Exam One Misc Facts and important info Flashcards
what are the two qualifiers that need to be met in order for a drug to become generic
- bioequivalency standards ( must contain same active ingredient, same dosage form, admin by same route )
- must have comparable bioavailability ( rate and extent of drug absorption and delivery to site of action must be equivalent )
Rx for controlled substances are NOT to exceed 7 days: no refills and no new Rx without exam..T or F
T
what are schedule 1 drugs
not commercially available ( marijuana) we don’t rx schedule 1
what are schedule 2 drugs
examples like codeine, morphine, oxycodone, hydrocodone, and cocaine ( in many states ODs cant Rx hydrocodone)
what are schedule 3 drugs
aspirin and Tylenol with codeine
what are schedule IV drugs
tramadol and diazepam
what are schedule V drugs
lyrica
what does q.h.s stand for
at bedtime
T or F: Always use a zero before the decimal pt
T
T or F: Always write a zero by itself after a decimal pt
F: Never do that
this type of antagonist will compete with the agonist in order to bind to the receptor; this antagonist will displace the agonist
competitive agonist
this antagonist will bind to the receptor and will remain bound to the receptor so that the agonist can no longer bind at all
irreversible antagonist
know how to calculate the 1/2 life of a drug
remember its the time it takes for one half of the drug to be eliminated
what is the normal tear film volume
8-10 uL
how much tear film volume can be held after given a drop if the lids are not squeezed and the cul de sac is utilized
30 uL
how much is a typical ophthalmic drop and where does the excess fluid go
50 uL: drains through the nasolacrimal duct, absorbed through the nasal mucosa or swallowed , drains over the lid margins to the face ( wasted)
T or F: 20 drops = 1.0 mL
T
what is the tip size limit
25 uL
what are the three techniques to maximize the effect of each drop
Fraunfelder “ pouch” technique, looking down, punctal occlusion
this technique involves pulling on the inferior lid to form a “pouch” , instilling the drop, having the pt close their eyes and look down ( turn cornea inferiorly), and punctal occlude
fraunfelder “ pouch technique
this technique involves closing the eye and applying gentle pressure over the lacrimal sac
punctal occlusion
what are some hurdles in dosing of the anterior segment
tears ( dilute the medication and also flushes it down the drainage system or out of the eye to the cheek,) the cornea is a barrier bc you need a biphasic nature for the drug to penetrate , and aqueous humor is always being filtered through the TM
what kind of drugs penetrate the corneal epithelium
lipophilic drugs ; this resists drugs like Flourescein ( hydrophilic)
T or F: Flourescein is hydrophilic
T
what kind of drugs penetrate the corneal stroma
hydrophilic drugs
this kind of drug is an inactive compound that gets activated in the body to its active compound
pro drug ( ie, increase penetration of cornea, propine penetrates cornea 10x as readily as parent compound epinephrine) and ( ie, enters cornea /anterior chamber and is then transformed into an active form like ZIrgan
how do you get max therapeutic effect of a drug
increase drug concentration ( higher concentration or fortified Ab), more frequent dosing , loading dose , residence time
these drugs are compounded from injectable strength Ab
fortified Ab
with drug delivery kinetics what happens when you are above the therapeutic range
we aren’t getting any increased effect but will have toxicity
what happens with drug delivery kinetics when you go into the subtherapeutic range
re-drop
what is the goal of drug delivery kinetics
to keep people within the therapeutic window
what is used to reach the eff. concentration sooner
loading dose
how can you increase the residence time of the drug
put in a punctal plug which can jam up the puncta and prevent tears from flowing out of the eye keeping the drop in longer, or punctal occlusion
how do you store solutions and suspensions
in the fridge which reduces bacterial growth
what does “chilling “ the bottle do
reduces sting
what are some instillation techniques for kids
drop in closed eyes - open and goes in nasal canthus or spray with open or closed eyes
this type of medication has a green cap
miotic
this type of medication has a red cap
Mydriatic/cycloplegic
this type of medication has a brown cap
Antibiotic
this type of medication has a grey cap
NSAID
this type of medication has a yellow cap
0.5% beta blocker
this type of medication has a light blue cap
0.25% beta blocker
this type of medication has a has a purple cap
alpha agonist
this type of medication has a teal/clear cap
prostaglandin analogue
this type of medication has a orange cap
CAI
what are the diff routes of admin.
topical ( solutions and suspensions, ointments and fels, lid therapy/scrubs, solid delivery devices, continuous flow devices), periocular admin., intraocular admin. , parenteral admin., oral admin.
this is a solid in a liquid - always transparent and light passes through; no shaking required
solution
this is a solid in a liquid; cloudy mixture of two or more substances that settle on standing ; need to shake
suspension
this is a liquid in a liquid ; includes emulsions; intermediate / hybdir between a solution and suspension ; these are cloudy; does not need shaking
colloid
what is a steroid emulsion that is now available
Durezol
what are advantages of ophthalmic ointments
longer contact time, gradual melt and nasolacrimal drainage, pediatric pts, tx with patching
what are the disadvantages of ointments
blurred vision, limited # conc. available, ointments block the absorption of another drop, increased contact time for allergic reactions
when is ointment CI
in jagged or flap like corneal lacerations ( ok for superficial abrasions), corneal ulcers , and can interfere with other topical meds
this is an ointment/eyedrop hybrid; its thicker so it increases retention time, may blur vision temporarily, timed release type effect, apply qhs usually
gels
what is a newer gel ; upon dosing, the gel becomes a viscous liquid ; does not require shaking
lotemax
this is a kit that seals the corneal incision like glue ; the kit comes as two liquid solutions that the surgeon mixes together ; within 20 sec of applying the liquid to eye tissue, a gel forms that adheres to the eye and seals the incision ; gel breaks over 7 days
ReSure corneal sealant gel
T or F: Lid scrubs are good for blepharitis and recalcitrant blepharitis
T
what is a way to tx MGD
heat and hot soak compresses , anti inflammatory Tx ( topical and oral )- doxycycline and omega 3 FAs
what is the ocusert delivery device
uses pilocarpine ; replaced every 7 days , inserted on the sclera
what is lacrisert
solid delivery device ; slow release artificial tear ; apply to inferior sac and it melts throughout the day
what is the morgan lens
continuous flow device; continuous irrigation system ; Cls hooked up to a saline drip ; fluid comes down through the hose and the Cls is placed onto the eye -> provides continuous infusion
what are some periocular admin
subconj, sub tenons, retrobulbar
can you do subconj injection for corneal ulcer
yes : for non compliance
what is the most common injection
subconj; obtain high local conc.
why are subconj inje. indicated
for drugs that penetrate cornea poorly, pts that don’t reliably use topical meds ; used as new tx for glaucoma
what can you do retrobulbar injections for
anesthetics ( in cat sx) , corticosteroids , and alcohol
what are the diff types of intraocular injections
intravitreal and intracameral
what is the intravitreal inj
posterior segment, usually anti VEGF and implants like vitrasert and steroids
what are intracameral inj
used for anterior seg
what are the parenteral route of injections
subcutaneous, intramuscular, and intravenous
Which drugs are CI in cardiovascular disease
adrenergics
which drugs are CI in diabetes
corticosteroids
which drugs are CI in pregnancy
almost all except mild topicals
which drugs are CI in asthma and stevens Johnson syndrome
stevens johnsone- sulfacetamide and asthma ( Timolol)
what is Youngs Rule for Pediatric Dosage
Adult dose x ( age of child / age of child +12 )
what is clarks rule for ped. dosage
adult dose x (wt in kg / 70) OR adult dose x ( wt in lbs/ 150)
T or F: Child weight in lbs/ 2.2= wt in kg
T
what is the combo for the ped. cyclo spray
15 ml sol of 0.5% cyclopentolate, 2.5% phenyl, and 0.5% tropicamide
T or F: one spray = 105 ul or about 1 drop
F : one spray =n 105 ul or 2 drops
this is an obligate ic org.; depends on host cell for multiplication controlled by response ot pts immune system
virus
how do viruses invade the host cell
virions invade the host cell- they take over metabolic machinery- they produce new viral nucleic acid and capsid protein coat- and the host cell releases new virus to infect other cells
this virus is from STD, mainly affects cornea/lid and lips
herpes simplex
this virus is periocular, causes ocular uveitis, herpes zoster
varicella zoster ( herpes zoster)
this virus is adenoviral, EKC, PCF
adenoviral keratoconjunctivitisi
this virus is retinal assoc with immune compromise
CMV
this virus effects the lacrimal gland / dacryoadenitis
Epstein barr virus
this infection is systemic- flu like symptoms ; assoc with follicular conjunctivitis and vesicles on eyelid or periorbital skin
HSV 1
this Herpes virus is typically above the belt
HSV 1 ( oral “ cold sore) , ocular, or latent in trigeminal nerve
This herpes virus is below the belt
HSV II ( genital, STD, can be transmitted to eye , neonatal)
at primary resolution where does the HSV reside
trigeminal ganglion
what are some triggers for reactivation of HSV
trauma, immunosuppression, sunlight, stress/illness, menstration, PRK, laser Sx, Prostaglangin analogs
what is recurrent HSV keratitis
HSV I or II; viruses produced in trigeminal nerve- sensory nerves to cornea infect epithelial cells ; will have dendritic pattern
signs and symptoms with Recurrent HSV
pain , photophobia, PA noes, corneal hypoesthesia , conj. hyperemia, corneal keratitis -> stellate-> dendritic
this is a virus characterizied by febrile illness and crops of pruritic maculopapular and vesicular lesions ; lesions begin on the scalp, face, or trunk , vesicles crust over and slough with healing ; virus becomes latent
varicella ( chickenpox)
T or F: highest incidence of VZV is in the US
T
what % of adults aged >40 are at risk for Zoster bc they have had chickenpox
99.5%
what % of zoster pts suffer from ophthalmic zoster
10-25%
where does the VZV virus est latency
dorsal root ganglion
this is an infection of CN5 ganglia by VZV- chicken pox/shingles ( dormant in trigeminal ganglia) ; its a reactivation of VZV; cutaneous rash with small blisters , painful and reactivation via immunosuppresions
HZO
what are the Sub and Obj, findings of HZO
S: facial pain, fever, malaise
O: vesicular skin rash along dist. of ophthalmic and maxillary ; respects midline; tip of nose = hutchinsons sign ( eye)
what does VZV target
neurons, T lymphocytes, and epithelial cells of the skin
what is the incubation period of adenovirus
8 days; then you begin to get red eye with some SPK and for about 2 wks you are infectious ; the immune system ramps up to fight the virus so you will have infiltrates that manifest themselves in the cornea as white spots
tx options for adenovirus
no Antivirals are “approved:” ; can take topical steroids to improve signs and symptoms
this is an iodine based antiseptic that is found in first aid kits. It kills fungi, bascteria, and viruses. Can be used off label in a wash with pts that are affected severly with Adenovirus
betadine: povidine- iodine
this is usually yeasts or molds; has nucleus and DNA; rigid cell wall of chitin ; cell membrane made of ergosterol
fungi
what are the most common yeast infections of the eyes
candida, and cryptococcus
what are the most common mold infections of the eye
aspergillus, fusarium, curvularia, acremonium, and microsporidium
these are protozoans, infections from it are tough to treat; they like to hang around water sources
acanthamoeba
what are the two life forms of acanthamoeba
trophozite stage ( active form under favorable conditions) and the cyst stage ( harsh conditions)
what is a ring infiltrate
usually made by an acanthamoeba infection when it has been around for a long time
whats the ribosomal makeup of a bacterial cell
large subunit is 50S and small subunit is 30S; total 70S
T oF: bacterial cell contains DNA, ribosomes, and a plasma membrane, cell wall
T
what is contained in the bacterial cell wall that provides structural integrity
peptidoglycan ( carb backbone of alternating NAM and NAG bonded by a beta 1,4 glycosidic linkage , contains aa attached to NAM)
what are the two types of cell walls
gram positive and gram negative ( if the cell wall takes the stain= gram positive , if it doesn’t take stain = gram negative )
this type of bacterial cell has an outer lipid membrane ( LPS) in the cell wall that prevents the stain from entering the cell
gram negative
this type of bacterial cell has a thick peptidoglycan cell wall that can take up the purple stain ; these bacteria also have lipoteichoic acid
gram positive
these type of bacteria are gram positive
cocci : staph aureus and epidermis ; streptococcus : pneumoniae, Pyogenes, viridans
these type of bacteria are gram negative
cocci: Neisseria- gonorrhoeae and meningitides, Moraxella catarrhalis
coccobacillus - Haemophilus species
bacilli: pseudomonas, proteus mirabilis, enteric rods
example of spirochete bacteria
Treponema pallidum ( syphilis)
example of chlamydia
chlamydia trachomatis
example of actinomycetes
actinomyces israelii
this term means to kill bacteria
bactericidal
this is the min. concentration of drug which can kill 99.9% of the population
min. bactericidal concentration
what are some bactericidal agents
PCN, cephalosporin, aminoglycosides, flouroquinolones, bacitracin
this term means to slows the growth of bacteria
bacteriostatic
this the min. concentration of drug which can inhibit the growth of bacteria
min. inhibitory concentration
what are some bacteriostatic agents
tetracyclines, erythromycins, trimethoprims, and sulfa
this is when bacteria that were initially susceptible to an Ab become resistant to the action of the drug-makes it harder to eliminate infections as existing drugs become less effective
bacterial resistance
what are the 4 diff ways bacteria can become resistant
- bacteria alter the target site to reduce or block binding of Ab
- bacteria produce an enzyme that destroys/ inactivates an Ab
- bacteria actively transport the Ab out of the cell
- bacteria prevent entry of the Ab into the cell
T or F: Do not taper AB
T
T or F: LOW MIC = potent drug
T
If MIC is higher, what does that mean
the bacteria is resistant to the drug ( bc it takes more drug to kill the bacteria )
what were the findings of the OCular Trust Study ( 200-2006)
it evaluated antimicrobial susceptibility of Staph Aureus to diff Ab; Trimethoprim found to have high activity against MRSA
MRSA is 50% susceptible to which drug
tobramycin
What were the findings of the ARMOR study ( 2009- present);
Antiobiotic Resistance Monitoring in OCular Microorganisms; designed to continue the efforts of the Ocular trust study
what is the gold standard for MRSA
vancomycin ( new is besifloxacin)
what are the main tx options for MRSA
vancomycin, trimethoprim, Besivance, and tobramycin
what is the MOA of antimicrobials
impacts cell wall, DNA synthesis, protein synthesis, and cell membrane
this is the sum of the hosts defenses to infectious or noxious stimuli
inflammation
what are the features of inflammation
rubor, tumor ( swelling), calor, dolor, loss of function
what is the inflammatory response pathway
- cells in the tissue become damaged
- pathogens invade
- complement proteins release cytokines, increases bv permeability, induces mast cells to release histamine, attracts WBCs to site
- kinins increase bv permeability, vasodilation and activate phospholipase A
what is the enzyme involved with the inflammatory process
phospholipase A2
what do the leukotrienes do
cause bronchoconstriction and increase vascular permeability
what do the COX1 do
cytoprotective prostaglandins that protect the gastric mucosa, renal protection and aid platelet aggregration
what do the COX 2 do
these are inflammatory prostaglandins that increase vascular permeability and recruit inflammatory cells ; sensitize skin pain receptors ; fever
these cells secrete factors that kill and degrade pathogens and also remove pathogens by phagocytosis
neutrophils
these remove pathogens by phagocytosis and secrete cytokines to attract other immune cells to the site and initiate tissue repair
monocytes
what are the local hormones produced in inflammation
arachidonic acid ( FA) which goes to Leukotrienes, COX 1 and COX 2
MOA of steroids
they inhibit phospholipase A2 so the local hormones cannot be produced to cause inflammation
this category of steroids controls reabsorption of inorganic ions by the kidney ie corticosterone, aldosterone
mineralocorticoids
this category of steroids reduces the inflammatory response ; produced naturally by the adrenal gland
glucocorticoids
this is the main/ principle glucocorticoid hormone
cortisol
SE of steroids
immunosuppression, increased blood glucose and bp, osteoporosis, gastritis, kidney stones, weight gain, redist. of fat to face, back of the neck, and abdomen, increased IOP , cataracts
when are steroids CI
infectious, Diabetes, HTN , CHF, osteoporosis, peptic ulcer disease, chronic renal failure, pregnancy, cushings disease
what are the ketone based steroids
prednisolone, dexamethasone, fluourmetholone, difluprednate
what are the ester based steroids
loteprednol ( less SE than other steroids) has a chloromethyl ester in place where the ketone would be
T or F: loteprednol is site specific
T : broken down in the cornea and anterior chamber
a steroid response to increased IOP is an increase > 10 mm Hg .. T or F
T- usually you add an IOP lowering med to the steroid tx ( ie Timolol which decreases aqueous production) -
this is the DOC for steroid responders
Loteprednol
what are the three analgesic meds mechanisms to manage acute ocular pain
- anesthetic agents
- peripherally acting agents ( NSAIDS and Aspirin)
- Centrally acting opioids ( Vicodin and Percocet)
these initiate pain signal
nociceptors ( anesthetics work on the nociceptors)
these are involved with Na blockade of peripheral nerves
anesthetics
these are peripheral acting agents; they block the generation of the pain signal by inhibiting synthesis of PGE2
NSAIDS and ASA
these are central acting meds that act on opioid receptors in the brain - for moderate to severe pain and often in combo with anti inflammatories
opioids ( they block the perception of and emotional response to pain)
these peripheral acting analgesics inhibit COX1 and COX2
NSAIDS
these sensitize the nociceptors
prostaglandins
indications for topical NSAIDS
allergies sometimes, pain control ( ie abrasions), cystoid macular edema
what is the diff between dry and wet ARMD
dry has drusen ( means there is no blood 90% of cases) and wet has choroidal neovascular membranes ( there is blood)
whats a huge risk factor for ARMD
smoking
what is drusen
metabolic debris or waste products that are polluting the local area and leading to degeneration; when the drusen builds up enough it can cause a break in Bruchs membrane and this allows neovascularization of the choroid to occur with leakage
What did they find in the age related eye disease study 1
there is a reduced risk of progression to ARMDS with antioxidants and zinc ; antioxidants + zinc is better than antioxidants or zinc oxide alone ; AMD can be treated or prevented through the use of antioxidant supplements by 25% BUT beta carotene was found to increase risk of lung cancer in smokers so they came up with AREDs2
What was the alteration to the AREDS2 study
lutein and zeaxanthin was also added and tested ; done to see if beta carotene and zinc were necessary
what are the main carotenoids found in human retina
lutein and zeaxanthin - make up macular pigment optical density - pts with lower levels are exposed to more harmful IV blue light increasing risk for ARMD ; these pigments act as filters , absorbing harmful UV/blue light
what were the results of AREDS2
removing beta carotene- no effect, decreasing zinc- no effect, adding lutein/zeaxanthin = no additional bft , omega 2 FA = no additional bft ; overall a 26% reduction in risk for highest risk sub type
AREDS1 vs AREDS2
recommend AREDS2 for dry ARMD; beta carotene removed and replaced with L/Z instead ; reduced Zn levels …less GI upset
these are humanized monoclonal Ab that are poten inhibitors of Anti VegF molecules; used mainly for intravitreal injection into the eyes for diabetic macular edema, wet ARMD, CRVO BRVO assoc macular edema
Anti Vegf Agents ( ie. Macugen , Avastin, Lucentis, EYelea);
MOA of Anti Vegf
ANti VEGF agents bind to free floating VEGF molecules to prevent attachment of VEGF to endothelial surface receptors responsible for the neovascular growth signal
clinical duration of action of anti vegf?
up to 4-10 weeks
what is the treat and extend approach for anti vegf
monthly injections until dry; inject again on dry exam; extend out 2 wks ; if recurrence, tx then reduce FU by 2 wk
what does VEGF cause
neovascularization, vascular migration, and increased capillary permeability
