nursing Implications:
√ electrolytes
√ allergy to SULFA
Contraindicated in pregnancy

Drug Class: Cholinergic Agents

Example: pilocarpine (Isopto-Carpine, Pilopine HS)

Action: cholinergic → miosis (ciliary body contraction) → IOP↓

Side effects:
↓ Visual acuity @ night
Blurred vision 1-2 hr. after admin.
Headache/conjunctival irritation

Serious Side Effects- may be signs of excessive administration→toxicity:

Bradycardia/Hypotension
Diaphoresis/Salivation/Abdominal discomfort
Nursing Implications:
√ heart rate
Block inner canthus 3-5 minutes
Safety (blurred vision)

Note: These drugs must be administered 4 x day. Use is ↓ due to side effects and preference for
drugs that need either daily or bid administration.

Drug Class: Alpha Adrenergic Agents

Example: phenylephrine (Prefrin, Mydfrin)

Action: mydriasis; ↑ outflow of aqueous humor, ↓ production of aqueous humor

Use: mydriasis for ophthalmic diagnostic procedures

↓IOP in open angle
lowers redness from irritation

Side effects:
Systemic: ↑ HR, ↑ BP
Sensitivity to light
Conjunctival irritation/lacrimation

Nursing Implications:
√ HR, BP
Block inner canthus
Sunglasses
Use with caution in patients with bronchial asthma

Drug Class: Beta-Adrenergic Blocking Agents

Examples: betaxolol (Betoptic); timolol (Timoptic)

Use: first line drugs for open-angle glaucoma

↓IOP

Action: unknown (? ↓ production aqueous humor)

Side effects:
Systemic: BP↓ HR↓

Nursing Implications:
√ BP, HR @ specific intervals
Block inner canthus 3-5 minutes
√ interactions (other BB)

Drug Class: Prostaglandin Agonists

Examples: latanoprost (Xalatan); travoprost (Travatan); bimatoprost (Lumigan)

Action: ↑ outflow of aqueous humor→ ↓ IOP

Dosage: usually once daily; don't exceed dosage

Side effects:
Mild irritation, stinging
Eye pigment changes (Blue>Brown)
Eyelash growth

Nursing Implications: Teaching

Side effects
Do not admin. with contacts
Avoid products with Thimerosol

Drug Class: Anticholinergic Agents

Example: Mydriacyl

Use: mydriasis & cycloplegia (extreme dilation for eye exams)

Contraindication: closed angle glaucoma

Side effects: light sensitivity; ↑ IOP

Drug Class: Antifungals

Example: natamycin (Natacyn)

Use: yeasts such as Candida, Aspergillus

Side effects: photosensisitivity; blurred vision

Teach: symptoms should improve in a few days; notify physician if worsening or no improvement

Drug Class: Antivirals

Example: trifluridine

Use: herpes keratitis

Side effects: light sensitivity, blurring, stinging, tearing

Teaching: notify physician if no improve-ment in 7 -14 days

Drug Class: Ophthalmic Antibiotics

Example: erythromycin

Uses:
bacterial infections
prophylaxis for gonorrhea & chlamydia blindness in newborns

Teach: prolonged use can cause hypersensitivity & resistant organisms

Drug Class: Corticosteroids

Examples:
dexamethasone
(Dexasol)- ointment; (Maxidex)-suspension

Uses: Allergic reactions of the eye/ acute, non-infectious inflammatory conditions.

Prolonged ocular steroid therapy may cause glaucoma and cataracts

Drug Class: Ophthalmic Anti-Inflammatory Agents
Example: Flurbiprofen sodium, Diclofenac sodium, nepafenac and bromfenac

Action: anti-inflammatory, antipyretic, and analgesic by inhibiting biosynthesis of prostaglandins

which ↑intraocular inflammation & pressure. Also inhibit miosis .

Uses:
Flurbiprofen (Ocufen) - inhibits miosis during Cataract surgery
Diclofenac sodium(Voltaren), nepafenac (Nevanac) and bromfenac (Xibrom)- treat postoperative
inflammation after cataract extraction
Ketorolac tromethamine (Acular) - relieves ocular itching with seasonal allergic conjunctivitis

Drug Class: Antihistamines

Example: Patanol (olopatadine)

Uses:
Relief of Sx associated with allergies

Administration:
For best results, administer before exposure to allergens

Drug Class: Antiallergic

Action: Inhibit release of histamine

Examples: Bepreve, Crolom, Alomide, Alamast

Use: Treat allergic ocular disorders

(ie.vernal keratoconjuctivitis)

Drug Class: Diagnostic Agent Sodium Fluorescein

Used for:
Identifying foreign bodies, abraded, & ulcerated areas
Fitting contact lenses

Topical - 2% topical solution (strips)

10% & 25% for injection into aqueous humor

*An abraded cornea

is highly susceptible to infection*

Drug Class: Artificial Tear Solutions

Example: Tears Naturale, Murine

Used for:
Dry eyes
Artificial eyes
Decreased protective reflexes

Caution: sensitivity to preservatives

Drug Class: Ophthalmic Irrigants

Example: Eye-Stream, Blinx, Optigene

Uses:
Cleansing the eye
Foreign bodies
Chemical exposure

Eye wash station

Macular Degeneration
Deterioration of the macula- small area in retina. Age-related macular degeneration. (AMD)

Symptoms: blurriness, dark areas, distortion. Peripheral vision NOT affected.

"Dry" (atrophic) AMD

Caused by aging and thinning of the macular tissues.

Vision loss is gradual

Most common form of AMD

"Wet" (exudative) AMD

Abnormal blood vessels form underneath the retina at back of the eye. Leak fluid or blood and blur
central vision.

Vision loss may be rapid and severe

Drug Class: Vascular Endothelial Growth Factor Antagonist

Examples: pegaptanib (Macugen) (q 6 weeks)
and ranibizumab (Lucentis) (q month)

Action: antagonists that bind to VEGF to prevent it from forming new blood vessels which contribute
to wet form of AMD

*Watch for redness, light sensitivity, pain, ↓vision.

Report immediately to ophthalmologist*

Ophthalmic Med Administration

Should be labeled "For Ophthalmic Use"

Gloves & sterile technique

Cleanse eyelashes & eyelids (with separate gauze)- inner canthus outward

Drops should be @ room temperature

Positioning

For Systemic medications:

Pre-medication assessment
Hold pressure @ inner canthus 3-5 minutes
If >1 eye med is ordered, wait at least 5 minutes between meds.

DROPS > OINTMENT

Don't remove impaled objects

Post-operative restrictions
Prevent Increase in IOP

Head position

No: bending,
coughing, Valsalva maneuver

The nurse is teaching a patient with open-angle glaucoma about the disease and its treatment. Which
statement by the patient best indicates that teaching has been successful?
A. "I need to use my eye drops regularly if I want to regain my vision."
B. "I will use a separate bottle of eye drops for each eye so I can't spread the infection."
C. "I will refill my eye drop prescription a few days ahead of time so I am certain not to run out."
D. "I won't touch my eyes because it increases the pressure in them."
C. "I will refill my eye drop prescription a few days ahead of time so I am certain not to run out."

What is the best measure of drug effectiveness in the treatment of open-angle glaucoma?

A. Intraocular pressure
B. Visual acuity
C. Speed of convergence
D. Change in peripheral vision
A. Intraocular pressure

Which ophthalmic medication does the nurse expect to administer when preparing a patient for
cataract surgery?

A. Ketorolac tromethamine (Acular)

B. Timolol maleate (Timoptic)
C. Diclofenac sodium (Voltaren)
D. Flurbiprofen sodium (Ocufen)
D. Flurbiprofen sodium (Ocufen)

A patient admitted to the eye clinic has been diagnosed with "wet" macular degeneration (exudative)
in the right eye. Which medication does the nurse anticipate the ophthalmologist will order for this
patient?

A. Latanoprost (Xalatan)
B. Metipranolol (OptiPranolol)
C. Ranibizumab (Lucentis)
D. Tropicamide (Mydriacyl)
C. Ranibizumab (Lucentis)
A patient is taking bimatoprost (Lumigan) and timolol maleate (Timoptic) eye drops. How does the
nurse instruct the patient to administer the drops?

A. At the same time

B. At least 1 minute apart
C. At least 5 minutes apart
D. At least 30 minutes apart
C. At least 5 minutes apart