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NU 560 - Adv. Pharmacotherapeutics > Unit 1 Exam > Flashcards

Unit 1 Exam Flashcards

1
Q

Phases of Clinical Trials

A

Pre-Clinical Trials
Phase I-IV

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2
Q

Pre-Clinical Trials

A

Animal testing

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3
Q

Phase I

A

20-100 healthy individuals

Focuses on pharmacodynamics

Most effective administration routes and dosage ranges are determined.

Occurs inpatient (overnight/weekend).

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4
Q

Phase II

A

Up to several hundred people with the disease the drug is intended to treat.

Same testing focus as phase I.

Performed outpatient. Serum levels, tolerance, side effects, and effectiveness are monitored.

Approval of the application means the drug can be marketed, but only by the company seeking the approval.

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5
Q

Phase III

A

1000 of patents

It begins once FDA determines that the drug causes no apparent side effects and that the dosing range is appropriate.

Double-blind research methods.

Most risk is discovered in this phase.

Either approved or rejected by FDA after this phase.

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6
Q

Phase IV

A

Post-marketing studies/surveillance.

Objectives:
1. Compare drugs to other drugs on the market.
2. Monitor long-term effectiveness and impact on QOL.
3. Analyze cost effectiveness.

Drugs can be taken off the market due to additional findings about the drugs and their side effects.

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7
Q

What is the Controlled Substances Act of 1970?

A

From the FDA

A way to categorize risk for addition and abuse.

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8
Q

What is the Controlled Substances Act of 1970?

A

From the FDA

A way to categorize risk for addition and abuse.

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9
Q

Drug Schedule

A

I, II, III, IV, V

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10
Q

Example of Schedule I Drugs

A

Heroin, cocaine

Highest abuse / addictive potential

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11
Q

Example of Schedule II Drugs

A

Morphine, dilaudid, methadone

Short interval of use

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12
Q

Example of Schedule III Drugs

A

Percocet

Low abuse potential / high addictive potential

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13
Q

Example of Schedule IV Drugs

A

Benzos

Low abuse / some addiction

Those who “NEED” it are likely to abuse it

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14
Q

Example of Schedule V Drugs

A

Robotussin w/ codeine, adderall

Least abuse / lowest addition

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15
Q

How to monitor adherence to therapy?

A

Lab testing
Pill count
Patient diary (BP or BG journal)

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16
Q

Therapeutic Window

A

Range of drug concentration in the blood between a minimally effective level and toxic level.

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17
Q

Pharmacogenomics

A

Personalized medicine
How genetic variations impact response to therapy
Single nucleotide polymorphism
Enables targeted therapy/focus resources
Expedites clinical improvements
Targeted risk reduction strategies
Area of tremendous amount of research.

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18
Q

Pharmacotherapeutics

A

Utilization of drugs to diagnose, prevent, or treat disease or illness.

Includes pharmacokinetics and pharmacodynamics.

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19
Q

Pharmacokinetics

A

What the body does to the drug.

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20
Q

Pharmacodynamics

A

What the drug does to the body.

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21
Q

Pharmacokinetics includes what 4 phases?

A

Absorption
Distribution
Metabolism
Excretion

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22
Q

Gender and Pharmacokinetics

A

Women have a higher % body fat which can alter the pharmacokinetics of different drugs.

Most drugs are tested more on men than women so need to consider hormonal changes and different patterns of fat.

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23
Q

Absorption

A

How administered drugs are absorbed into the body.

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24
Q

What affects absorption?

A

Bioavailability and route of administration

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25
Q

Bioavailability

A

The rate and extent drugs are absorbed from substances and are available at the site of action.

The fraction or % of an administered dose of a drug that reaches the circulation in its unmetabolized form.

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26
Q

What affects bioavailability?

A

First pass effect
Prodrugs
Drug formulation (Ex. ER vs. IR)
GI motility
Blood flow

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27
Q

First Pass Affect

A

Metabolism that occurs in the liver before passing into circulation.

PO drugs are subject to first pass effect.

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28
Q

Pro-Drugs

A

Drugs w/ no biological activity itself

Once metabolised in the liver, it becomes an active metabolite.

Precursor to active drug.

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29
Q

Drug Formulation

A

IR - Delivered to GI tract quickly for quick onset of action.

ER - Extends activity of drugs in the body to level out the high peaks to low troughs of concentrations.

EC - Slow drug to be dissolved in the intestines rather than the stomach.

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30
Q

GI Motility

A

Gastric emptying - Increases absorption and bioavailability.

Decreased intestinal motility - Greater absorption and bioavailability.

Increased intestinal motility - Less absorption and bioavailability.

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31
Q

Blood Flow

A

Based on adequate perfusion

Gut and intestinal perfusion is important for absorption.

Shock states affect blood flow and delivery of drugs.

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32
Q

Route of Administration

A

Enteral vs. Parenteral (all routes not involving GI)

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33
Q

Distribution

A

How drugs are distributed to the site of action

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34
Q

What affects distribution?

A

Blood flow

Lipid or water solubility

Protein binding

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35
Q

Passive Diffusion

A

High-concentration to low-concentration

No energy needed

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36
Q

Facilitated Diffusion

A

High-concentration to low-concentration

Via carrier proteins

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37
Q

Active Transport

A

Low-concentration to high-concentration

Utilizes ATP

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38
Q

Protein Binding

A

After absorption, drugs circulate through the body as unbound (free drug) or bound to proteins (commonly albumin).

Drug unbound (free drug) = Biologically active.

Low albumin states can result in toxicity.

ATBs have higher affinity to albumin than warfarin -> free warfarin -> increased INR.

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39
Q

Metabolism

A

Biotransformation of the drug from active form to inactive form.

Preparation for elimination.

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40
Q

What organ is primarily responsible for metabolism?

A

Liver

Also kidneys and intestines

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41
Q

Two Phases of Metabolism

A

Phase 1 - Enzymatic process that involves oxidation or reduction (hydrolysis).

Phase 2 - Adding a conjugate to the parent drug or metabolized drug to further increase water solubility and enhance excretion.

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42
Q

Cytochrome P-450 System (CYP450)

A

Composed of superfamilies of more than 100 enzymes.

3 families (15 enzymes) are responsible for drug metabolism in about 90% of cases.

Drugs may be substrate, inducer, or inhibitors of the CYP450 system.

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43
Q

Inducer

A

Stimulates production of enzymes which increase the amount of enzymes available for metabolism.

Ex. Phenytoin, Rifampin, St. John’s Wort

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44
Q

Inhibitors

A

Inhibits the production of CYP enzymes, decreasing the metabolism of drugs and increasing circulating levels.

Ex. Grapefruit juice, Azoles, Protease inhibitors.

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45
Q

Excretion

A

Removal of inactive drug from the body.

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46
Q

Primary organ of excretion

A

Kidneys

Important to know GFR to help dose drugs.

Other areas include lungs, skin, and GI tract.

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47
Q

Half-Life (t 1/2)

A

Time required for 50% of a drug to be eliminated from the body.

Ex. If t 1/2 is 10 hrs, then each 10 hrs, 50% of what is remaining will be eliminated.

Drug is considered fully eliminated after 4-5 half-lives.

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48
Q

Factors Interfering w/ Elimination

A

Renal failure → Increased t1/2 → dose less

Hepatic failure → Impacts prodrugs + CYP450 enzymes → increases t1/2

Exercise (regular vs. intermittent) → Impacts blood flow, GI motility, and body temp.

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49
Q

Factors affecting pharmacodynamics

A

Receptor abundance

Receptor affinity

Post-receptor changes and sensitivities

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50
Q

Types of receptors

A

Agonists

Antagonists

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51
Q

Agonist

A

Creates a response

Dose dependent

Depended on receptor sensitivity

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52
Q

Antagonist

A

Creates no biological response

Blocks receptors from agonists

Compete for receptor sites

Noncompentative sites.

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53
Q

Autonomic Nervous System receptors

A

Alpha-1, alpha-2, beta-1, beta-2

Flight or fight

Neurotransmitter is NE

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54
Q

Parasympathetic Nervous System Receptors

A

Cholinergic and muscarinic receptors

Neurotransmitter is ACH (acetylcholine)

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55
Q

How is pharmacotherapy different in the pediatric population?

A

Each property of pharmacokinetics is different.

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56
Q

Factors affecting drug delivery in pregnant women

A

Increased blood volume (30-50%), increased body water (~8lbs), and increased circulation -> Dilutional effect

Decreased serum albumin -> Increased free drug.

Increased progesterone + decreased Gi motility -> Increased absorption + bioavailability.

Maternal fat distribution + GI pH increased.

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57
Q

Factors promoting placental transfer

A

Lipid solubility.

Smaller, lighter molecules.

Unbound or “free drug”.

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58
Q

Factors Inhibiting placental transfer

A

Highly ionized molecules (requires active transport).

Larger, heavier molecules.

Drugs with high protein binding.

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59
Q

Beers Criteria

A

Guidelines for inappropriate medication use in older adults.

American Geriatric Society

Medicare Part-D may not pay for some of these meds.

Commonly prescribed meds are on that list.

Ex. Alpha-blockers prescribed for BPH.

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60
Q

Active Immunization

A

Administration of all or part of a microorganism or modified product of that microorganism.

Live or attenuated.

Evokes a natural immune response that mimics the body’s response to natural infection.

Ex. PNA vaccine/MMR

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61
Q

Passive Immunization

A

For people who have been exposed or have the potential to be exposed to specific infectious agents.

Administration of a preformed antibody when the recipient has a congenitally acquired defect or is immunodeficient.

Ex. Rabies

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62
Q

Vaccination Rates Across Lifespan

A

3 y/o = 90% - Infants/peds consistently visit their PCP.

18-64 y/o = 33-70%

Most vaccine series end around 11/12 y/o

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63
Q

Pediatric PNA Vaccine

A

Under 2 years, receive 4 doses of PCV-13

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64
Q

Elderly PNA Vaccine

A

> 65 years receive 1 dose of PPSV-23, even if unknown.

65
Q

Immunocompromised PNA Vaccine

A

Under or over 65 years may receive bost PPSV-23 + PCV-13 at different times.

66
Q

Influenza Vaccine Ages

A

Ages 6 months and up.

Not recommended for ages 6 months or less.

67
Q

Inactivated Influenza Vaccine (IIV)

A

Given IM

Healthcare workers + immunocompromised

68
Q

Live Attenuated Influenza Vaccine (LAIV)

A

Nasal spray

Recommended for ages 2-49 years.

Contraindicated in immunocompromised, household members of immunocompromised, and healthcare workers.

69
Q

Tobacco Use Disorder Key Features

A

Continued use despite wanting to quit.

Prior attempts to quit.

Persistent use despite physical illness.

Tolerance.

Presence of withdrawal symptoms.

70
Q

APA Criteria for Tobacco Use Disorder (2 or more in 12 month period)

A
  1. Tobacco is taken in larger amounts over a longer period of time than was intended.
  2. There exists a persistent desire to cut down or control tobacco use, or unsuccessful efforts are made to cut down or control tobacco use.
  3. A significant amount of time is spent in activities necessary to obtain or use tobacco.
  4. Craving, or a strong desire or urge to use tobacco, exists.
  5. Recurrent tobacco use results in a failure to fulfill important obligations or responsibilities at work, school, or home.
  6. Tobacco use continues despite its contribution to persistent or recurrent social or interpersonal problems (e.g., tobacco use causes or contributes to arguments with others).
  7. Tobacco use results in the individual giving up important social, occupational, or recreational activities.
  8. Tobacco use recurs in situations that are physically hazardous (e.g., smoking in bed).
  9. Persistent tobacco use despite knowledge of having chronic tobacco-related physical or psychosocial problems
  10. Tolerance to tobacco exists, with tolerance being defined as either one of the following: (1) the need for a markedly increased amount of tobacco to produce the intended effect or (2) a markedly diminished effect with the continued use of the same amount of tobacco.
  11. Withdrawal occurs. Withdrawal is manifested by either one of the following: (1) presence of characteristic co-relate withdrawal symptoms; (2) tobacco, or other nicotine containing products, is taken to relieve or avoid withdrawal symptoms.
    Irritability, anxiety, difficulty concentrating, restless, depression, increased appetite, insomnia.
71
Q

Fagerstrom Tolerance Test (Point System)

A

Time to first cigarette (TTFC)

Number of cigarettes per day.

Total score should range 0-10
-Score 6-7 suggest high level of physical dependence to nicotine.
-Score of 8-10 suggests a very high level of physical dependence to nicotine.

72
Q

Nicotine Replacement Therapy

A

Transdermal patch
Gum
Lozenge
Nasal spray (req. rx)
Inhaler (req. rx)

No concurrent smoking

73
Q

Buproprion SR (Zyban) MOA

A

MOA → Unknown

Takes 1 week to take effect → Smoke 1st week of therapy.

74
Q

Buproprion SR (Zyban) Caution + SE

A

Avoid other antidepressants → OD could cause delirium

May cause insomnia and dry mouth

75
Q

Varenicline (Chantix) MOA

A

Binds to the subunit of the nicotinic acetylcholine receptor.

Activates “reward system” without nicotine.

76
Q

Varenicline (Chantix) Side Effects

A

Mood changes
Anxiety
Suicidal ideation
Vivid dreams

77
Q

Normal BMI

A

18.5-24.9 kg/m2

78
Q

Obese BMI

A

> 30 kg/m2

79
Q

Severely Obese BMI

A

> 40 kg/m2

80
Q

Adjunctive weight loss therapy with pharmacotherapy is recommended for…

A

> 30 kg/m2

> 27 kg/m2 w/ comorbidity (DM2, HTN, HLD)

81
Q

Weight Loss Drug Therapy

A

Appetite suppressants

Lipase inhibitors

Glucagon-like peptide-1 receptor agonists

82
Q

Appetite Suppressants

A

Benzphetamine

Diethylpropion ER

83
Q

Appetite Suppressants MOA

A

Decreases appetite by stimulating the hypothalamus to release norepinephrine.

84
Q

Appetite Suppressants Caution / SE

A

Schedule III or IV → Potential for abuse

SE: Increased BP and HR

Avoid in patients taking MAOIs → can lead to hypertensive crisis

85
Q

Lipase Inhibitors

A

Orlistat (Xenical, Alli, Zenicol)

86
Q

Lipase Inhibitors MOA

A

Acts locally in the GI tract.

GI pancreatic lipase inhibitor that lowers the absorption of dietary fat.

Spread fat throughout the day.

87
Q

Lipase Inhibitors Contraindications

A

Malabsorption syndrome

Can increase INR → d/t decreased absorption of vitamin K

88
Q

Lipase Inhibitors Side Effects

A

Frequent BMs
Bowel urgency
Fatty stools
Flatulence
Nausea
Abdominal pain

89
Q

Glucagon-Like Peptide-1 Receptor Agonists

A

Saxenda (Victoza for DMII)

90
Q

Glucagon-Like Peptide-1 Receptor Agonists MOA

A

Stimulates glucose-dependent insulin secretion, decreases glucagon secretion, and slows gastric emptying.

Activates proopiomelanocortin neurons, which results in a feeling of satiety.

91
Q

Glucagon-Like Peptide-1 Receptor Agonists Side Effects

A

Nausea/vomiting
Diarrhea
Constipation

***Block box warning = medullary thyroid cancer, endocrine neoplasias type-2 seen in animal studies.

92
Q

Combination Weight Loss Drugs

A

Phentermine EF / Topiramate

Naltrexone SR / Bupropion

93
Q

Blepharitis

A

Meibomian glands secrete an oily film that prevents tears from evaporating → inflammation of eyelid margin.

94
Q

Blepharitis Presentation

A

Present with irritated red eyes, burning sensation, increased tearing, blinking, photophobia, and sticking of eyelids.

95
Q

Types of Blepharitis

A

Bacterial
Seborrheic
Meibomian Gland Dysfunction (MGD)

96
Q

Bacterial/Staphylococcal Blepharitis Presentation

A

Loss of eyelashes or misdirection with matted, scaling, and crusting.

97
Q

Seborrheic Blepharitis Presentation

A

Greasy deposits

98
Q

MGD Blepharitis Presentation

A

Fatty foam deposits

99
Q

First-Line Treatment of Bacterial Blepharitis

A

Bacitracin or Erythromycin ointment

If undesirable, then…

Moxifloxacin (Vigamox) or Azithromycin (AzaSite) solution.

*Avoid in corneal abrasion, slows wound healing.

100
Q

Second-Line Treatment of Bacterial Blepharitis

A

If no improvment to 1st line after several weeks or condition worsens → refer to ophthalmologist.

101
Q

First-Line Treatment of Seborrheic Blepharitis

A

Eye care specialist

102
Q

First-Line Treatment of MGD Blepharitis

A

Eyelid massage following warm compress is used to remove excess oil, then use eyelid cleaner or baby shampoo.

103
Q

Bacterial Conjunctivitis Presentation

A

Purulent discharge

Starts in one eye

104
Q

First-Line Treatment of Bacterial Conjunctivitis

A

Erythromycin - 1cm x6 per day for 5-7 days.

Polymyxin B Trimethoprim (Polytrim) - 1 drop q 3-4 hrs for 5-7days

Targeting S. aureus, S. pneumoniae, H. influenzae.

105
Q

Second-Line Treatment of Bacterial Conjunctivitis

A

Fluroquinolones (“-oxacin”) → Gram (+) coverage

Moxifloxacin (Vigamox) - 1 drop TID for 7 days

Ofloxacin (Ocuflox) - 1-2 drops q 2-4 hrs for 48 hrs, then 1-2 drops QID for 5 days.

106
Q

Treatment of Chlamydial Conjunctivitis in Newborns

A

Erythromycin only

107
Q

First-Line Treatment of DED

A

Mild → Artificial tears (GenTeal, Systane)

Mod/Severe → PF artificial tear sub as much as hourly

Sjogren’s → Cholinergic Agonists

108
Q

Cholinergic Agonists

A

Pilocarpine
Cevimeline

109
Q

Cholinergic Agonist MOA (DED)

A

Binds to muscarinic receptors, stimulating the secretion of salivary and sweat glands.

110
Q

Cholinergic Agonist Contraindications + SE

A

Uncontrolled asthma, acute iritis, and narrow-angle glaucoma

SE: Excessive sweating

111
Q

Second-Line Treatment of DED

A

Cyclosporine solution
Lifitegrast (Xiidra) 5% solution
Topical corticosteriods

112
Q

Cyclosporine MOA (DED)

A

Increases aqueous tear production and decreases ocular irritation by preventing T cells from activating and releasing cytokines.

113
Q

Liftiegrast 5% MOA

A

Blocks interaction of cell surface proteins LFA-1 and intracellular adhesion molecule 1 and may inhibit T-cell-related inflammation.

114
Q

Topical Corticosteriods Use

A

Max use of 2 weeks → to suppress irritation and inflammation

Long-term use → ocular infection, cataract formation, and glaucoma.

115
Q

Third-Line Treatment of DED

A

If all other therapies fail → refer to ophthalmology for permanent occlusion or tarsorrhaphy.

Helps eyes stay lubricated longer.

116
Q

First-Line Treatment of Glaucoma

A

Prostaglandin Analogs

117
Q

Prostaglandin Analogs

A

Bimatoprost (Lumigan)
Latanoprost (Xalatan)
Travoprost (Travatan Z)

“-oprost”

118
Q

Prostaglandin Analogs MOA

A

Reduce IOP by improving uveoscleral outflow of aqueous humor, reducing IOP by 25-33%

119
Q

Prostaglandin Analog Side Effects

A

Irreversible iris discoloration → periocular hyperpigmentation

120
Q

Prostaglandin Analog Considerations

A

Refrigerate
Discard after 6 weeks
Travoprost should not be used during pregnancy

121
Q

Second-Line Treatment of Glaucoma

A

Beta-blockers OR add beta-blocker if 1st agent fails to decrease IOP

122
Q

Non-Selective Beta-Blockers

A

Timolol (Timoptic)
Levobunolol (Betavan)
Carteolol
Metiproanolol

123
Q

Non-Selective Beta-Blocker Contraindications

A

Severe asthma/COPD

124
Q

Beta-1 Selective Beta-Blockers

A

Betaxolol (Betopic S)

125
Q

Beta-1 Selective Beta-Blocker Contraindications

A

Bradycardia
Heart block
CHF
Cardiogenic Shock

126
Q

Beta-Blockers MOA

A

Reduce adenylyl cyclase activity, reducing the production of aqueous humor in the ciliary body, lowering IOP by 20-25%

127
Q

Third-Line Treatment of Glaucoma

A

Topical Carbonic Anhydrase Inhibitors
OR
Adrenergic Agonists

128
Q

Carbonic Anhydrase Inhibitors

A

Brinzolmide (Azopt)
Dorzolamide (Truopt)

“-zolamide”.

129
Q

Carbonic Anhydrase Inhibitors MOA

A

Reduces aqueous humor production by the ciliary body by reducing the production of HCO3 ions and decreasing movement of HCO3, Na, and fluid into the posterior chamber. Reduces IOP by 15-26%.

130
Q

Carbonic Anhydrase Inhibitors Contraindications

A

Severe renal impairment
Respiratory acidosis
Electrolyte disorders

131
Q

Systemic Carbonic Anhydrase Inhibitors

A

Acetazolamide (Diamox)
Methanzolamide (Neptazane)

Most potent (reduces IOP by 25-40%)

132
Q

Adrenergic Agonists

A

Brimonidine (Alphagan P) → Selective alpha-2 agonist → little to no a-1 activity.

Apraclonidine (Iopidine) → Selective Alpha-2 Agonist → Some A-1 acivity

133
Q

Adrenergic Agonist MOA

A

Inhibits the release of norepinephrine, which reduces the formation of aqueous humor. Reduces IOP by 18-27%.

134
Q

Nitric Oxide Donating Prostaglandin Analogs

A

Lantanoprostene Bunod (Vyzulta)

135
Q

Nitric Oxide Donating Prostaglandin Analogs MOA

A

Prostaglandin analog improves uveoscleral outflow of aqueous humor, and NO reduces cellular contractility and volume, facilitating outflow of aqueous humor through trabecular meshwork and Schlemm’s canal.

136
Q

Nitric Oxide Donating Prostaglandin Analogs Considerations

A

Requires refrigeration

May cause iris discoloration

137
Q

Cholinergic Agonists

A

Pilocarpine (Isopto Carpine)

138
Q

Cholinergic Agonists MOA (Glaucoma)

A

Stimulates the parasympathetic muscarinic receptor site to increase aqueous outflow through the trabecular meshwork.

Reduces IOP by 20-30%.

139
Q

Rho Kinase Inhibitors

A

Netarsudil (Rhopressa)

140
Q

Rho Kinase Inhibitors MOA

A

Increases aqueous humor outflow by relaxing cells that line Schlemm’s canal, reducing resistance to the flow of aqueous humor.

Reduces IOP by 14-22%.

141
Q

Glaucoma Combination Products

A

Promotes adherence to therapy.

Combination therapy provides additional reduction in IOP than a single drug alone.

Ex.
Brimonidine + Timolol (Combigan)
Dorzolamide + Timolol (Cosopt)

142
Q

Education Regarding Glaucoma Ophthalmic Solutions

A

Wash hands.
Make sure contacts are removed.
Apply medication to the inner aspect of the lower eyelids.
Tip of the container should not touch any part of the eye.
Multiple drops should be separated by at least 10 minutes.

143
Q

Otitis Media

A

Occurs when the eustachian tube is obstructed due to inflammation of mucous membranes.

144
Q

OTC Treatment of Otitis Media

A

OTC → NSAIDS/Tylenol

Topical benzocaine/procaine for pain relief for children >5 years old.

145
Q

First-Line Treatment of Otitis Media

A

PCN (Amoxicillin) or Cephalosporins (Cefdinir if allergic to PCNs)

146
Q

Second-Line Treatment of Otitis Media

A

Failure to improve in 72 hrs, change to Augmentin

Failure of augmentin, change to ceftriaxone single IM or IM x3 days.

147
Q

Third-Line Treatment of Otitis Media

A

For reoccurrence, refer to ENT for tympanostomy tubes.

148
Q

Amoxicillin Dosing for Children with Otitis Media

A

80-90 mg/kg/d PO BID

149
Q

Amoxicillin-Clavulanate Dosing for Children with Otitis Media

A

Augmentin 80-90 mg/kg/d PO BID

150
Q

Cephalosporin Dosing for Children with Otitis Media

A

Cefdinir - 14 mg/kg/day PO BID

Cefpodoxime - 10 mg/kg/day PO QD

Cefuroxime - 30 mg/kg/day PO BID

Ceftriaxone - 50 mg/kg/day IM QD 1-3 days

151
Q

Antibiotic Duration for Children with Otitis Media

A

Age <2 = 10-day course

Age 2-5 = 7-day course

Age >6 = 5-day course

152
Q

Medications No Longer Recommended for Otitis Media

A

Macrolides and clindamycin

Due to the ineffectiveness to S. pneumoniae and H. influenzae

153
Q

First-Line Treatment of Otitis Externa

A

Fluoroquinolones

154
Q

Fluoroquinolones

A

Ofloxacin (Floxin Otic)

Ciprofloxacin 0.3% - Dexamethasone 0.1% (Ciprodex)

155
Q

Second-Line Treatment of Otitis Externa

A

Aminoglycosides

156
Q

Aminoglycosides

A

Neomycin-Polymyxin B

Neomycin Sulfate-Polymyxin B-Hydrocortisone Acetate (Cortisporin)

157
Q

Aminoglycosides Side Effects

A

Superinfection
Contact dermatitis
Ototoxicity with prolonged use

158
Q

Aminoglycoside Contraindications

A

Herpes, fungal or viral otic infections

Perforated eardrum

Caution in breastfeeding / pregnancy

NU 560 - Adv. Pharmacotherapeutics (5 decks)

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