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Ocular Pharm > Exam One Misc Facts and important info > Flashcards

Exam One Misc Facts and important info Flashcards

1
Q

what are the two qualifiers that need to be met in order for a drug to become generic

A
  1. bioequivalency standards ( must contain same active ingredient, same dosage form, admin by same route )
  2. must have comparable bioavailability ( rate and extent of drug absorption and delivery to site of action must be equivalent )
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2
Q

Rx for controlled substances are NOT to exceed 7 days: no refills and no new Rx without exam..T or F

A

T

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3
Q

what are schedule 1 drugs

A

not commercially available ( marijuana) we don’t rx schedule 1

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4
Q

what are schedule 2 drugs

A

examples like codeine, morphine, oxycodone, hydrocodone, and cocaine ( in many states ODs cant Rx hydrocodone)

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5
Q

what are schedule 3 drugs

A

aspirin and Tylenol with codeine

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6
Q

what are schedule IV drugs

A

tramadol and diazepam

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7
Q

what are schedule V drugs

A

lyrica

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8
Q

what does q.h.s stand for

A

at bedtime

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9
Q

T or F: Always use a zero before the decimal pt

A

T

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10
Q

T or F: Always write a zero by itself after a decimal pt

A

F: Never do that

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11
Q

this type of antagonist will compete with the agonist in order to bind to the receptor; this antagonist will displace the agonist

A

competitive agonist

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12
Q

this antagonist will bind to the receptor and will remain bound to the receptor so that the agonist can no longer bind at all

A

irreversible antagonist

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13
Q

know how to calculate the 1/2 life of a drug

A

remember its the time it takes for one half of the drug to be eliminated

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14
Q

what is the normal tear film volume

A

8-10 uL

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15
Q

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

A

30 uL

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16
Q

how much is a typical ophthalmic drop and where does the excess fluid go

A

50 uL: drains through the nasolacrimal duct, absorbed through the nasal mucosa or swallowed , drains over the lid margins to the face ( wasted)

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17
Q

T or F: 20 drops = 1.0 mL

A

T

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18
Q

what is the tip size limit

A

25 uL

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19
Q

what are the three techniques to maximize the effect of each drop

A

Fraunfelder “ pouch” technique, looking down, punctal occlusion

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20
Q

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

A

fraunfelder “ pouch technique

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21
Q

this technique involves closing the eye and applying gentle pressure over the lacrimal sac

A

punctal occlusion

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22
Q

what are some hurdles in dosing of the anterior segment

A

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

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23
Q

what kind of drugs penetrate the corneal epithelium

A

lipophilic drugs ; this resists drugs like Flourescein ( hydrophilic)

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24
Q

T or F: Flourescein is hydrophilic

A

T

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25
Q

what kind of drugs penetrate the corneal stroma

A

hydrophilic drugs

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26
Q

this kind of drug is an inactive compound that gets activated in the body to its active compound

A

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

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27
Q

how do you get max therapeutic effect of a drug

A

increase drug concentration ( higher concentration or fortified Ab), more frequent dosing , loading dose , residence time

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28
Q

these drugs are compounded from injectable strength Ab

A

fortified Ab

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29
Q

with drug delivery kinetics what happens when you are above the therapeutic range

A

we aren’t getting any increased effect but will have toxicity

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30
Q

what happens with drug delivery kinetics when you go into the subtherapeutic range

A

re-drop

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31
Q

what is the goal of drug delivery kinetics

A

to keep people within the therapeutic window

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32
Q

what is used to reach the eff. concentration sooner

A

loading dose

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33
Q

how can you increase the residence time of the drug

A

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

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34
Q

how do you store solutions and suspensions

A

in the fridge which reduces bacterial growth

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35
Q

what does “chilling “ the bottle do

A

reduces sting

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36
Q

what are some instillation techniques for kids

A

drop in closed eyes - open and goes in nasal canthus or spray with open or closed eyes

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37
Q

this type of medication has a green cap

A

miotic

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38
Q

this type of medication has a red cap

A

Mydriatic/cycloplegic

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39
Q

this type of medication has a brown cap

A

Antibiotic

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40
Q

this type of medication has a grey cap

A

NSAID

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41
Q

this type of medication has a yellow cap

A

0.5% beta blocker

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42
Q

this type of medication has a light blue cap

A

0.25% beta blocker

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43
Q

this type of medication has a has a purple cap

A

alpha agonist

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44
Q

this type of medication has a teal/clear cap

A

prostaglandin analogue

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45
Q

this type of medication has a orange cap

A

CAI

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46
Q

what are the diff routes of admin.

A

topical ( solutions and suspensions, ointments and fels, lid therapy/scrubs, solid delivery devices, continuous flow devices), periocular admin., intraocular admin. , parenteral admin., oral admin.

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47
Q

this is a solid in a liquid - always transparent and light passes through; no shaking required

A

solution

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48
Q

this is a solid in a liquid; cloudy mixture of two or more substances that settle on standing ; need to shake

A

suspension

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49
Q

this is a liquid in a liquid ; includes emulsions; intermediate / hybdir between a solution and suspension ; these are cloudy; does not need shaking

A

colloid

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50
Q

what is a steroid emulsion that is now available

A

Durezol

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51
Q

what are advantages of ophthalmic ointments

A

longer contact time, gradual melt and nasolacrimal drainage, pediatric pts, tx with patching

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52
Q

what are the disadvantages of ointments

A

blurred vision, limited # conc. available, ointments block the absorption of another drop, increased contact time for allergic reactions

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53
Q

when is ointment CI

A

in jagged or flap like corneal lacerations ( ok for superficial abrasions), corneal ulcers , and can interfere with other topical meds

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54
Q

this is an ointment/eyedrop hybrid; its thicker so it increases retention time, may blur vision temporarily, timed release type effect, apply qhs usually

A

gels

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55
Q

what is a newer gel ; upon dosing, the gel becomes a viscous liquid ; does not require shaking

A

lotemax

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56
Q

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

A

ReSure corneal sealant gel

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57
Q

T or F: Lid scrubs are good for blepharitis and recalcitrant blepharitis

A

T

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58
Q

what is a way to tx MGD

A

heat and hot soak compresses , anti inflammatory Tx ( topical and oral )- doxycycline and omega 3 FAs

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59
Q

what is the ocusert delivery device

A

uses pilocarpine ; replaced every 7 days , inserted on the sclera

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60
Q

what is lacrisert

A

solid delivery device ; slow release artificial tear ; apply to inferior sac and it melts throughout the day

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61
Q

what is the morgan lens

A

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

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62
Q

what are some periocular admin

A

subconj, sub tenons, retrobulbar

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63
Q

can you do subconj injection for corneal ulcer

A

yes : for non compliance

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64
Q

what is the most common injection

A

subconj; obtain high local conc.

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65
Q

why are subconj inje. indicated

A

for drugs that penetrate cornea poorly, pts that don’t reliably use topical meds ; used as new tx for glaucoma

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66
Q

what can you do retrobulbar injections for

A

anesthetics ( in cat sx) , corticosteroids , and alcohol

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67
Q

what are the diff types of intraocular injections

A

intravitreal and intracameral

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68
Q

what is the intravitreal inj

A

posterior segment, usually anti VEGF and implants like vitrasert and steroids

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69
Q

what are intracameral inj

A

used for anterior seg

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70
Q

what are the parenteral route of injections

A

subcutaneous, intramuscular, and intravenous

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71
Q

Which drugs are CI in cardiovascular disease

A

adrenergics

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72
Q

which drugs are CI in diabetes

A

corticosteroids

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73
Q

which drugs are CI in pregnancy

A

almost all except mild topicals

74
Q

which drugs are CI in asthma and stevens Johnson syndrome

A

stevens johnsone- sulfacetamide and asthma ( Timolol)

75
Q

what is Youngs Rule for Pediatric Dosage

A

Adult dose x ( age of child / age of child +12 )

76
Q

what is clarks rule for ped. dosage

A

adult dose x (wt in kg / 70) OR adult dose x ( wt in lbs/ 150)

77
Q

T or F: Child weight in lbs/ 2.2= wt in kg

A

T

78
Q

what is the combo for the ped. cyclo spray

A

15 ml sol of 0.5% cyclopentolate, 2.5% phenyl, and 0.5% tropicamide

79
Q

T or F: one spray = 105 ul or about 1 drop

A

F : one spray =n 105 ul or 2 drops

80
Q

this is an obligate ic org.; depends on host cell for multiplication controlled by response ot pts immune system

A

virus

81
Q

how do viruses invade the host cell

A

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

82
Q

this virus is from STD, mainly affects cornea/lid and lips

A

herpes simplex

83
Q

this virus is periocular, causes ocular uveitis, herpes zoster

A

varicella zoster ( herpes zoster)

84
Q

this virus is adenoviral, EKC, PCF

A

adenoviral keratoconjunctivitisi

85
Q

this virus is retinal assoc with immune compromise

A

CMV

86
Q

this virus effects the lacrimal gland / dacryoadenitis

A

Epstein barr virus

87
Q

this infection is systemic- flu like symptoms ; assoc with follicular conjunctivitis and vesicles on eyelid or periorbital skin

A

HSV 1

88
Q

this Herpes virus is typically above the belt

A

HSV 1 ( oral “ cold sore) , ocular, or latent in trigeminal nerve

89
Q

This herpes virus is below the belt

A

HSV II ( genital, STD, can be transmitted to eye , neonatal)

90
Q

at primary resolution where does the HSV reside

A

trigeminal ganglion

91
Q

what are some triggers for reactivation of HSV

A

trauma, immunosuppression, sunlight, stress/illness, menstration, PRK, laser Sx, Prostaglangin analogs

92
Q

what is recurrent HSV keratitis

A

HSV I or II; viruses produced in trigeminal nerve- sensory nerves to cornea infect epithelial cells ; will have dendritic pattern

93
Q

signs and symptoms with Recurrent HSV

A

pain , photophobia, PA noes, corneal hypoesthesia , conj. hyperemia, corneal keratitis -> stellate-> dendritic

94
Q

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

A

varicella ( chickenpox)

95
Q

T or F: highest incidence of VZV is in the US

A

T

96
Q

what % of adults aged >40 are at risk for Zoster bc they have had chickenpox

A

99.5%

97
Q

what % of zoster pts suffer from ophthalmic zoster

A

10-25%

98
Q

where does the VZV virus est latency

A

dorsal root ganglion

99
Q

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

A

HZO

100
Q

what are the Sub and Obj, findings of HZO

A

S: facial pain, fever, malaise

O: vesicular skin rash along dist. of ophthalmic and maxillary ; respects midline; tip of nose = hutchinsons sign ( eye)

101
Q

what does VZV target

A

neurons, T lymphocytes, and epithelial cells of the skin

102
Q

what is the incubation period of adenovirus

A

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

103
Q

tx options for adenovirus

A

no Antivirals are “approved:” ; can take topical steroids to improve signs and symptoms

104
Q

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

A

betadine: povidine- iodine

105
Q

this is usually yeasts or molds; has nucleus and DNA; rigid cell wall of chitin ; cell membrane made of ergosterol

A

fungi

106
Q

what are the most common yeast infections of the eyes

A

candida, and cryptococcus

107
Q

what are the most common mold infections of the eye

A

aspergillus, fusarium, curvularia, acremonium, and microsporidium

108
Q

these are protozoans, infections from it are tough to treat; they like to hang around water sources

A

acanthamoeba

109
Q

what are the two life forms of acanthamoeba

A

trophozite stage ( active form under favorable conditions) and the cyst stage ( harsh conditions)

110
Q

what is a ring infiltrate

A

usually made by an acanthamoeba infection when it has been around for a long time

111
Q

whats the ribosomal makeup of a bacterial cell

A

large subunit is 50S and small subunit is 30S; total 70S

112
Q

T oF: bacterial cell contains DNA, ribosomes, and a plasma membrane, cell wall

A

T

113
Q

what is contained in the bacterial cell wall that provides structural integrity

A

peptidoglycan ( carb backbone of alternating NAM and NAG bonded by a beta 1,4 glycosidic linkage , contains aa attached to NAM)

114
Q

what are the two types of cell walls

A

gram positive and gram negative ( if the cell wall takes the stain= gram positive , if it doesn’t take stain = gram negative )

115
Q

this type of bacterial cell has an outer lipid membrane ( LPS) in the cell wall that prevents the stain from entering the cell

A

gram negative

116
Q

this type of bacterial cell has a thick peptidoglycan cell wall that can take up the purple stain ; these bacteria also have lipoteichoic acid

A

gram positive

117
Q

these type of bacteria are gram positive

A

cocci : staph aureus and epidermis ; streptococcus : pneumoniae, Pyogenes, viridans

118
Q

these type of bacteria are gram negative

A

cocci: Neisseria- gonorrhoeae and meningitides, Moraxella catarrhalis
coccobacillus - Haemophilus species
bacilli: pseudomonas, proteus mirabilis, enteric rods

119
Q

example of spirochete bacteria

A

Treponema pallidum ( syphilis)

120
Q

example of chlamydia

A

chlamydia trachomatis

121
Q

example of actinomycetes

A

actinomyces israelii

122
Q

this term means to kill bacteria

A

bactericidal

123
Q

this is the min. concentration of drug which can kill 99.9% of the population

A

min. bactericidal concentration

124
Q

what are some bactericidal agents

A

PCN, cephalosporin, aminoglycosides, flouroquinolones, bacitracin

125
Q

this term means to slows the growth of bacteria

A

bacteriostatic

126
Q

this the min. concentration of drug which can inhibit the growth of bacteria

A

min. inhibitory concentration

127
Q

what are some bacteriostatic agents

A

tetracyclines, erythromycins, trimethoprims, and sulfa

128
Q

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

A

bacterial resistance

129
Q

what are the 4 diff ways bacteria can become resistant

A
  1. bacteria alter the target site to reduce or block binding of Ab
  2. bacteria produce an enzyme that destroys/ inactivates an Ab
  3. bacteria actively transport the Ab out of the cell
  4. bacteria prevent entry of the Ab into the cell
130
Q

T or F: Do not taper AB

A

T

131
Q

T or F: LOW MIC = potent drug

A

T

132
Q

If MIC is higher, what does that mean

A

the bacteria is resistant to the drug ( bc it takes more drug to kill the bacteria )

133
Q

what were the findings of the OCular Trust Study ( 200-2006)

A

it evaluated antimicrobial susceptibility of Staph Aureus to diff Ab; Trimethoprim found to have high activity against MRSA

134
Q

MRSA is 50% susceptible to which drug

A

tobramycin

135
Q

What were the findings of the ARMOR study ( 2009- present);

A

Antiobiotic Resistance Monitoring in OCular Microorganisms; designed to continue the efforts of the Ocular trust study

136
Q

what is the gold standard for MRSA

A

vancomycin ( new is besifloxacin)

137
Q

what are the main tx options for MRSA

A

vancomycin, trimethoprim, Besivance, and tobramycin

138
Q

what is the MOA of antimicrobials

A

impacts cell wall, DNA synthesis, protein synthesis, and cell membrane

139
Q

this is the sum of the hosts defenses to infectious or noxious stimuli

A

inflammation

140
Q

what are the features of inflammation

A

rubor, tumor ( swelling), calor, dolor, loss of function

141
Q

what is the inflammatory response pathway

A
  1. cells in the tissue become damaged
  2. pathogens invade
  3. complement proteins release cytokines, increases bv permeability, induces mast cells to release histamine, attracts WBCs to site
  4. kinins increase bv permeability, vasodilation and activate phospholipase A
142
Q

what is the enzyme involved with the inflammatory process

A

phospholipase A2

143
Q

what do the leukotrienes do

A

cause bronchoconstriction and increase vascular permeability

144
Q

what do the COX1 do

A

cytoprotective prostaglandins that protect the gastric mucosa, renal protection and aid platelet aggregration

145
Q

what do the COX 2 do

A

these are inflammatory prostaglandins that increase vascular permeability and recruit inflammatory cells ; sensitize skin pain receptors ; fever

146
Q

these cells secrete factors that kill and degrade pathogens and also remove pathogens by phagocytosis

A

neutrophils

147
Q

these remove pathogens by phagocytosis and secrete cytokines to attract other immune cells to the site and initiate tissue repair

A

monocytes

148
Q

what are the local hormones produced in inflammation

A

arachidonic acid ( FA) which goes to Leukotrienes, COX 1 and COX 2

149
Q

MOA of steroids

A

they inhibit phospholipase A2 so the local hormones cannot be produced to cause inflammation

150
Q

this category of steroids controls reabsorption of inorganic ions by the kidney ie corticosterone, aldosterone

A

mineralocorticoids

151
Q

this category of steroids reduces the inflammatory response ; produced naturally by the adrenal gland

A

glucocorticoids

152
Q

this is the main/ principle glucocorticoid hormone

A

cortisol

153
Q

SE of steroids

A

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

154
Q

when are steroids CI

A

infectious, Diabetes, HTN , CHF, osteoporosis, peptic ulcer disease, chronic renal failure, pregnancy, cushings disease

155
Q

what are the ketone based steroids

A

prednisolone, dexamethasone, fluourmetholone, difluprednate

156
Q

what are the ester based steroids

A

loteprednol ( less SE than other steroids) has a chloromethyl ester in place where the ketone would be

157
Q

T or F: loteprednol is site specific

A

T : broken down in the cornea and anterior chamber

158
Q

a steroid response to increased IOP is an increase > 10 mm Hg .. T or F

A

T- usually you add an IOP lowering med to the steroid tx ( ie Timolol which decreases aqueous production) -

159
Q

this is the DOC for steroid responders

A

Loteprednol

160
Q

what are the three analgesic meds mechanisms to manage acute ocular pain

A
  1. anesthetic agents
  2. peripherally acting agents ( NSAIDS and Aspirin)
  3. Centrally acting opioids ( Vicodin and Percocet)
161
Q

these initiate pain signal

A

nociceptors ( anesthetics work on the nociceptors)

162
Q

these are involved with Na blockade of peripheral nerves

A

anesthetics

163
Q

these are peripheral acting agents; they block the generation of the pain signal by inhibiting synthesis of PGE2

A

NSAIDS and ASA

164
Q

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

A

opioids ( they block the perception of and emotional response to pain)

165
Q

these peripheral acting analgesics inhibit COX1 and COX2

A

NSAIDS

166
Q

these sensitize the nociceptors

A

prostaglandins

167
Q

indications for topical NSAIDS

A

allergies sometimes, pain control ( ie abrasions), cystoid macular edema

168
Q

what is the diff between dry and wet ARMD

A

dry has drusen ( means there is no blood 90% of cases) and wet has choroidal neovascular membranes ( there is blood)

169
Q

whats a huge risk factor for ARMD

A

smoking

170
Q

what is drusen

A

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

171
Q

What did they find in the age related eye disease study 1

A

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

172
Q

What was the alteration to the AREDS2 study

A

lutein and zeaxanthin was also added and tested ; done to see if beta carotene and zinc were necessary

173
Q

what are the main carotenoids found in human retina

A

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

174
Q

what were the results of AREDS2

A

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

175
Q

AREDS1 vs AREDS2

A

recommend AREDS2 for dry ARMD; beta carotene removed and replaced with L/Z instead ; reduced Zn levels …less GI upset

176
Q

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

A

Anti Vegf Agents ( ie. Macugen , Avastin, Lucentis, EYelea);

177
Q

MOA of Anti Vegf

A

ANti VEGF agents bind to free floating VEGF molecules to prevent attachment of VEGF to endothelial surface receptors responsible for the neovascular growth signal

178
Q

clinical duration of action of anti vegf?

A

up to 4-10 weeks

179
Q

what is the treat and extend approach for anti vegf

A

monthly injections until dry; inject again on dry exam; extend out 2 wks ; if recurrence, tx then reduce FU by 2 wk

180
Q

what does VEGF cause

A

neovascularization, vascular migration, and increased capillary permeability

Ocular Pharm (3 decks)

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