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Pharmacology: Exam I > Exam I > Flashcards

Exam I Flashcards

1
Q

Schedule I Controlled Substances

A

high potential for abuse

heroine

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2
Q

Schedule II Controlled Substances

A

high potential for abuse
physical and psychological dependency
oxycodone, hydrocodone, hydromorphone

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3
Q

Schedule III Controlled Substances

A

some potential for abuse
limited psychological and physical dependency
up to 5 renewals in 6 months
testosterone

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4
Q

Schedule IV Controlled Substances

A

low potential for abuse
limited psychological and physical dependency
alprazolam, phentermine, tramadol

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5
Q

Schedule V Controlled Substances

A

subject to state/local regulation
may be sold Rx or OTC in some states
pregabalin

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6
Q

Pregnancy Category A

A

no risk to fetus in first trimester

no evidence of risk in later trimesters

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7
Q

Pregnancy Category B

A

no risk to fetus in animal studies, but no well-controlled studies in pregnant women

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8
Q

Pregnancy Category C

A

adverse effects on fetus in animal studies, but no well-controlled studies in pregnant women
benefits may outweigh risks

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9
Q

Pregnancy Category D

A

positive human fetal risk has been reported

considering potential benefit versus risks may, in some select cases, warrant the use of these drugs in pregnant women

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10
Q

Pregnancy Category X

A

fetal abnormalities were reported, and positive evidence of fetal risk in humans is available from animal or human studies
risks clearly outweigh the benefits
drugs should not be used in pregnant women

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11
Q

Recommendations for Writing Prescriptions

A

legible; verbal orders should be minimized
include purpose when appropriate
use metric system except for therapies that use standard units, in which case write out units
oral doses should be expressed with metric weight or volume and always include concentration or mg dose when using mL
include patient age and weight when appropriate
include drug name, exact metric weight or concentration, and dosage form
a leading zero should always be used before a decimal and a terminal zero should never be used after a decimal
avoid abbreviations

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12
Q

Report Medication Errors to:

A

FDA: MedWatch
Institute for Safe Medication Practices (ISMP)
Medication Errors Reporting (MER) Program/ US Pharmacopeia
US/MEDMARX (anonymous)

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13
Q

Pharmacodynamics

A

what drugs do to the body
mechanism of action
biochemical/physiologic effects

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14
Q

Pharmacokinetics

A

what the body does to the drugs

absorption, distribution, metabolism, excretion, half life

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15
Q

Pharmacology

A

the study of pharmacodynamics and pharmacokinetics

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16
Q

Drug

A

any substance that is used for diagnosis, cure, treatment, or prevention of disease/condition

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17
Q

Drug Receptors

A

bind to a drug molecule (with high affinity) and send (transduce) a signal/do something
not all drug receptors do something
what happens depends on the drug molecule

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18
Q

Affinity

A

strength of the binding between a drug and its receptor

what gets the drug bound to the receptor

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19
Q

Efficacy

A

ability of a drug to initiate max biological effect/stimulate receptor to produce pharmacological response
dictates what happens to the drug

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20
Q

Potency

A

measure of the ability of a set dose of an agonist or antagonist to produce its maximum pharmacological effect
used to compare drugs
ex. 10 mg Drug A = 5 mg Drug B

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21
Q

Quantity

A

amount of drug that reaches the receptor

may lose drug to first pass metabolism, can’t reach drug receptor site, etc.

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22
Q

Agonist

A

resembles naturally occurring hormone, neurotransmitter, or enzyme
bind and activate the receptor
act longer than the natural substances that they mimic

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23
Q

What are the two types of Agonists?

A

Full Agonist - acts with max effect

Partial Agonist - acts with less than max effect

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24
Q

Antagonist

A

bind to receptor and block the action of an endogenous agonist

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25
Q

What are the two types of Antagonist?

A

Competitive: competes with agonist and can be overcome by increasing concentrations of agonist
Noncompetitive: irreversibly bound

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26
Q

Binding Mechanisms for Receptors

A

ionic bonding
Van der Waals bonding
Hydrogen bonding

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27
Q

Selectivity

A

preference of a drug for certain receptor sites

non-selective drugs cause more side effects

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28
Q

How do drugs act on drug receptors?

A

direct activation of ion channel
G-protein activation of ion channel
G-protein activation of second messenger system
Receptor activation of intracellular enzyme (tyrosine kinase)
transcription factors
act on enzymes

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29
Q

Effective Dose 50 (ED50)

A

50% of people respond

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30
Q

Lethal Dose 50 (LD50)

A

50% of people die

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31
Q

Toxic Dose 50 (TD50)

A

50% of people (animals) show toxicity

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32
Q

Therapeutic Index (TI)

A

a window of dosage in which a drug is effective, but not toxic
TD50/ED50
the larger the TI, the safer the drug; the higher the dose to be toxic over the smaller dose to be effective if best
lower TI means a risky drug

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33
Q

Five Basic Parameters of Pharmacokinetics

A 
absorption
distribution
metabolism
excretion
half-life
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34
Q

Most drugs pass cell membranes by….?

A

passive transport

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35
Q

Absorption

A

when a drug is taken from the site of administration to the bloodstream
determined by: the drug’s properties (pH, lipid solubility/insolubility, ionized/unionized, molecular weight), drug formulation, route of administration
must be in a solution (ex. tablets must dissolve)
must cross cell membranes to reach the bloodstream (except IV)

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36
Q

Drugs cross cell membranes easier if they are…?

A

lipid soluble and unionized (like cell membranes!)

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37
Q

Bioavailability

A

the extent and rate that a drug enters systemic circulation

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38
Q

What affects Bioavailability?

A

largely determined by the properties of dosage form and the site of administration

drugs can be digested in first-pass metabolism, may be poorly absorbed in the GI tract, and/or may not be completely absorbed

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39
Q

First-Pass Metabolism

A

when drugs are digested before reaching the blood stream

mainly a function of the liver

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40
Q

Generic Drugs

A

drugs that replace brand name drugs on the market

must prove that they have the same bioavailability as the brand-name drug; the same amount of drug has to reach the bloodstream at the same rate

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41
Q

Oral Route of Administration

A

tablets, liquid, chewable tablets

usually the most convenient, easiest, and least expensive route

most commonly used route of administration

about 30 min - 2 hr onset

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42
Q

In order to be absorbed, Oral Routes must….

A

survive pH, GI secretions, and enzymes
have enough time to be absorbed/be absorbed quickly (food slows gastric secretion and may affect absorption)
have adequate blood flow to the intestines

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43
Q

What is Enteric Coating, and why is it important?

A

Enteric coating can be added to oral routes of administration. Some drugs can harm the lining of the stomach and cause irritation. Enteric coating can help prevent drugs from dissolving in the stomach, but still allows for dissolution in the small intestine.

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44
Q

Subcutaneous Injection Route

A

can be formulated to prolong absorption (internal depot)

can be irritating

30 min onset

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45
Q

Intramuscular Injection Route

A

for injecting larger volumes than subcutaneous (short term depot)

more blood flow than subcutaneous

can be irritating

5 min onset

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46
Q

Intravenous Injection Route

A

30 sec onset of peak plasma drug levels - fast!
precise administration
sell controlled
short duration in the body

good for irritating solutions (inject into larger veins) or water soluble solutions

more difficult to administer, uncomfortable, and once it is administered, you cannot get it back

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47
Q

Intrathecal Injection Route

A

inserted into spinal theca

rapid/local effects to CSF

rapid side effects

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48
Q

Sublingual and Buccal Route

A

absorbed under the tongue or between the gums and cheek; not swallowed

rapid absorption, but may be incomplete or erratic

ex. Nitroglycerin for the heart

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49
Q

Rectal Route

A

suppositories, solutions, creams, ointments, and foams

in general, any drug that can be given orally, can be given rectally, so rectal administration is useful when eating is difficult or impossible

absorption is faster that in oral routes and can be local or systemic, but absorption can also be unpredictable and erratic

affected by first pass metabolism

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50
Q

Vaginal Route

A

suppositories, solutions, creams, ointments, foams, and tablets

absorption can be local or systemic, but can also be variable

long-term absorption is possible (IUD)

less drug degradation than oral

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51
Q

Ocular Route

A

liquids (may run off quickly) and gels (remains in the eyes better than liquid, but may blur vision)

local absorption; if it is absorbed systemically, it may cause side effects

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52
Q

Otic Route

A

solutions or suspensions

local absorption

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53
Q

Nasal Route

A

atomized (small droplets)

drug is rapidly absorbed through the nasal mucous membrane

systemic or local effects

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54
Q

Inhalation Route

A

absorbed in the lungs, so these are rarely used, except for lung medications or gasses for general anesthesia

atomized/aerosolized (smaller than nasal routes)

ex. inhaleres

1 min onset or less

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55
Q

Nebulization Route

A

aerosolized

requires nebulizer

easier for young children or those who struggle with inhalers

1 min onset

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56
Q

Cutaneous Route

A

ointment, cream, lotion, solution, powder, or gel

typically used for local effect, but can have systemic absorption

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57
Q

Transdermal Route

A

patch

can be used for long periods of time and provide continuous dosing of drugs (external depot), but are only useful for potent, lipophilic drugs

can cause skin irritation

slower than subcutaneous route (» 30 min onset)

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58
Q

Distrubution

A

when drug moves from the bloodstream to the tissues

depends on:

  • blood perfusion - more blood, more drug to tissues (ex. inramuscular administration)
  • tissue mass (fat stores drugs, so more body fat leads to more drug storage)
  • ability to permeate capillaries and move from blood to tissue
  • amount of free/unbound drug in the blood stream
  • tissue binding (volume of distribution)
  • accumulation (storage in body)
  • blood brain barrier
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59
Q

Volume of Distribution

A

theoretical volume necessary to contain total amount of administered drug at the same concentration that is observed in the plasma; theoretical volume of fluid in which a drug administered would have to be diluted to produce the same concentration of drug observed in plasma

high for drugs that primarily bind to tissues

low for drugs that primarily remain in the bloodstream

= total amount of drug in the body/concentration in the plasma

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60
Q

Accumulation of Drugs in the Body

A

accumulation of drugs stored in body components (tissues and bone) can prolong drug action; it is released as plasma concentrations are used up

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61
Q

Blood Brain Barrier

A

made up of endothelium of brain capillaries and the astrocytic sheath

tight junctions between endothelial cells slow diffusion of water-soluble drugs

lipid-soluble drugs can enter the brain, but polar compounds, protein-bound drugs, and ionized drugs cannot

some unintended drugs pass the blood brain barrier and cause side-effects (sedation)

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62
Q

Relationship of Metabolism Rate and Drug Concentration

A

metabolism rate has an upper limit based on the number of occupied enzyme sites

most enzyme sites are not occupied, so metabolism increases with drug concentration

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63
Q

Pro-Drug

A

drugs that are weakly active or inactive, but have active metabolites; need to be metabolized to work

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64
Q

Excretion

A

removal of drugs and metabolites

primarily carried out by the kidneys through urine, but also in bile/feces, saliva, sweat, tears, breast milk, lungs

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65
Q

Renal Clearance

A

total amount of drug excreted by over time through kidneys; rate that drugs are excreted form the kidneys

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66
Q

Kidney Excretion

A

Glomerular Filtration - filtration moves drugs from blood to urine; protein-bound drugs and other high molecular weight drugs are not filtered (take longer to be excreted); glomerular filtration rate measures how well the kidneys are filtering

Tubular Reabsorption - most water and electrolytes are reabsorbed into circulation, along with lipid-soluble drugs

Tubular Excretion - polar and ionized compounds (most drugs and metabolites) are not reabsorbed and are instead excreted in urine unless there are active transport systems in place to assist them

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67
Q

How does urine pH affect drug reabsorption?

A

increases reabsorption and decreases excretion of weak acids, decreases reabsorption and increases excretion of weak bases

68
Q

Half-Life

A

measure of how long it will take for half of a drug to be eliminated from the bloodstream

helps determine dosing intervals, time it takes to reach ‘steady state,’ and when a drug is cleared

Does not determine absorption of drug!

5-6 half-lives to eliminate a drug from the body

rate of drug release from tissues affects half-life; some drugs remain bound in tissues longer than others

69
Q

Onset of Routes of Administration: Fastest (30 sec - 1 min)

A

IV

inhalation

70
Q

Onset of Routes of Administration: Fast (5 min)

A

intramuscular

71
Q

Onset of Routes of Administration: Mid (30 min)

A

subcutaneous

oral

72
Q

Onset of Routes of Administration: Slow (2 hours +)

A

transdermal

oral

73
Q

Duration that drugs act on the body depend on:

A

half life, body clearance, and the drug

can be extended by depot (internal, external)

74
Q

CYP450

A

enzyme involved with metabolism that is found in all tissues of the body; metabolize many drugs

variable depending on genetics, race/ethnicity, and age

can be induced or inhibited by drugs

75
Q

Drug Interactions and Metabolism

A

can prevent or increase the action of a drug
can make toxic effects more likely
can slow or speed up excretion of a drug
can increase or decrease metabolism of a drug

76
Q

Hepatic Impairment

A

liver failure, impairment, disease, etc. can impact how drugs are metabolized, and may affect efficacy and excretion

drug dose adjustment may be necessary

77
Q

Loading Dose

A

an initial high dose of drug given at the beginning of a course of treatment to reach and remain above the minimum effective drug concentration in the body; following doses are lower to maintain steady state

78
Q

Where are most otic drugs administered?

A

the external auditory ear canal, but some are for the middle ear

79
Q

What is the correct way to administer ear drops?

A

wash hands
adults - gently pull ear up and back
children - gently pull ear down and back
keep ear facing up for several minutes after administering drops
use cotton plug in the ear to maintain medicine within the canal

80
Q

Are eardrops absorbed in the skin?

A

Not typically; only absorbed through the skin if the skin is broken

81
Q

Otitis Externa

A

infection of the outer ear

pain on movement of the pinna

etiology: history of swimming or exposure to contaminated water

typically caused by gram-negative rods or fungi

rarely life-threatening

get culture, if it is still present after one week of treatment

82
Q

How is Otitis Externa generally treated?

A

Otic Anti-Infectives with or without corticosteroids

Acid-Alcohol Solutions

83
Q

Bacteriostatic

A

antibiotic or anti-infective that prevents the growth of bacteria

84
Q

Bacteriocidal

A

kill bacteria

85
Q

What is the usual administration route of Otic Anti-infectives?

A

topical; not usually absorbed through the skin

86
Q

Why are steroids sometimes combined with otic anti-infectives?

A

corticosteroids are used for their anti-inflammatory, antipruritic, and anti-allergenic effects; reduce inflammation, relieve symptoms, and the reduction in inflammation may help the topical meds reach more of the ear

anti-infectives with corticosteroids are more commonly prescribed than those without

87
Q

What risks should you be aware of when prescribing otic anti-infectives?

A

risk of ototoxicity, especially formulations containing neomycin

do not prescribe if you believe the patient might have ruptured ear drums or tubes in their ears

88
Q

What would you prescribe for serious cases of Otitis Externa? (if cellulitis is present)

A

fluoroquinolones: ciprofloxacin or ofloxacin

kill pseudomonas

89
Q

What are the most commonly prescribed medications for Otitis Externa?

A

ciprofloxacin/hydrocortisone

ciprofloxacin/dexamethasone

90
Q

Adverse Reactions of Otic Anti-Infectives

A

similar for with or without steroids
ear pain
ear discomfort or irritability
ear residue
ototoxicity - neomycin, tubes, perforated eardrum
contact dermatitis - itchy rash (Neomycin)

91
Q

Otic Anti-infectives Contraindications

A

hypersensitivity to active ingredients or vehicle (other stuff in the medication that holds the drug)
Neomycin - tubes or perforated eardrums

92
Q

Acid-Alcohol Solutions

A

supplement natural defense mechanism of the ear (naturally acidic environment)

induce drying of cellular infective agents (bacteria cannot survive)

provide topical, antibacterial, and antifungal effect

used for superficial infections of the external auditory canal

93
Q

Adverse Effects of Acid-Alcohol Solutions

A

stinging and burning

local irritation

do not use with perforated eardrums or ear tubes

Anti-infectives with steroids are more commonly prescribed

94
Q

How do you treat water-clogged ears?

A

95% isopropyl alcohol and 5% anhydrous glycerin (swimmer’s ear, Auro Dri drops, FDA approved)

50:50 acetic acid (5%) and isopropyl alcohol (95%) (recommended by American Academy of Otolaryngology)

95
Q

Otitis Media

A

middle ear infection

common in children

1/2 of cases are bacterial (S. pneumonia, Haemophilus influenza, Moraxella catarrhalis, Streptococcus pyrogenes)

1/2 of cases are viral

be cautious when prescribing antibiotics - they will not work for viral infections, but will cause side-effects

96
Q

How is Acute Otitis Media pain treated?

A

pain should be assessed and treated with acetaminophen and/or ibuprofen

97
Q

In what cases would you prescribe antibiotics for Acute Otitis Media?

A

6 mo+ with bilateral or unilateral Acute Otitis Media and severe signs and symptoms

6-23 mo with bilateral Acute Otitis Media

98
Q

In what cases would you watch and wait and consider proscribing antibiotics for Acute Otitis Media?

A

6 mo-23 mo with non-severe unilateral Acute Otitis Media

24 mo+ with nonsevere Acute Otitis Media

99
Q

What antibiotics are used to treat Acute Otitis Media?

A

Amoxicillin is the drug of choice

Amoxicillin/Clavulanate provides B-lactase coverage that is necessary if Amoxicillin was recently used or the patient had previous Amoxicillin resistance

Oflaxacin can be a good choice if the patient has tubed ears

100
Q

Cerumenolytics

A

cerumen softening agents

aimed at softening and removing ear wax from the external auditory canal

water based, oil based, nonwater/nonoil based

101
Q

Adverse Effects of Cerumenolytics

A 
mild itching
burning
ear pain
erythema of the ear canal
allergic reactions (emergency)
102
Q

Contraindications of Cerumenolytics

A

perforated ear drum or ear tubes

ear discharge, pain, rash, or irritation around the ear

103
Q

How to Use Cerumen-Softening Agents?

A

instill in ear

once wax is softened, follow with warm water irrigation using otic syringe

ensure drops are removed completely with irrigation (leaving drops in longer than 30 minutes causes irritation)

don’t use q-tips to clean out wax

104
Q

How to Administer Eyedrops

A

wash hands before and after administration

remove contacts unless using contact-safe formulations

look up, pull lower lid down, and instill drops

close eye to allow medication to have max effect (can occlude tear duct with finger - punctual occlusion)

don’t touch dropper tip

wait 5+ minutes between different eye drop meds and use ointments after drops

105
Q

Two Classes of Ophthalmic Anesthetics

A

amino esters: tetracaine and proparacarpine

amino amide: lidocaine

106
Q

Clinical Use of Ophthalmic Anesthetics

A

to produce local anesthesia for ophthalmic procedures, removing foreign bodies or sutures, scraping for diagnosis

107
Q

Improper use of Ophthalmic Anesthetics can cause…?

A

deep corneal infiltrates, ulceration, and perforation

only to use on occasion; do not prescribe

108
Q

Ophthalmic Anesthetics Mode of Action

A

penetrate to sensory nerve endings in the corneal tissue where they bind to receptors within the sodium channels and block the movement of sodium, inhibiting depolarization along the axon and preventing the pain stimulus from reaching the spinal cord

109
Q

Ophthalmic Anesthetics Pharmacokinetics

A

work within 20-30 seconds and last up to 15 minutes (may need to be re-dosed)

A: rapid at corneal capillaries; local action
D: protein binding is high (protein-bound remain in bloodstream)
M: unknown in the eye/skin; some may be metabolized if it’s systemically absorbed
E: unknown for lidocaine, but tetracaine and proparacaine through bile
T 1/2: proparacaine is shortest, lidocaine is intermediate, and tetracaine is longest

110
Q

Ophthalmic Anesthetics Adverse Reactions

A

burning and stinging upon application

if used over days: severe keratitis, opacification, scarring of the cornea and loss of vision possible (rare)

111
Q

Conjunctivitis

A

inflammation of the conjunctiva

caused by allergens, bacteria, viruses, and fungi (rare)

112
Q

Ophthlamic Anti-Infectives Adverse Reactions

A

local irritation

blurry vision

super infections possible with long-term use/ resistance

hypersensitivity to sulfacetamide is possible (sulfa allergy is a contraindication)

little to no systemic absorption

113
Q

Allergic Conjunctivitis Symptoms and Etiology

A 
Symptoms:
chronic and recurring itching
slightly red eyes
tearing and blurring
little discharge
Etiology:
animal hair
pollen
ragweed
plants
114
Q

Ophthalmic Mast Cell Stabilizers

A

inhibit degranulation of mast cells after exposure to antigen - reduces histamine release

used for allergic conjunctivitis and keratitis

no significant systemic absorption

used less often than antihistamines

115
Q

Ophthalmic Mast Cell Stabilizers Adverse Effects

A 
transient stinging and burning
blurry vision
photophobia
mydriasis
rhinitis
sinusitis
headache
116
Q

Ophthalmic Antihistamines

A

block the effects of histamines released during allergic reactions and blunt its symptoms

H1 blockers - bind and block H1 receptors, preventing a normal signal from sending (antagonists)

temporarily relieve itching associated with allergic conjunctivitis

little to no systemic absorption

117
Q

Which Ophthalmic Antihistamines are prescribed more often?

A

ketotifen and olopatadine

118
Q

Ophthalmic Antihistamine Adverse Effects

A 
transient stinging and burning
blurry vision
photophobia
Mydriasis
Rhinitis
Headache
119
Q

Ophthalmic Vasoconstrictors/Decongestants

A

weak sympathomimetic (raise blood pressure and constrict blood vessels in the conjunctiva)

used to temporarily relieve eye redness

not for dry eyes

not usually recommended because of adverse reactions

120
Q

Ophthalmic Vasoconstrictors/Decongestants Adverse Reactions

A

Avoid if: heart disease, high blood pressure, enlarged prostate, narrow-angle glaucoma, or are a contact wearer

contraindication: narrow-angle glaucoma - these drugs cause mydriasis which could worsen glaucoma and result in permanent eye damage

systemic adverse effects: tachycardia and aggravation of arrythmias

local adverse effects: burning, stinging, and blurry vision

interactions: increase pressor effects if used with MAOIs and tricyclics

121
Q

Dry Eye

A

caused by tear film instability due to deficiency of any tear film component

Presentation: 
ocular discomfort
desire to rub eyes
blurred vision
burning
reness
122
Q

Ophthalmic Lubricants

A

contain agents that provide hydration, maintain moisture, and protect the eye

Used:

  • to supplement natural tears, when relief of dry eyes is needed or to wash away irritants
  • as viscosity enhancers that promote increased contact time of an ophthalmic agent with the ocular surface
  • for secondary corneal edema

recommended preservative free if used frequently

123
Q

Artificial Tears

A

act as demulcents (protective film) to mimic mucin (glyocprotein of mucus

124
Q

Ocular Emollients

A

protects and prevents drying

125
Q

Ocular Ointments

A

have longer contact

more likely to cause blurred vision

often prescribed to take at bedtime

126
Q

Corneal Edema

A 
Symptoms: 
foggy vision
halos around lights
photophobia
irritation
sensation of a foreign body
extreme pain

caused by prolonged contact lens wearing, infection, gluacoma, or iritis

treated with Sodium Chloride (2-5%)

127
Q

Pupillary Dilation Agents

A

used to dilate pupils (mydriasis) - inhibition of circular muscle

MOA: muscarinic agents - block parasympathetic receptors that would normally cause pupils to constrict if stimulated

128
Q

Pupillary Dilation Agents Averse Reactions

A 
tachycardia
flushing of cheeks
blurry vision
photophobia
dry mouth
slurred speech, drowsiness, hallucinations
congestion
irritated eyes

contraindications: closed angle glaucoma - dilation can occlude outflow of aqueous humor, increasing intraoccular pressure, further impeding outflow

129
Q

Mydriatic

A

dilates pupils

130
Q

Miotic

A

constricts pupils

131
Q

Gluacoma

A

increased intraocular pressure (IOP) - causes pathologic changes in optic nerve and visual field defects

Pathogenesis: changes in aqueous humor outlfow that result in increased intraocular pressure - leads to optic nerve atrophy and loss of vision

Intraocular pressure increases due to decreased elimination of aqueous humor or increased production of aqueous humor

132
Q

Angle-Closure Glaucoma (Closed-Angle)

A

aqueous humor cannot leave the anterior chamber

shallow anterior chamber leads to a narrow angle, so iris dilation can block the angle and comprise aqueous humor filtration

pupillary blockage of aqueous humor outflow; as aqueous humor increases in the anterior chamber, the lens if pushed further, and blocks the angle further

EMERGENCY

can be triggered by many drugs (pupillary dilators and vasoconstrictors)

133
Q

Open-Angle Glaucoma

A

the canal of Schlemm is blocked

angle of the anterior chamber remains open, but filtration of aqueous humor is gradually diminished because of the tissues of the angle

80-90% of glaucoma cases

decreased elimination of aqueous humor as it passes through trabecular meshwork

134
Q

Glaucoma Treatment Principles

A

reduce IOP to prevent optic nerve damage and visual field loss

use topical medications as first-line treatment

acute angle-closure glaucoma is an emergency

135
Q

Prostaglandin Analogues

A

Treat Glaucoma

1st line treatment

increase outflow of intraocular aqueous humor through uveoscleral pathway

-prost

136
Q

B Antagonists/ Beta Blockers

A

Treat Glaucoma

blockade of sympathetic nerve endings in ciliary epithelium, decreasing aqueous humor formation and lowing intraocular pressure

B-blockers bind to receptors in the ciliary body and prevent some aqueous humor formation

-olol

137
Q

Adrenergic Agonists

A

Treat Glaucoma

decreases aqueous humor production, maybe increases outflow

vasoconstriction leads to decrease in production

bind to alpha 2 receptors in the ciliary body and cause vasoconstriction

138
Q

Carbonic Anhydrase Inhibitors

A

Treat Glaucoma

decrease volume of aqueous humor by slowing action of carbonic anhydrase (enzyme)

carbonic anhydrase is involved in formation of aqueous humor

139
Q

Cholinergics

A

Treat Glaucoma

cause parasympathetic response, which causes miosis

direct - directly stimulate ocular cholinergic receptors (act like acetylcholine)

indirect - bind to and inactivate cholinesterases (break down acetylcholine) –> keep acetylcholine around

140
Q

Cholinergics Mechanism of Action

A

contracts the iris sphincter muscle, resulting in miosis

ciliary muscles attach to the trabecular meshwork; contraction opens the canal of Schlemm, increasing the outflow of aqueous humor, and decreases IOP

141
Q

Glaucoma treatments that slows down production of aqueous humor

A

beta blockers, alpha 2 agonists, carbonic anhydrase inhibitors

142
Q

Glaucoma treatments that increase outflow of aqueous humor

A

prostaglandins and cholinergics/muscarinics

143
Q

Allergic Rhinitis

A

exposure to allergens causes nasal symptoms

allergen binds B-cell - B-cell triggers plasma cell - plasma cell releases antibodies - mast cells find antibodies bound to allergens - mast cells degranulate to histamine and other chemicals (cytokines) - histamine and other chemicals cause smooth muscle contraction, mucus secretion, vascular permeability, sensory nerve stimulation

Presentation:
Nasal - congestion, rhinorrhea, nasal pruritis, sneezing, post-nasal drip
Ocular - itching, lacrimation, redness, irritation
General - headache, malaise, mood swings, irritability

144
Q

Allergic Rhinitis Nonpharmacologic Treatment

A

avoid allergens

145
Q

Allergic Rhinitis Pharmacologic Treatment

A

mild - 2nd generation, non-sedating antihistmines prn

moderate - combinations of intranasal steroids, antihistamines, and decongestants for nasal symptoms, and ophthalmic antihistamine for ocular symptoms

severe - refer to specialty/immunology

146
Q

Intranasal Corticosteroids

A

reduce ocular symptoms, nasopharyngeal itching, sneezing, and rhinorrhea

decrease influx of inflammatory cells, inhibit release of cytokines, which reduce inflammation of mucosa

onset is less than 30 minutes

need to be taken for 2-4 weeks for max efficacy

more effective than antihistamines in persistent and more severe cases

147
Q

Antihistamines

A

reduce nasopharyngeal itching, sneezing, and rhinorrhea

H1 receptor antagonists; block histamine receptor

1st generation - cause sedation, non-selective
2nd generation - selective, low incidence of sedation

onset: 15-30 minutes

immediate, temporary relief for once in awhile usage

148
Q

Antihistamine Pharmacokinetics

A 
A: rapid
D: 60-70% protein bound
M: minimal; desloratadine is a prodrug
E: fexofenadine, desloratadine, and loratadine through feces and urine; all others through urine
T 1/2: variable
149
Q

Oral Decongestants

A

reduce rhinorrhea

alpha-adrenergic agonists - vasoconstriction; constriction of blood vessels decrease blood supply to the nasal mucosa, decreasing nasal edema

no effect on histamine

15-30 minute onset

just helps with symptoms

150
Q

Oral Decongestant Side Effects

A

headache
elevated blood pressure - bad for glaucoma
tremor
urinary retention
dizziness
tachycardia
insomnia - ask for shorter acting and don’t take at HS

Contraindications: hypertension, heart disease, diabetes, hyperthyroidism, enlarged prostate, narrow-angle glaucoma, blood pressure

151
Q

Topical Decongestant

A

reduces rhinorrhea

alpha agonists act locally as vasoconstrictors; constriction of blood vessels decreases blood supply to nose, which decrease mucosal edema

no effect on histamine

Side Effects: 
minimal systemic absorption (good option for patients with other conditions)
local burning
nasal irritation and dryness
sneezing

REBOUND CONGESTION - don’t use for mroe than 3-5 days

152
Q

Immunotherapy

A

subcutaneous injections of allergen

5-7 years; can last up to 12

can be very effective

reserved for patients:
unresponsive to usual treatment
who cannot tolerate usual treatment
who want to avoid long-term med use
with allergic asthma
153
Q

Common Cold

A

usually viral

results in release of numerous inflammatory mediators - cytokines

Presentation:
sore throat
nasal symptoms
watery eyes
sneezing
cough
malaise
low-grade fever

gradual onset, slow progression
1-2 weeks

154
Q

Nonpharmacologic Cold Treatments

A

humidifiers, increase fluid intake, rest

155
Q

Pharmacologic Cold Treatments

A

Decongestants - nasal congestion
Analgesics - pain, headache
Local Anesthetic - lozenges, sprays

156
Q

Treat Fever

A

acetominophen

NSAIDS (non-steroidal anti-inflammatory drugs): ibuprofen and naproxen

157
Q

Who should you avoid prescribing cough medicine to?

A

children under 6 yo

158
Q

What might be effective alternative treatments for cough?

A 
high-dose inhaled corticosteroids
buckwheat honey
nasal irrigation with saline
vapor rub
zinc sulfate
159
Q

Cough Treatments

A

Antitussives
Expectorant
Sore Throat Remedies

160
Q

Sore Throat/ Cough Remedies

A

saline gargle
sprays, lozenges (benzocaine, dyclonine, phenol, menthol)
honey
lots of water

161
Q

Innate Immunity

A

natural immunity

162
Q

Two Types of Acquired Immunity

A

Humoral - antibodies and B cells

Cellular - no antiboidies and T cells

163
Q

Gell and Coombs Hypersensitivity Classification Types

A

Type I: IgE-mediated (anaphylaxis/allergy)
Type II: Cytotoxic Reaction - antibodies attack drug coated cells
Type III: Immune Complex - drug-antibody deposits on tissues; 1-3 weeks after exposure
Type IV: Delayed, Cell-mediated; drug rash; 2-7 days after exposure

164
Q

Type I Hypersensitivity

A

IgE-mediated

Mild - allergic rhinitis

Moderate - Urticaria (Hives) and Andioedema (Swelling)

Severe - Anaphylaxis

165
Q

Biphasic Reaction

A

a second reaction of Anaphylaxis that can occur hours later

Pharmacology: Exam I (4 decks)

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