Exam I Flashcards
Schedule I Controlled Substances
high potential for abuse
heroine
Schedule II Controlled Substances
high potential for abuse
physical and psychological dependency
oxycodone, hydrocodone, hydromorphone
Schedule III Controlled Substances
some potential for abuse
limited psychological and physical dependency
up to 5 renewals in 6 months
testosterone
Schedule IV Controlled Substances
low potential for abuse
limited psychological and physical dependency
alprazolam, phentermine, tramadol
Schedule V Controlled Substances
subject to state/local regulation
may be sold Rx or OTC in some states
pregabalin
Pregnancy Category A
no risk to fetus in first trimester
no evidence of risk in later trimesters
Pregnancy Category B
no risk to fetus in animal studies, but no well-controlled studies in pregnant women
Pregnancy Category C
adverse effects on fetus in animal studies, but no well-controlled studies in pregnant women
benefits may outweigh risks
Pregnancy Category D
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
Pregnancy Category X
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
Recommendations for Writing Prescriptions
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
Report Medication Errors to:
FDA: MedWatch
Institute for Safe Medication Practices (ISMP)
Medication Errors Reporting (MER) Program/ US Pharmacopeia
US/MEDMARX (anonymous)
Pharmacodynamics
what drugs do to the body
mechanism of action
biochemical/physiologic effects
Pharmacokinetics
what the body does to the drugs
absorption, distribution, metabolism, excretion, half life
Pharmacology
the study of pharmacodynamics and pharmacokinetics
Drug
any substance that is used for diagnosis, cure, treatment, or prevention of disease/condition
Drug Receptors
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
Affinity
strength of the binding between a drug and its receptor
what gets the drug bound to the receptor
Efficacy
ability of a drug to initiate max biological effect/stimulate receptor to produce pharmacological response
dictates what happens to the drug
Potency
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
Quantity
amount of drug that reaches the receptor
may lose drug to first pass metabolism, can’t reach drug receptor site, etc.
Agonist
resembles naturally occurring hormone, neurotransmitter, or enzyme
bind and activate the receptor
act longer than the natural substances that they mimic
What are the two types of Agonists?
Full Agonist - acts with max effect
Partial Agonist - acts with less than max effect
Antagonist
bind to receptor and block the action of an endogenous agonist
What are the two types of Antagonist?
Competitive: competes with agonist and can be overcome by increasing concentrations of agonist
Noncompetitive: irreversibly bound
Binding Mechanisms for Receptors
ionic bonding
Van der Waals bonding
Hydrogen bonding
Selectivity
preference of a drug for certain receptor sites
non-selective drugs cause more side effects
How do drugs act on drug receptors?
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
Effective Dose 50 (ED50)
50% of people respond
Lethal Dose 50 (LD50)
50% of people die
Toxic Dose 50 (TD50)
50% of people (animals) show toxicity
Therapeutic Index (TI)
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
Five Basic Parameters of Pharmacokinetics
absorption distribution metabolism excretion half-life
Most drugs pass cell membranes by….?
passive transport
Absorption
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)
Drugs cross cell membranes easier if they are…?
lipid soluble and unionized (like cell membranes!)
Bioavailability
the extent and rate that a drug enters systemic circulation
What affects Bioavailability?
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
First-Pass Metabolism
when drugs are digested before reaching the blood stream
mainly a function of the liver
Generic Drugs
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
Oral Route of Administration
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
In order to be absorbed, Oral Routes must….
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
What is Enteric Coating, and why is it important?
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.
Subcutaneous Injection Route
can be formulated to prolong absorption (internal depot)
can be irritating
30 min onset
Intramuscular Injection Route
for injecting larger volumes than subcutaneous (short term depot)
more blood flow than subcutaneous
can be irritating
5 min onset
Intravenous Injection Route
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
Intrathecal Injection Route
inserted into spinal theca
rapid/local effects to CSF
rapid side effects
Sublingual and Buccal Route
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
Rectal Route
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
Vaginal Route
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
Ocular Route
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
Otic Route
solutions or suspensions
local absorption
Nasal Route
atomized (small droplets)
drug is rapidly absorbed through the nasal mucous membrane
systemic or local effects
Inhalation Route
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
Nebulization Route
aerosolized
requires nebulizer
easier for young children or those who struggle with inhalers
1 min onset
Cutaneous Route
ointment, cream, lotion, solution, powder, or gel
typically used for local effect, but can have systemic absorption
Transdermal Route
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)
Distrubution
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
Volume of Distribution
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
Accumulation of Drugs in the Body
accumulation of drugs stored in body components (tissues and bone) can prolong drug action; it is released as plasma concentrations are used up
Blood Brain Barrier
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)
Relationship of Metabolism Rate and Drug Concentration
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
Pro-Drug
drugs that are weakly active or inactive, but have active metabolites; need to be metabolized to work
Excretion
removal of drugs and metabolites
primarily carried out by the kidneys through urine, but also in bile/feces, saliva, sweat, tears, breast milk, lungs
Renal Clearance
total amount of drug excreted by over time through kidneys; rate that drugs are excreted form the kidneys
Kidney Excretion
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
How does urine pH affect drug reabsorption?
increases reabsorption and decreases excretion of weak acids, decreases reabsorption and increases excretion of weak bases
Half-Life
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
Onset of Routes of Administration: Fastest (30 sec - 1 min)
IV
inhalation
Onset of Routes of Administration: Fast (5 min)
intramuscular
Onset of Routes of Administration: Mid (30 min)
subcutaneous
oral
Onset of Routes of Administration: Slow (2 hours +)
transdermal
oral
Duration that drugs act on the body depend on:
half life, body clearance, and the drug
can be extended by depot (internal, external)
CYP450
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
Drug Interactions and Metabolism
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
Hepatic Impairment
liver failure, impairment, disease, etc. can impact how drugs are metabolized, and may affect efficacy and excretion
drug dose adjustment may be necessary
Loading Dose
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
Where are most otic drugs administered?
the external auditory ear canal, but some are for the middle ear
What is the correct way to administer ear drops?
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
Are eardrops absorbed in the skin?
Not typically; only absorbed through the skin if the skin is broken
Otitis Externa
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
How is Otitis Externa generally treated?
Otic Anti-Infectives with or without corticosteroids
Acid-Alcohol Solutions
Bacteriostatic
antibiotic or anti-infective that prevents the growth of bacteria
Bacteriocidal
kill bacteria
What is the usual administration route of Otic Anti-infectives?
topical; not usually absorbed through the skin
Why are steroids sometimes combined with otic anti-infectives?
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
What risks should you be aware of when prescribing otic anti-infectives?
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
What would you prescribe for serious cases of Otitis Externa? (if cellulitis is present)
fluoroquinolones: ciprofloxacin or ofloxacin
kill pseudomonas
What are the most commonly prescribed medications for Otitis Externa?
ciprofloxacin/hydrocortisone
ciprofloxacin/dexamethasone
Adverse Reactions of Otic Anti-Infectives
similar for with or without steroids
ear pain
ear discomfort or irritability
ear residue
ototoxicity - neomycin, tubes, perforated eardrum
contact dermatitis - itchy rash (Neomycin)
Otic Anti-infectives Contraindications
hypersensitivity to active ingredients or vehicle (other stuff in the medication that holds the drug)
Neomycin - tubes or perforated eardrums
Acid-Alcohol Solutions
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
Adverse Effects of Acid-Alcohol Solutions
stinging and burning
local irritation
do not use with perforated eardrums or ear tubes
Anti-infectives with steroids are more commonly prescribed
How do you treat water-clogged ears?
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)
Otitis Media
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
How is Acute Otitis Media pain treated?
pain should be assessed and treated with acetaminophen and/or ibuprofen
In what cases would you prescribe antibiotics for Acute Otitis Media?
6 mo+ with bilateral or unilateral Acute Otitis Media and severe signs and symptoms
6-23 mo with bilateral Acute Otitis Media
In what cases would you watch and wait and consider proscribing antibiotics for Acute Otitis Media?
6 mo-23 mo with non-severe unilateral Acute Otitis Media
24 mo+ with nonsevere Acute Otitis Media
What antibiotics are used to treat Acute Otitis Media?
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
Cerumenolytics
cerumen softening agents
aimed at softening and removing ear wax from the external auditory canal
water based, oil based, nonwater/nonoil based
Adverse Effects of Cerumenolytics
mild itching burning ear pain erythema of the ear canal allergic reactions (emergency)
Contraindications of Cerumenolytics
perforated ear drum or ear tubes
ear discharge, pain, rash, or irritation around the ear
How to Use Cerumen-Softening Agents?
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
How to Administer Eyedrops
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
Two Classes of Ophthalmic Anesthetics
amino esters: tetracaine and proparacarpine
amino amide: lidocaine
Clinical Use of Ophthalmic Anesthetics
to produce local anesthesia for ophthalmic procedures, removing foreign bodies or sutures, scraping for diagnosis
Improper use of Ophthalmic Anesthetics can cause…?
deep corneal infiltrates, ulceration, and perforation
only to use on occasion; do not prescribe
Ophthalmic Anesthetics Mode of Action
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
Ophthalmic Anesthetics Pharmacokinetics
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
Ophthalmic Anesthetics Adverse Reactions
burning and stinging upon application
if used over days: severe keratitis, opacification, scarring of the cornea and loss of vision possible (rare)
Conjunctivitis
inflammation of the conjunctiva
caused by allergens, bacteria, viruses, and fungi (rare)
Ophthlamic Anti-Infectives Adverse Reactions
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
Allergic Conjunctivitis Symptoms and Etiology
Symptoms: chronic and recurring itching slightly red eyes tearing and blurring little discharge
Etiology: animal hair pollen ragweed plants
Ophthalmic Mast Cell Stabilizers
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
Ophthalmic Mast Cell Stabilizers Adverse Effects
transient stinging and burning blurry vision photophobia mydriasis rhinitis sinusitis headache
Ophthalmic Antihistamines
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
Which Ophthalmic Antihistamines are prescribed more often?
ketotifen and olopatadine
Ophthalmic Antihistamine Adverse Effects
transient stinging and burning blurry vision photophobia Mydriasis Rhinitis Headache
Ophthalmic Vasoconstrictors/Decongestants
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
Ophthalmic Vasoconstrictors/Decongestants Adverse Reactions
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
Dry Eye
caused by tear film instability due to deficiency of any tear film component
Presentation: ocular discomfort desire to rub eyes blurred vision burning reness
Ophthalmic Lubricants
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
Artificial Tears
act as demulcents (protective film) to mimic mucin (glyocprotein of mucus
Ocular Emollients
protects and prevents drying
Ocular Ointments
have longer contact
more likely to cause blurred vision
often prescribed to take at bedtime
Corneal Edema
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%)
Pupillary Dilation Agents
used to dilate pupils (mydriasis) - inhibition of circular muscle
MOA: muscarinic agents - block parasympathetic receptors that would normally cause pupils to constrict if stimulated
Pupillary Dilation Agents Averse Reactions
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
Mydriatic
dilates pupils
Miotic
constricts pupils
Gluacoma
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
Angle-Closure Glaucoma (Closed-Angle)
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)
Open-Angle Glaucoma
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
Glaucoma Treatment Principles
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
Prostaglandin Analogues
Treat Glaucoma
1st line treatment
increase outflow of intraocular aqueous humor through uveoscleral pathway
-prost
B Antagonists/ Beta Blockers
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
Adrenergic Agonists
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
Carbonic Anhydrase Inhibitors
Treat Glaucoma
decrease volume of aqueous humor by slowing action of carbonic anhydrase (enzyme)
carbonic anhydrase is involved in formation of aqueous humor
Cholinergics
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
Cholinergics Mechanism of Action
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
Glaucoma treatments that slows down production of aqueous humor
beta blockers, alpha 2 agonists, carbonic anhydrase inhibitors
Glaucoma treatments that increase outflow of aqueous humor
prostaglandins and cholinergics/muscarinics
Allergic Rhinitis
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
Allergic Rhinitis Nonpharmacologic Treatment
avoid allergens
Allergic Rhinitis Pharmacologic Treatment
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
Intranasal Corticosteroids
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
Antihistamines
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
Antihistamine Pharmacokinetics
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
Oral Decongestants
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
Oral Decongestant Side Effects
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
Topical Decongestant
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
Immunotherapy
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
Common Cold
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
Nonpharmacologic Cold Treatments
humidifiers, increase fluid intake, rest
Pharmacologic Cold Treatments
Decongestants - nasal congestion
Analgesics - pain, headache
Local Anesthetic - lozenges, sprays
Treat Fever
acetominophen
NSAIDS (non-steroidal anti-inflammatory drugs): ibuprofen and naproxen
Who should you avoid prescribing cough medicine to?
children under 6 yo
What might be effective alternative treatments for cough?
high-dose inhaled corticosteroids buckwheat honey nasal irrigation with saline vapor rub zinc sulfate
Cough Treatments
Antitussives
Expectorant
Sore Throat Remedies
Sore Throat/ Cough Remedies
saline gargle
sprays, lozenges (benzocaine, dyclonine, phenol, menthol)
honey
lots of water
Innate Immunity
natural immunity
Two Types of Acquired Immunity
Humoral - antibodies and B cells
Cellular - no antiboidies and T cells
Gell and Coombs Hypersensitivity Classification Types
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
Type I Hypersensitivity
IgE-mediated
Mild - allergic rhinitis
Moderate - Urticaria (Hives) and Andioedema (Swelling)
Severe - Anaphylaxis
Biphasic Reaction
a second reaction of Anaphylaxis that can occur hours later
