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DEENT > Exam 1 Material > Flashcards

Exam 1 Material Flashcards

1
Q

tears

A

coat the conjunctiva and cornea
contains nutrients, enzymes, and immunoglobulins to support and protect the cornea

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2
Q

POAG glaucoma

A

usually gradual until visual field loss occurs
obstructed trabecular meshwork
drainage canal blocked

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3
Q

PACG

A

connected with shape of the eye
medical emergency
significant pain
quickly decrease IOP
pressure pushes iris against cornea, blocking trabecular meshwork
iris and lens stick together

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4
Q

B receptor antagonists for glaucoma MOA

A

block the beta-2 adrenoceptor on the ciliary body

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5
Q

B receptor antagonists for glaucoma pharm action

A

reduce aqueous production by the ciliary body (decrease inflow)
not much effect on outflow

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6
Q

Nonspecific B-blocking agents for glaucoma

A

timolol
levobunolol

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7
Q

relatively B1-selective agent glaucoma

A

betaxolol

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8
Q

nonspecific blocker with intrinsic sympathomimetic activity for glaucoma

A

caretolol

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9
Q

B receptor antagonists for glaucoma side effects

A

ocular
-sting and burning, decreased corneal sensitivity, diplopia, blurred or cloudy vision, decreased night vision, and ptosis
systemic
-cardiac: bradycardia and hypotension
-respiratory: bronchospasm in asthmatics
headache, insomnia, taste perversion, depression, impotence

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10
Q

a2 agonists for glaucoma MOA

A

bind to a2 rec on the ciliary body
binds to the uveosclera

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11
Q

a2 agonists for glaucoma pharm effect

A

decreases rate of aqueous humor production (decrease inflow)
some increase in uveoscleral outflow
neuroprotective

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12
Q

a2 agonists for glaucoma

A

apraclonidine
brimonidine

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13
Q

apraclonidine side effects

A

ocular-burning and stinging, blurred vision, foreign body sensation, ocular pruritus
systemic-hypotension, oral dryness, allergic rxns

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14
Q

brimonidine side effects

A

ocular-foreign body sensation and ocular pruritus
systemic-oral dryness, dizziness, fatigue, somnolence, reduction in blood pressure and pulse
more systemic SE

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15
Q

carbonic anhydrase inhibitors for glaucoma MOA

A

prevents the conversion of CO2 and water to carbonic acid
reduces availability of sodium and bicarbonate for secretion

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16
Q

carbonic anhydrase inhibitors for glaucoma pharm effect

A

decreases ciliary body aqueous humor secretion (decrease inflow)

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17
Q

oral carbonic anhydrase inhibitors for glaucoma

A

acetazolamide
methazolamide

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18
Q

ophthalmic carbonic anhydrase inhibitors for glaucoma

A

dorzolamide
brinzolamide

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19
Q

carbonic anhydrase inhibitors for glaucoma side effects

A

ocular: burning or stinging, hypersensitivity, headache, bitter, sour, or unusual taste, dry eye, foreign body sensation, and blurred vision
oral: altered taste and smell, dry mouth, excessive thirst, increased urination, systemic acidosis, and depression

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20
Q

M3 agonists for glaucoma

A

carbachol
pilocarpine

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21
Q

AChE inhibitor for glaucoma

A

echothiophate

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22
Q

M3 agonists for glaucoma MOA

A

agonist at M3 receptor on sphincter muscle and trabecular meshwork

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23
Q

M3 agonists for glaucoma pharm effect

A

contraction of the sphincter muscle and trabecular meshwork increase outflow
opens meshwork

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24
Q

M3 agonists for glaucoma side effects

A

ocular: burning and stinging, painful ciliary muscle spasm->headache, blurred vision, myopia, poor vision in dim light, increased visibility of floaters and lacrimation
systemic: diarrhea, salivation, sweating, and rhinorrhea

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25
Q

AChE inhibitor for glaucoma MOA

A

irreversible acetylcholinesterase inhibitor
increase of acetylcholine

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26
Q

AChE inhibitor for glaucoma pharm effect

A

contraction of the sphincter muscle and trabecular meshwork (increase outflow)

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27
Q

AChE inhibitor for glaucoma side effects

A

ocular: burning and stinging, blurred vision, eye pain, lacrimation, headache, brow-ache, twitching of eyelids
systemic: diarrhea, salivation, sweating, and rhinorrhea

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28
Q

prostaglandin agonists for glaucoma

A

bimatoprost
latanoprost
latanoprostene bunod
travaprost
tafluprost

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29
Q

prostaglandin agonists for glaucoma MOA

A

agonist at the PFG2a receptor causing relaxation of the ciliary muscle

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30
Q

prostaglandin agonists for glaucoma pharm effect

A

reduces IOP by increasing uveoscleral and trabecular outflow of aqueous humor (increase outflow)
does NOT affect aqueous humor production
may be more effective in hazel/brown colored eyes than blue/green

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31
Q

prostaglandin agonists for glaucoma side effects

A

blurred vision, burning and stinging, eye pain lid edema and ocular hyperemia
increased brown pigmentation of iris and eyelids
hypertrichosis and hyperpigmentation of lashes
hair growth in other areas
few systemic side effects

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32
Q

rho kinase inhibitor for glaucoma

A

netarsudil

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33
Q

rho kinase inhibitor for glaucoma pharm effect

A

increases outflow

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34
Q

rho kinase inhibitor for glaucoma side effects

A

conjunctival hyperemia-vasodilation
corneal vericillate; did not change vision
instillation site pain
conjunctival hemorrhage

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35
Q

combo products for glaucoma

A

timolol and dorzolamide
timolol and brimonidine
brinzolamide and brimonidine

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36
Q

histamine

A

released from storage granules as a result of the interaction of antigen with IgE antibodies on the mast cell surface
immediate hypersensitivity and allergic rxns

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37
Q

effects of histamine release

A

itching and stimulates secretion from nasal mucosa
contracts smooth muscles-bronchi and gut
relaxes other smooth muscles-small blood vessels
stimulus of gastric acid secretion
edema and stimulation of sensory nerve endings

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38
Q

ophthalmic antihistamines for allergic conjunctivitis MOA

A

H1 inverse agonists
mast cell stabilization

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39
Q

H1 inverse agonists

A

reduce constitutive activity of receptor and compete with histamine binding to the receptor

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40
Q

mast cell stabilization

A

reduces release of mast cell mediators during an allergic response
anti-inflammatory prop, reducing cytokine secretion, decreased adhesion molecule expression, and inhibition of eosinophil infiltration

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41
Q

ophthalmic antihistamines for allergic conjunctivitis pharm action

A

reduce the symptoms of an allergic rxn such as edema, itch, inflammation, and watery eyes

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42
Q

ophthalmic antihistamines for allergic conjunctivitis

A

alcaftadine
azelastine
bepotastine
cetirizine
epinastine
ketotifen
olopatadine

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43
Q

alcaftadine

A

H1 antagonist and mast cell stabilization
H4 receptor antagonism
v little anticholinergic activity
little penetration into CNS
low incidence of side effects

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44
Q

azelastine

A

H1 antagonist and mast cell stabilization
also as nasal spray for allergic rhinitis

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45
Q

bepotastine

A

H1 antagonist and mast cell stabilizer

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46
Q

cetirizine

A

H1 antagonist
has minimal anticholinergic effects
negligible CNS penetration, but still causes drowsiness

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47
Q

epinastine

A

H1 antagonist and mast cell stabilization
H2 antagonist, which may reduce eyelid edema

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48
Q

ketotifen

A

H1 antagonist and mast cell stabilizer

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49
Q

olopatadine

A

H1 antagonist and mast cell stabilization
also as nasal spray

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50
Q

ophthalmic decongestants for allergic conjunctivitis MOA

A

adrenergic (alpha) receptor agonist

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51
Q

ophthalmic decongestants for allergic conjunctivitis pharm action

A

vasoconstrictors for local application to the nasal mucous membrane or the eye
reduces redness

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52
Q

a2 agonists for ophthalmic decongestants

A

naphazoline
oxymetazoline
tetrahydrozoline
brimonidine tartrate

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53
Q

ophthalmic antihistamine/decongestant combo for allergic conjunctivitis

A

naphazoline/pheniramine

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54
Q

ophthalmic mast cell stabilizers for allergic conjunctivitis pharm effect

A

prevents release of inflammatory and constricting mediators like histamine, leukotrienes, cytokines, and degradative enzymes from activated mast cells
prevents thee allergic event rather than alleviating symptoms

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55
Q

ophthalmic mast cell stabilizers for allergic conjunctivitis

A

cromolyn sodium
nedocromil

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56
Q

ophthalmic mast cell stabilizers for allergic conjunctivitis side effects

A

cromolyn-burning and stinging, dryness and styes
nedocromil-headache, burning/stinging, photophobia

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57
Q

glucocorticoids for allergic conjunctivitis MOA

A

immunosuppression to reduce inflammation

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58
Q

glucocorticoids for allergic conjunctivitis side effects

A

cataracts

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59
Q

glucocorticoids for allergic conjunctivitis products

A

fluorometholone
hydrocortisone
loteprednol
prednisolone Na+ phosphate
rimexolone

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60
Q

dry eye

A

aka keratoconjunctivitis sicca
onset is unpredictable but may correlate with environment (meds)
may present with or without redness of the eyes

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61
Q

risk factors for dry eye

A

increasing age and females

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62
Q

cyclosporine

A

calcineurin inhibitor class immunosuppressant
helps increase tear production

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63
Q

calcineurin inhibitor MOA

A

inhibits production of IL-2 needed for T cell proliferation (which reduces inflammation of eye)

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64
Q

calcineurin inhibitors for dry eye side effects

A

ocular burning, instillation site pain, conjunctival hyperemia, discharge, epiphora, eye pain, foreign body sensation, pruritus, stinging, or visual disturbances

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65
Q

loteprednol

A

anti-inflammatory to treat dry eye
corticosteroid

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66
Q

LFA-1 antagonist for dry eye MOA

A

lymphoma function-associated antigen 1 (LFA-1) antagonist
cell surface protein found on leukocytes
blocks interaction with intercellular adhesion molecule-1 (ICAM-1)
may inhibit T cell adhesion to ICAM-1 and secretion of inflammatory cytokines

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67
Q

lifitegrast

A

LFA-1 antagonist for dry eye

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68
Q

lifitegrast side effects

A

application site irritation, reduced visual acuity

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69
Q

intranasal varenicline

A

nicotinic acetylcholine receptor agonist
-increase production of basal tear film
typically for smoking cessation, but can also used for dry eye

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70
Q

intranasal varenicline side effects

A

acquired night blindness, blurred vision, retinal vascular disorder, subcapsular cataract, transient blindness, visual disturbance

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71
Q

cerumenolytics mechanisms

A

hydrate, soften, liquify, or disintegrate cerumen

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72
Q

three types of cerumenolytics

A

water based
oil based
nonwater, nonoil based

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73
Q

water based cerumenolytics

A

cerumenex
colace-docusate sodium
hydrogen peroxide

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74
Q

oil based cerumenolytics

A

olive oil

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75
Q

nonwater, nonoil based cerumenolytics

A

debrox-carbamide peroxide
prepared in diff solvent-glycerol

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76
Q

docusate Na

A

water-based cerumenolytics
surfactant which increases water entry and emulsifies
has both hydrophilic and lipophilic parts

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77
Q

carbamide peroxide

A

debrox
nonwater, nonoil based cerumenolytics
releases H2O2, which generates effervescing O2
effervescence breaks up ear wax

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78
Q

tooth decay causes

A

bacteria forms plaque on teeth and gums
bacteria also converts sugars into acids which erode enamel leading to cavities
acid drinks can also erode enamel

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79
Q

tooth decay prevention

A

fluoride based toothpastes or gels
non-fluoride toothpastes
mouth rinses
cavity treatments

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80
Q

fluoride based toothpastes or gels

A

enamel is made up of hydroxyapatite (vulnerable to acid erosion)
fluoride ions toothpastes convert hydroxyapatite into fluorapaptite which is more resistant to acid erosion

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81
Q

fluoride ions in toothpastes or gels

A

form fluorapatite from hydroxyapatite
enhance mineral deposition (mineralization)
but too much fluoride can cause enamel fluorosis

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82
Q

non-fluoride toothpastes

A

abrasives/pH modifiers/remineralizers
sodium bicarbonate
nanohydroxyapatite
calcium sodium phosphosilicate (CSPS)
amorphous calcium phosphate (ACP)

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83
Q

sodium bicarbonate

A

abrasive and mouth pH elevating agent

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84
Q

nanohydroxyapatite (10% nHA)

A

small crystals which bond to hydroxyapatite

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85
Q

calcium sodium phosphosilicate (CSPS)

A

bioactive glass that reacts with oral fluids to deposit crystalline hydroxycarbonate apatite (HCA)

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86
Q

amorphous calcium phosphate (ACP)

A

reactive salt mixture that releases Ca and PO4 ions to remineralize enamel upon contact with salvia

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87
Q

mouth rinses

A

for plaque/gingivitis/bad breath/tooth decay/pain management
chlorhexidine gluconate
cetylpyridinium chloride
fluoride
NaHCO3
carbamide peroxide
thymol/eucalyptol/methyl salicylate/menthol
benzocaine

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88
Q

chlorhexidine gluconate

A

mouth rinses
bisbiguanide salt
bind to cell wall and disrupt its integrity

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89
Q

cetylpyridinium chloride

A

mouth rinse
pyridinium salt

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90
Q

fluoride mouth rinse

A

promote remineralization and prevent caries

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91
Q

NaHCO3 mouth rinse

A

increase saliva pH
decrease growth of acidic bacteria

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92
Q

carbamide peroxide mouth rinse

A

for canker cores

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93
Q

benzocaine mouth rinse

A

anesthetic agent

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94
Q

thymol/eucalyptol/methyl salicylate/menthol mouth rinse

A

listerine

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95
Q

teeth whitening

A

whiteners remove stains
range from abrasives to H2O2 bleaching agents
carbamide peroxides and hydrogen peroxides

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96
Q

alpha2 agonists chem

A

aryl imidazolines
decrease inflow and increase outflow
clonidine
apraclonidine
brimonidine tartrate

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97
Q

SAR for alpha2 agonists

A

X=CH2; alpha1 receptor agonists
X=NH2; alpha2 receptor agonists

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98
Q

beta antagonists chem

A

aryloxypropanolamine
decrease inflow
timolol, betaxolol, levobunolol, caretolol

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99
Q

SAR of beta antagonists

A

aryloxypropanolamine is more potent that arylethanolamines
most have mixed B1+B2 activities
S-OH isomers are preferred
most p-aryloxypropanolamine are B1 antagonists

100
Q

carbonic anhydrase (CA) inhibitor chem

A

Zn-metalloenzyme which modulates aqueous humor production through pH changes
increases pH
sulfonamides-inhibits CA to decrease inflow
acetazolamide, methazolamide, brinzolamide, dorzolamide

101
Q

carbonic anhydrase (CA) inhibitor metabolism

A

undergo CYP N-deethylation to active metabolites
ionic interactions with Zn, glutamic, NH2, threonine

102
Q

direct acting cholinergics chem

A

increases outflow
carbamates and esters
carbachol, pilocarpine

103
Q

direct acting cholinergics SAR

A

acyloxy group for H bonding to nicotinic/muscarinic receptors (non-selective)
ionizable amine (N) group
N-methyl groups
2-C spacer btwn O and N

104
Q

indirect acting cholinergics

A

organophosphate
echothiophate iodide-irreversible

105
Q

extent of AChE inhibition depends on the FG present

A

phosphoryl>carbamate> ester

106
Q

prostaglandins chem

A

all increase outflow via FP or PGF2a receptor activation
prodrug activation via esterase

107
Q

prostaglandins SAR

A

carboxylic acids and amides are active drugs
esters are prodrugs
C-15=OH or halogens (prevents 15-OH oxidation)

108
Q

rho kinase (ROCK) inhibitors chem

A

isoquinolines
netarsudil
increases outlofw
an ester prodrug

109
Q

a1/a2 agonists decongestants chem

A

aryl imdiazoline
oxymetazoline, xylometazoline, tetrahydrometazoline, naphazoline

110
Q

mast cell stabilizers chem

A

chromone and oxamic acid
inhibit granule histamine release from mast cells
ionized/ionizable FG
locally active

111
Q

dual acting agents (antihistamines + mast cell stabilizing) chem

A

multicyclic
ionizable FGs

112
Q

glucocorticoid steroids chem

A

activate the GR complex to produce proteins which in turn suppress pro-inflammatory protein
a-face away
B-face towards you
hydrocortisone, dexamethasone

113
Q

glucocorticoid steroids SAR

A

anti-inflammatory activity is increased by
-double bond btwn C1 and C2
-6a-F
11B-OH

114
Q

risk factors POAG

A

older age
family history of glaucoma
high IOP
use of corticosteroids
African descent

115
Q

clinical presentation POAG

A

remains asymptomatic until severe with vision loss and decreased quality of life from lack of ability to perform daily activities
early intervention is essential to slow progression of disease

116
Q

first line therapy for POAG

A

prostaglandins
some contain BAK preservative and some don’t
once daily dosing
reduces IOP by 33%
better 24 hr IOP control
good tolerance
lower cost

117
Q

side effects of prostaglandins

A

blurred vision, stinging, burning, elongation and darkening of eyelashes, induced iris darkening, periocular skin pigmentation

118
Q

contraindications for prostaglandins

A

macular edema
history of herpetic keratitis

119
Q

second line or preferred adjunctive for POAG

A

ophthalmic beta blockers
timolol, levobunolol, carteolol, bexatolol
reduces 20-30% may use initial monotherapy if prostaglandins CI or not tolerated
good tolerance

120
Q

ophthalmic beta blockers side effects

A

stinging on application, dry eyes, blepharitis, blurred vision, decreased HR and BP, bronchospasm, cardiac effects

121
Q

ophthalmic beta blockers precaution

A

asthma/COPD
bradycardia/heart block
advanced heart disease
heart failure
on PO B-blocker therapy

122
Q

ophthalmic beta blockers product selection

A

adverse effect potential
-more systemic SE with non-selective agents
-rapidly absorbed into systemic circulation
individual patient response
cost

123
Q

adjunctive therapy for POAG

A

alpha2-adrenergic agonists
-brimonidine
-apraclonidine

124
Q

alpha2 agonists can also be used to

A

increase IOP postoperative or post-laser treatment

125
Q

why are alpha2 agonists adjunctive

A

moderate IOP reduction
-10-27%
freq: every 8-12 hrs

126
Q

alpha2 agonists side effects

A

lid edema, eye discomfort, foreign-object sensation, itching, dizziness, fatigue, somnolence, dry mouth, slight BP or HR reduction

127
Q

alpha2 agonist precaution

A

advanced CV diseases
renal compromise
history of stroke
diabetes
taking blood pressure lowering agents, MAOIs, and TCAs

128
Q

Last lines for POAG

A

topical carbonic anhydrase inhibitors
oral carbonic anhydrase inhibitors

129
Q

why are topical carbonic anhydrase inhibitors last line

A

IOP reduction: 15-26%
freq: every 8-12 hr

130
Q

topical carbonic anhydrase inhibitors side effects

A

burning, stinging, ocular discomfort, blurred vision, tearing
minimal systemic SEs

131
Q

why are oral carbonic anhydrase inhibitors last line

A

IOP reduction: 25-40%
intolerable adverse effects: topical first, no combo of oral and topical together, often used for short-term admin to lower IOP

132
Q

oral carbonic anhydrase inhibitors side effects

A

older adults do NOT tolerate CAIs as well as younger patients
A LOT of systemic SEs
systemic acidosis

133
Q

carbonic anhydrase inhibitors precaution

A

sulfa allergies (cross sensitivity is v low)
sickle cell disease
pulmonary disorders
electrolyte imbalance

134
Q

Last last line for POAG

A

cholinergic agonists (miotic agents)
pilocarpine
carbachol
echothiophate

135
Q

why are cholinergic agonists last last line for POAG

A

poor tolerance
frequent dosing-every 6 hrs
side effects

136
Q

cholinergic agonists (miotic agents) side effects

A

burning, stinging, blurred vision upon application, eyebrow ache, may precipitate acute angle-closure glaucoma
excessive sweating, nausea, vomiting, diarrhea, cramping, bronchospasm, heart block

137
Q

rho-kinase (ROCK) inhibitor

A

rhopressa
-triple mechanism for lowering IOP
conjunctival hyperemia->relatively high number of discontinuation rates and adverse events

138
Q

novel combo agent: rocklatan

A

prostaglandin and ROCK inhibitor
IOP reduction of 30% or greater

139
Q

follow up on POAG

A

4-6 weeks after therapy initiation
every 3-4 months once target IOP are achieved

140
Q

refrigerate before opening; once opened, store at room temp medication

A

latanoprost
lataoprostene bunod
tafluprost

141
Q

refrigerate before opening; once opened, store at room temp for < 6 weeks medication

A

netarsudil

142
Q

drugs that can increase IOP (POAG)

A

ophthalmic corticosteroid (high risk)
systemic corticosteroids
nasal/inhaled corticosteroids
ophthalmic anticholinergics

143
Q

intolerance of medications for POAG

A

reduce conc (if possible)
change formulations
switch to alternative class

144
Q

combigan

A

brimonidine tartrate/timolol
alpha2 agonist/B-blocker

145
Q

cosopt

A

dorzolamide/timolol
CAI/B-blocker

146
Q

simbrinza

A

brinzolamide/brimonidine
CAI/alpha2 agonist

147
Q

nonpharm interventions for POAG

A

surgical and laser treat

148
Q

PACG risk factors

A

females
older
Asian (Southeast Asian)
first degree relatives of patients

149
Q

management of acute PACG

A

medical emergency->ER to avoid blindness

150
Q

management of chronic PACG

A

laser surgery

151
Q

exclusions of self-treatment for ocular disorders

A

eye pain, ocular trauma, chem exposure, eye exposure to heat, blurred vision, light sensitivity, signs and symptoms of eyelid infection, except stye
untreated symptoms that persist over 72 hrs

152
Q

conjunctivitis

A

inflammation of the conjunctiva
most are viral
self-limiting

153
Q

allergic conjunctivitis

A

pink/red/clear, itchy, watery, bilaterally
inflammatory response to allergens (pollen, animal dander, and other environmental antigens)

154
Q

nonpharm treatment of allergic conjunctivitis

A

allergic avoidance
cold or warm compresses (3-4 times daily)
contacts should NOT be worn
common: pollen, mold, dust mites, pet dander

155
Q

preferred treatment for allergic conjunctivitis

A

artificial tears as needed-symptomatic relief

156
Q

after artificial tears, what do you give for allergic conjunctivitis

A

ophthalmic antihistamine/mast cell stabilizer/histamine type 1 antagonist
-olopatadine
-ketotifen

157
Q

after antihistamine/mast cell stabilizers, what do you use for allergic conjunctivitis

A

decongestants/alpha agonists
naphazoline
oxymetazoline
tetrahydrozoline
brimonidine

158
Q

adverse events of decongestants/alpha agonists

A

ocular dryness, which can exacerbate the symptoms
rebound congestion

159
Q

decongestants/alpha agonists contraindications

A

pregnancy
angle-closure glaucoma

160
Q

decongestants/alpha agonists precautions

A

HTN
CV disease
diabetes

161
Q

after decongestants/alpha agonists, what do you give for allergic conjunctivitis

A

2nd gen oral antihistamine
if symptoms persist with topical AH/mast cell stabilizer
loratadine, fexofenadine, cetrizine

162
Q

medical referral allergic conjunctivitis

A

if symptoms do NOT resolve after 72 hr of appropriate treatment

163
Q

viral conjunctivitis

A

self-limiting within 1-2 weeks
does NOT require treatment
detected with high sensitivity and specificity

164
Q

clinical presentation of viral conjunctivitis

A

highly contagious
pink eyes with amounts of watery discharge and crusting
presents unilateral and progresses to bilateral

165
Q

nonpharm treatment of viral conjunctivitis

A

hand washing
cold compresses
avoid sharing towels or objects
multi-dose eye drops, make up and other products
contact lens use should be avoided

166
Q

pharm treatment of viral conjunctivitis

A

no effective treatment
artificial tears, cold compresses, and ocular antihistamines->refer if no improvements occur within 7-10 days
AVOID topical steroids as they could worsen and prolong the infection unless corneal inflammation

167
Q

when to refer for viral conjunctivitis

A

no improvements occur within 7-10 days

168
Q

bacterial conjunctivitis

A

least common
transmitted btwn individuals or may result from abnormal proliferation of conjunctival bacterial flora
risk factors: dry eye, immunosuppression, or trauma

169
Q

risk factors for bacterial conjunctivitis

A

dry eye, immunosuppression, or trauma

170
Q

clinical presentation of bacterial conjunctivitis

A

unilateral or bilateral red eye
bilateral matting or crusting and sticking

171
Q

when to refer for bacterial conjunctivitis

A

if no improvements occur within 7 days or if topical antibiotics may be indicated

172
Q

referrals for ocular stuff should be made when

A

visual loss
moderate or severe pain
severe purulent discharge
photophobia
corneal inflammation
lack of response to therapy within 1 week
recurrent episodes of conjunctivitis
history herpes simplex viral eye disease

173
Q

dry eye

A

aging
discomfort and visual disability
acute cases: elimination of exacerbating factors
chronic: gets worse
can use artificial tears, but need referral

174
Q

risk factors of dry eye

A

older
female

175
Q

clinical presentation of dry eye

A

excessive tearing
foreign body sensation->gritty feeling
itching, irritation, and soreness with or without redness
intermittent blurred vision
symptoms are often worse at the end of the day

176
Q

treatment of blepharitis

A

scrub eyelids at the base of lash with a cotton swab dipped in baby shampoo, tea tree oil
apply warm compresses as necessary

177
Q

pharm treatment of dry eye

A

ocular lubricants

178
Q

ocular lubricants

A

drops>ointments
1-2x daily

179
Q

ophthalmic preservatives

A

benzalkonium chloride (BAK)
chlorhexidine
methyparaben
propylparaben
purite
thimerosal

180
Q

hordeolum

A

eyelid gland infection
tender to touch
palpable, tender, nodule present
eyelid swelling
lid redness

181
Q

chalazion

A

noninfectious granuloma located near, but NOT on the eyelid
NOT tender to the touch

182
Q

treatment of hordeolum and chalazion

A

warm compresses for 5-10 min 3-4x daily
stye may be treated with topical antibiotic ointment

183
Q

referral for hordeolum and chalazion

A

if the nodule does NOT drain after 1 week

184
Q

recurrent aphthous stomatitis (RAS)

A

canker sores
precipitated by stress and local trauma
peak onset: 10-19

185
Q

clinical presentation of recurrent aphthous stomatitis (RAS)

A

sores appear on nonkeratinized mucosa
ulcers are painful, rounded, flat, or crater-like lesions
range from gray to yellow with red halo of inflamed tissue
prodome may occur 24-48 hrs prior to when the ulcers appear
may inhibit normal daily activities
self-resolves in 10-14 days

186
Q

recurrent aphthous stomatitis (RAS) exclusions of self care

A

lesions > 14 days or if associated underlying pathology
frequent recurrence
symptoms of systemic illness (fever, swollen lymph nodes, malaise)
failure of prior self-care treatment

187
Q

recurrent aphthous stomatitis (RAS) nonpharm treatment

A

increase nutrients
eliminate offending food
avoid spicy/acidic foods
recommend bland foods
ice every 10 min
avoid toothpastes
stress reduction

188
Q

topical anesthetics

A

for recurrent aphthous stomatitis (RAS)
provide short term relief of the pain
-benzocaine
use with oral debriding agents

189
Q

oral debriding and wound cleansing agents

A

for recurrent aphthous stomatitis (RAS)
carbamide peroxide
hydrogen peroxide
up to 4x daily for NO > 7->black hairy tongue

190
Q

topical oral protectants

A

for recurrent aphthous stomatitis (RAS)
canker cover (menthol)
-disc placed against sore
coal and protect the area and provide relief
3-4x daily after meals, avoid drinking 30 min after

191
Q

oral rinses

A

recurrent aphthous stomatitis (RAS)
helps quickly heal ulcers
-listerine
helps sooth
-saline rinses

192
Q

systemic analgesics for recurrent aphthous stomatitis (RAS)

A

NSAIDs or tylenol for extra relief of pain

193
Q

referral to PCP recurrent aphthous stomatitis (RAS)

A

if symptoms do not abate after 7 days with agents
lesions do not heal in 14 days
symptoms worsen
systemic infection

194
Q

tooth hypersensitivity

A

loss of enamel or gingival recession
dentin tubules must be open to both oral cavity and the pulp
short, sharp pain results when stimuli touch exposed dentin, which stimulates the underlying nerves

195
Q

risk factors of tooth hypersensitivity

A

regular consumption of acidic beverages
whitening products
teeth clenching or grinding
excessive brushing with hard bristled toothbrush
regurgitation of gastric contents into the mouth (GERD)
orthodontal or periodontal procedures

196
Q

clinical presentation of tooth hypersensitivity

A

pain from hot, cold, sweet, or acidic beverages, or hot or cold air
pain varies from mild discomfort to sharp, excruciating pain
self-treatable

197
Q

toothache

A

bacterial invasion
pain that remains even in the absence of stimulus; intermittent, short, and sharp pain on stimulation may indicate reversible pain
continuous, dull, and throbbing pain without stimulation usually indicates irreversible damage

198
Q

tooth hypersensitivity: exclusions for self-care

A

toothache
fever or swelling
trauma to the mouth with bleeding, swelling, and soreness
loose teeth
bleeding gums
broken or knocked out teeth
severe tooth pain triggered or worsened by hot, cold, or chewing
mouth soreness from dentures

199
Q

nonpharm treatment of tooth hypersensitivity

A

eliminate predisposing factors-minimize consumption of acidic food or drinks
minimize symptoms of GERD-avoid larges, fattening meals/acidic or spicy foods
correct harsh toothbrushing-soft bristled toothbrush

200
Q

pharm treatment of tooth hypersensitivity

A

desensitizing toothpaste

201
Q

contraindication of desensitizing toothpaste

A

products containing potassium nitrate 5% are not recommended in children < 12 years->fluroride toothpaste

202
Q

referrals for tooth hypersensitivity

A

after 4 weeks if symptoms do NOT resolve with treatment
or if symptoms worsen

203
Q

relief of tooth hypersensitivity

A

takes several days to weeks

204
Q

do NOT recommend tooth hypersensitivity

A

eugenol (oil of cloves)
topical anesthetics

205
Q

teething discomfort

A

emergence of baby teeth through tissues
normal process
occurs over an 8 day period with each tooth

206
Q

clinical presentation of teething discomfort

A

reddening, irritation, mild pain, low grade fever, gum swelling, drooling, sleep disturbances
eruption cysts->LEAVE ALONE

207
Q

exclusions of self care for teething discomfort

A

vomiting, diarrhea, fever >101, nasal congestion, malaise, pain

208
Q

nonpharm treatment of teething discomfort

A

massage gums
cold (NOT frozen) teething rings
cold wet cloth
dry toast or teething biscuits
avoid foods high in sucrose

209
Q

pharm treatment for teething discomfort

A

AVOID unless nonpharm treatments do not provide adequate relief
acetaminophen: 10-15 mg/kg/dose every 4-6 hrs as needed
ibuprofen: 5-10 mg/kg/dose every 6-8 hrs

210
Q

when to refer to PCP for teething discomfort

A

do not resolve in 3-5 days of treatment or if pain worsens or new symptoms develop

211
Q

do NOT recommend teething discomfort

A

topical anesthetics->toxicity (methemoglobenemia) and death

212
Q

monitor and evaluate of teething discomfort

A

evaluate in 2 days of treatment

213
Q

herpes simplex labialis (HSL)

A

cold sores
caused by HSV-1
once host is infected, the virus undergoes periods of latency, but the host is infected for life

214
Q

common triggers of herpes simplex labialis (HSL)

A

stress, fatigue, cold, windburn, UV radiation, injury, fever, infections, or immunosuppression

215
Q

clinical presentation of herpes simplex labialis (HSL)

A

prodrome
HSL lesions
lips/border of lips
painful, small, red papules of fluid
if pus or pustules appear under crust, secondary infection should be considered and treated
may be surrounded in a red border

216
Q

exclusions for herpes simplex labialis (HSL)

A

no previous diagnosis of a cold sore
lesions present > 14 days
increased freq of outbreaks
immunocompromised
symptoms of systemic infection
recurrance

217
Q

nonpharm treatment of herpes simplex labialis (HSL)

A

keep lesions clean (warm water and mild soap)
wash hands
apply lip balm
avoid triggers

218
Q

pharm treatments of herpes simplex labialis (HSL)

A

topical analgesics
topical antivirals
OTC triple antibiotic (secondary bacterial infection)
systemic analgesics (NSAIDs, tylenol)

219
Q

topical analgesics for herpes simplex labialis (HSL)

A

relieve burning, itching, and pain
does NOT reduce duration of symptoms
use after meals
safe and effective products: benzocaine, camphor, or menthol
avoid eating or drinking for at least 30 minutes after application

220
Q

contraindication of topical analgesics for herpes simplex labialis (HSL)

A

> 1% menthol bc its a counterirritant

221
Q

topical antivirals for herpes simplex labialis (HSL)

A

docosanol 10%
-reduce duration and severity of HSL symptoms
-prevents viral replication
5 times daily for up to 10 days

222
Q

complimentary therapy herpes simplex labialis (HSL)

A

tea tree oil
lysine
lemon balm

223
Q

do NOT recommend herpes simplex labialis (HSL)

A

topical steroids
highly astringent products
zinc sulfate

224
Q

monitor and evaluate of herpes simplex labialis (HSL)

A

immunocompetent patients
-HSL is mild and self-limiting
-healing of lesions 10-14 days
referral to PCP

225
Q

referral to PCP for herpes simplex labialis (HSL)

A

lesions do NOT heal in 14 days
self-treatment measures do not relieve discomfort
signs or symptoms of systemic illness
symptoms change or worsen

226
Q

clinical presentation of xerostomia (dry mouth)

A

difficulty talking or swallowing
burning tongue
loss of sense of taste and appetite
decline in nutritional status
thrush
halitosis
stomatitis
tooth hypersensitivity
increased risk of dental caries

227
Q

xerostomia (dry mouth) exclusions

A

sjogren’s syndrome or salivary gland stone
bleeding and swelling +/-trauma
loose teeth or tooth erosion/decay
mouth soreness due to poor fitting dentures/reduced denture wearing time
presence of fever and swelling of lymph nodes
candidiasis/gingivitis/periodontitis
severe tooth pain triggered or worsened by hot, cold, or chewing

228
Q

xerostomia (dry mouth) nonpharm

A

discontinue meds and other substances that reduce salivation: tobacco, caffeine, hot spicy foods, alcohol; or take 1 hr prior to meals
maintain good oral hygiene
chew sugar free gum
increase water intake, especially if it is fluoridated
humidifiers-some relief
use soft bristle toothbrushes

229
Q

xerostomia (dry mouth) pharm treatment

A

artificial saliva products-NOT cure, replacement therapy

230
Q

xerostomia (dry mouth) referral

A

should occur if improvement is NOT seen within 7 days of treatment

231
Q

monitor and evaluate for xerostomia (dry mouth)

A

evaluation after 5-7 days of self-treatment
mouth dryness lessened
-continue using artificial saliva and fluoride products
-continue nonpharm
dryness becomes worse or additional symptoms of complications develop
-referral to PCP for further evaluation

232
Q

self treatment restricted of otic disorders

A

external disorders-auricle
external auditory canal (EAC)

233
Q

risk factors for cerumen excess or impaction

A

narrow or irregularly shaped ECAs
excessive hair growth in the ear canal
irritation from foreign objects
atrophy of ceruminous glands (older adults)
genetics

234
Q

clinical presentation for cerumen excess or impaction

A

fullness/pressure, mild, dull pain, chronic cough, gradual hearing loss, vertigo, tinnitus, impaired cognition (older adults)

235
Q

exclusions for self care for cerumen excess or impaction and water clogged ears

A

severe pain
signs of infection or ear discharge (irrigation or rash)
bleeding or signa of trauma
presence of ruptured tympanic membrane
tympanostomy tube(s) present
ear surgery within 6 weeks
<12 years of age
worsening of condition after attempted self-treatment

236
Q

nonpharm treatments of cerumen excess or impaction

A

may self-resolve in mild cases
remove cerumen by using a wet, wrung out wash cloth draped over a finger to prevent impact
DO NOT USE:
cotton swabs, Q tips, or other foreign objects

237
Q

treatment for cerumen excess or impaction

A
  1. cerumen softening agent
  2. follow with irrigating the ear canal with an otic bulb and warm water
  3. referral if no improvement is seen within 4 days of treatment or if worsening occurs
238
Q

cerumen softening agents

A

carbamide peroxide
others are least effective

239
Q

carbamide peroxide

A

2x daily for up to 4 days
intended use: children > 12 years

240
Q

water clogged ears

A

excessive moisture within the EAC

241
Q

risk factors for water clogged ears

A

physical or anatomic changes within EAC
-excessive hair growth and canal narrow->excessive ear wax or debris build up
excessive moisture from sweating, swimming, bathing or hot, humid climate

242
Q

clinical presentation of water clogged ears

A

feeling of wetness, fullness, gradual hearing loss, may lead to tissue maceration that can cause itching, pain, inflammation, or infection

243
Q

water clogged ears nonpharm treatment

A

pull on ear to get water out
blow dry
clear ears-will not prevent water from entering

244
Q

pharm treatment of water clogged ears

A

isopropyl alcohol 95% in anhydrous glycerin 5%: swim ear
no mini age

245
Q

referral for PCP for water clogged ears

A

after 4 days

DEENT (4 decks)

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