Ch5: HEENT Flashcards

(180 cards)

1
Q

majority of cases of acute rhinosinusitis is usually caused by…..

A

virus

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2
Q

less than ____% of viral URIs are complicated by acute bacterial rhinosinusitis

A

2%

and the majority will resolve without antimicrobial therapy!!!!

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3
Q

what is acute rhinosinusitis

A

inflammation of the mucosal lining of the nasal passages and paranasal sinuses lasting up to 4 weeks, caused by allergens, environmental irritants, and/or infection (viruses [majority], bacteria, or fungus)

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4
Q

what is acute bacterial rhinosinusitis

A

secondary bacterial infection of the paranasal sinuses, usually following a viral URI. relatively UNCOMMON

Less than 2% of viral URIs are complicated by bacterial infection. and the majority will resolve without antimicrobial therapy

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5
Q

DRSP

A

drug-resistant strep pneumonia

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6
Q

top (3) causative pathogens in ABRS

A
  • Strep pneumoniae (gram-positive)
  • H. influenzae (gram-negative)
  • M. catarrhalis (gram-negative)
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7
Q

in treating ARBS, an antimicrobial activity against gram ______ should be chosen

A

positive and negative

strep pneumoniae = gram pos

H. influenzae and M. catarrhalis = gram neg

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8
Q

do you need a culture of sinus drainage in order to give abx for ABRS?

A

no, empiric therapy knowing the most common causative agents

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9
Q

COMPS mnemonic is for conditions caused by which (2) bacteria

A
  1. Strep pneumonia

2. H. influenzae

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10
Q

Conditions caused by strep pneumonia

A

COMPS

  • conjunctivitis
  • otitis media
  • meningitis
  • pneumonia
  • sinusitis
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11
Q

Conditions caused by H. influenzae

A

COMPS

  • conjunctivitis
  • otitis media
  • meningitis
  • pneumonia
  • sinusitis
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12
Q

1 most common causative agent for acute bacterial rhinosinusitis

A

strep pneumoniae

gram-positive diplococci

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13
Q

strep pneumoniae

gram _____
shape:

A

gram positive

diplococci

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14
Q

% of strep pneumonia in the US that is drug-resistant (DRSP)

A

> 25%

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15
Q

2 most common causative agent of ABRS

A

H. influenzae

gram-negative bacillus

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16
Q

h. influenzae

gram_______
shape:

A

gram negative

bacillus

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17
Q

% of h. influenzae that is penicillin-resistant via production of beta lactamase

A

> 30%

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18
Q

most ______ [abx class] are stable in the presence of bacteria that produce beta-lactamase

A

cephalosporins

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19
Q

bacteria that produce beta lactamase will be…..

A

resistant to penicillins

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20
Q

clauvulanate (e.g., added to amoxicillin to make Augmentin) will neutralize….

A

beta lactamase

making the abx work against otherwise resistant bacteria

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21
Q

3 causative agent of ABRS

A

M. catarrhalis

gram-negative coccus

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22
Q

% of m. catarrhalis that are resistant to penicillins

A

> 90%

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23
Q

conditions caused by m. catarrhalis (2)

A
  • ABRS

- CAP (uncommon)

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24
Q

for whom is it appropriate to prescribe antibiotics with acute rhinosinusitis

A

URI-like symptoms and either:

  • persistent symptoms that are not improving after 10 or more days
  • severe symptoms for >3-4 days (fever >102, purulent nasal discharge, facial pain),
    OR
  • worsening or “double-sickening” (initial improvement followed by worsening with fever, headache, nasal discharge, usually after 5-6 days of illness)
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25
standard viral URI is gone within.....
7-10 days
26
why do you wait 10 days before initiating antibiotic therapy for acute rhinosinusitis?
most acute rhinosinusitis is caused by a VIRUS > viral infections typically last 7-10 days >> if it lasts longer than 10 days, consider a bacterial superinfection
27
Risk factors for antibiotic resistance (5)
MOST COMMON - age <2 or >65yo, daycare attendance - prior systemic antibiotics within the last month (oral or parenteral) LESS COMMON - hospitalization within previous 5 days - comorbidities - immunocompromised
28
how long should you prescribe abx for and when should they feel improvement in ABRS
complete 5-7 days of antibiotic therapy (consider 7-10 days if they have risk factors for resistance) they should experience improvement after 3-5 days
29
if you prescribe abx for ABRS and they have no improvement or worsening symptoms after 3-5 days, what is your next step?
broaden coverage or switch to a different antimicrobial class
30
if you prescribe abx for ABRS and they have no improvement or worsening symptoms after 3-5 days. you then switch antibiotic classes and they report no improvement in another 3-5 days. What is your next step?
- referral to specialist - CT or MRI to investigate non-infectious causes or suppurative complications (e.g., periorbital abscess) - sinus or meatal cultures for pathogen-specific therapy
31
Symptomatic treatment in ABRS
- saline nasal irrigation - intranasal corticosteroids when they are additionally accompanied by allergic rhinitis - abx as indicated
32
intranasal corticosteroids are only useful in ABRS when they have what comorbidity
allergic rhinitis
33
``` the US FDA advises that the adverse effects associated with what antibiotic class generally outweighs the benefits for patients with - acute sinusitis - acute bronchitis - uncomplicated UTI who have other treatment options ```
fluoroquinolones e.g., levofloxacin, ciprofloxacin, moxifloxacin
34
which antibiotic class is NOT recommended in ABRS treatment due to their rising resistance rates
macrolides & TMP-SMZ (Bactrim) e.g., azithromycin, clarithromycin, erythromycin coverage is very poor because azithromycin was incredibly over-used and now most strep pneumo is resistant
35
First line antibiotic therapy for ABRS
amoxicillin-clavulanate (Augmentin) 875/125mg PO BID x5-7 days
36
First & second line antibiotic therapy options for ABRS
FIRST LINE amoxicillin-clavulanate (Augmentin) 875/125mg PO BID x5-7 days amoxicillin-clavulanate (Augmentin) 500/125mg PO TID x5-7 days SECOND LINE amoxicillin-clavulanate (Augmentin) 2000mg/125mg PO BID doxycycline 100mg PO BID doxycycline 200mg PO QD
37
the clavulanate aspect of Augmentin specifically causes this particular side effect
GI upset is really hard on the stomach
38
how high a dose of amoxicillin-clavulanate do you need to overcome resistance in drug-resistant strep pneumo (DRSP)
3-4g (3000-4000mg) per day
39
can doxycycline be used in pregnancy
NO (teeth staining of the child)
40
beta-lactamase inhibitor drug
clavulanate
41
doxycycline in ABRS -- is it better against the gram positive (strep pneumo) or gram negative (h. flu or m. cat) organisms?
does well against the gram NEGATIVES (h. flu and m. cat) does ok against gram POS (strep pneumo), particularly bad if it is a drug-resistant strep pneumo (DRSP)
42
ABRS treatment options if they have an allergy to beta-lactams/penicillins (4)
doxycycline 100mg PO BID doxycycline 200mg PO QD levofloxacin 500mg PO QD x5 days moxifloxacin 400mg PO QD x5 days
43
what is the only advantage the respiratory fluoroquinolones have over doxycycline in ABRS
they have better activity against drug-resistant strep pneumo (DRSP)
44
what are the (3) RESPIRATORY fluoroquinolones
moxifloxacin, gemifloxacin, levofloxacin
45
what are your antibiotic treatment options for folks with ABRS who have failed initial therapy or who are at high risk for antibiotic resistance (3)
amoxicillin-clavulanate (Augmentin) 2000/125mg PO BID (4g total daily - HIGH DOSE) levofloxacin 500mg PO QD moxifloxacin 400mg PO QD
46
only (4) antibiotics we should consider for ABRS
- amoxicillin-clavulanate (Augmentin) - doxycycline (second line) - levofloxacin (last resort) - moxifloxacin (last resort)
47
CYP450 is an example of a ....
drug-metabolizing isoenzyme
48
what is a substrate
a medication or a substance that utilizes a specific enzymatic pathway (e.g., CYP450) to be metabolized and modified in some way such that it can reach the drug site of action and/or be eliminated
49
what % of all prescription drugs are substrates of CYP450 3A4
50% e.g., sildenafil (Viagra), atorvastatin, simvastatin, alprazolam (Xanax), and many many other
50
50% of all prescription drugs are substrates of this isoenzyme....
CYP450 3A4
51
what is a CYP450 inhibitor
blocks the activity of the isoenzyme, limiting substrate excretion >> allows an increase in substrate levels, and possible risk of substrate-induced toxicity
52
erythromycin and clarithromycin are CYP450 3A4 ______
inhibitors
53
clarithromycin + simvastatin = risk for......
statin-induced rhabdomyolysis d/t clarithromycin being a CYP450 inhibitor
54
clarithromycin + alprazolam = risk for.....
sedation and fall risk d/t clarithromycin being a CYP450 inhibitor
55
what is a CYP450 inducer
accelerates the activity of the isoenzyme so that the substrate is pushed out the exit pathway >> reduction of the substrate level
56
St. John's wort is a CYP450 3A4 _______
inducer
57
CYP inducers can lead to [increased vs. reduced] target drug levels
reduced target drug levels >> | diminished therapeutic effect
58
CYP inhibitors can lead to [increased vs. reduced] target drug levels
increased target drug levels >> risk for toxicities
59
St John's Wort + COCs = increased risk for.....
decreased COC efficacy, spotting, contraceptive failure d/t st johns wort being a CYP450 inducer
60
St John's Wort + cyclosporine = increased risk for....
decreased cyclosporine efficacy (organ transplant anti-rejection med)
61
never give this antibiotic to a patient whom you don't know every med that they are on
clarithromycin (CYP450 3A4 inhibitor)
62
what possible condition may occur after resolution of acute otitis media? (common, not considered treatment failure)
serous otitis (otitis media with effusion) the inner ear is filled with fluid that can last days-weeks after resolution of the otitis media infection can caused continued sensation of ear fullness and muffled speech sounds
63
what type of hearing impairment occurs in serous otitis
conductive hearing loss
64
conductive hearing loss is usually [temporary vs. permanent]
temporary
65
sensorineural hearing loss is usually [temporary vs. permanent]
permanent
66
Cause of conductive hearing loss
sound is being blocked by something in the outer ear or middle ear (earwax, foreign object, damaged ear drum, serous otitis media, bone abnormality)
67
Cause of sensorineural hearing loss
inner ear disorder whereby the vestibulocochlear nerve (CN VIII) becomes damaged caused by advancing age, ototoxic medications, immune disorders, trauma
68
ototoxic medications cause _____ hearing loss
sensorineural
69
ear infections cause _____ hearing loss
conductive
70
Weber hearing tests will localized to the side with.....
increased tissue density, consolidation e.g., fluid build-up in acute otitis media
71
Weber test results in conductive vs. sensorineural hearing loss
CONDUCTIVE - buzzing sound will lateralize to the AFFECTED ear, heard louder in the affected ear due to increased tissue density, e.g., fluid build-up SENSORINEURAL - buzzing sound lateralizes to the UNAFFECTED ear, heard better in the unaffected ear; the buzzing sound is heard less well or not at all in the affected ear
72
Rinne test results in conductive vs. sensorineural hearing loss
CONDUCTIVE - Negative: bone conduction heard better than air conduction SENSORINEURAL - Positive or Normal: air conduction is heard better than bone conduction
73
Generally-speaking, treatment options for conductive hearing loss
often self-limiting post-URI, AOM resolution, or cerumen impaction removal rarely, further pharmacological or surgical intervention is needed
74
Generally-speaking, treatment options for sensorineural hearing loss
hearing aids, cochlear implants, expert consultation
75
positive vs. negative Rinne test
POSITIVE = NORMAL (air > bone conduction) NEGATIVE = ABNORMAL (bone > air conduction)
76
what is allergic rhinitis
"asthma in the head" recurrent, inflammatory disease of the upper-airways mediated by IgE (just like asthma) due to genetic and environmental interactions characterized by nasal congestion, rhinorrhea (nasal drainage), sneezing, intraocular and/or nasal itching
77
characteristic of allergic rhinitis, not a common cold or URI
itch
78
first line therapy in any allergic disorder, including allergic rhinitis
allergen avoidance/environmental control patient education to avoid the allergen whenever possible
79
first line MEDICATION therapy in allergic rhinitis
CONTROLLER therapy, not PRN to prevent symptoms and preventing formation of inflammatory mediators FIRST LINE = intranasal corticosteroids high efficacy e. g., fluticasone propionate (Flonase), triamcinolone (Nasarcort AQ) * * both OTC and lower-price SECOND LINE = leukotriene modifiers e.g., Montelukast (Singulair) best as add-on therapy if symptoms are not adequate controlled with intranasal corticosteroids
80
anticipatory guidance for intranasal corticosteroids for allergic rhinitis
cannot expect results for a few days
81
Reliver therapies for acute symptoms of allergic rhinitis (second line to controller therapies)
block the action of histamine, which is a potent inflammatory mediator - 2nd gen oral antihistamines (loratidine [Claritin], cetirizine [Zyrtec], levocetirizine [Xyxal - most potent] * *avoid first-gen like diphenhydramine (Benadryl) due to sedation - intranasal antihistamines (azelastine [Astelin, Astepro]) - ocular antihistamines for allergic conjunctivitis (olopatadine, aezlastine, bepotastine)
82
Most potent of the oral antihistamines for allergic rhinitis
levocetirizine (Xyxal)
83
examples of ocular antihistamines for allergic rhinitis
eyedrops filled with antihistamines - olopatadine (Patanol, Pataday) - azelastine (Optivar) - bepotastine (Bepreve)
84
examples of intranasal antihistamines for allergic rhinitis
- azelastine (Astelin, Astepro)
85
Treatment option for patients with allergic rhinitis refractory to standard therapies
sublingual or injection immunotherapies to reduce IgE production, requires specialty consultation can also consider acupuncuture
86
examples of 2nd-gen oral antihistamines for allergic rhinitis
- loratadine (Claritin) - cetirizine (Zyrtec) - levocetirizine (Xyxal)
87
examples of intranasal corticosteroids for allergic rhinitis
- fluticasone (Flonase) | - triamcinolone (Nasacort AQ)
88
example leukotriene modifier for allergic rhinitis
montelukast (Singulair)
89
WBC that is activated in allergic disorders
eosinophils
90
"dandruff of the eyelids"
blepharoconjunctivitis treat with baby shampoo on a q-tip
91
____ lymph nodes are tender
infected non-tender enlarged notes tend to be infected
92
medical term for canker sore
aphthous stomatitis
93
classic presentation of squamous cell carcinoma of the mouth
painless, persistent oral lesion indurated margins associated nontender firm lymphadenopathy h/o cigarette smoking, h/o HPV 16
94
inhaled corticosteroids puts folks at risk for oral.....
thrush
95
95% of oral cancers are....
squamous cell carcinoma
96
what are the 12 cranial nerves
OOOTTAFAGVAH ``` I = olfactory II = optic III = oculomotor IV = trochlear V = trigeminal VI = abducens VII = facial VIII = acoustic IX = glossopharyngeal V = vagus VI = accessory, spinal VII = hypoglossal ```
97
Risk factors for squamous cell carcinoma of the mouth
STRONG - longstanding HPV, especially HPV16 - tobacco use - alcohol abuse LESS POTENT - male - older age (>55yo)
98
60yo male pt with h/o tobacco use and HPV presents with a painless, ulcerating oral lesion x3 months with immobile, nontender lymphadenopathy to the ipsilateral cervical chain. You suspect...
oral squamous cell carcinoma
99
Function of CN I
olfactory = smell
100
Function of CN II
optic = vision
101
Function of CN III
oculomotor = eyelid and eyeball movement eye movements upward, medial, and downward
102
Function of CN IV
trochlear = innervates the superior oblique, turns eye downwards and laterally eye movements inward and downward
103
Function of CN V
trigeminal = chewing, face and mouth sensation, touch and pain touch the forehead & cheek clench teeth
104
Function of CN VI
abducens = turns eye laterally ability to look to each side
105
Function of CN VII
facial = controls most facial expressions, secretion of tears and saliva, taste smiling, taste for the anterior 2/3 of the tongue
106
Function of CN VIII
acoustic = hearing, equilibrium, sensation
107
Function of CN IX
glossopharyngeal = taste, senses carotid blood pressure taste for posterior 1/3 of the tongue
108
Function of CN X
vagus - senses aortic blood pressure, slows the HR, stimulates digestive organs, defecation, taste
109
Function of CN XI
spinal accessory = controls trapezius and sternocleidomastoid muscles, controls swallowing movements shoulder shrug
110
Function of CN XII
hypoglossal = controls movement of the tongue
111
Tongue movements tests Cranial Nerve....
12 (CN XII) - hypoglossal
112
Shoulder shrug tests Cranial Nerve ....
11 (CN XI) - spinal accessory
113
Facial expresses tests Cranial Nerve....
7 (CN VII) - facial
114
Eye movements in all directions tests Cranial Nerves ....
3 (CN III) - oculomotor 4 (CN IV) - trochlear 6 (CN VI) - abducens
115
Perceiving light sensation to the face tests Cranial Nerve....
5 (V) - trigeminal
116
Sense of smell tests Cranial Nerve....
1 (I) - olfactory
117
Vision tests cranial nerve....
2 (II) - optic
118
Hearing tests Cranial Nerve....
8 (VIII) - acoustic
119
"puff out your cheeks" tests which cranial nerve
CN VII (facial)
120
"shrug your shoulders" tests which cranial nerve
CN XI (spinal accessory)
121
"raise your eyebrows" tests which cranial nerve
CN VII (facial)
122
"do you recognize this scent" tests which cranial nerve
CN I (olfactory)
123
paralysis of cranial nerve VII is called....
bell's palsy
124
does bell's palsy require special imaging or labs for diagnosis
no, clinical diagnosis
125
most appropriate initial therapy for bell's palsy
initiating a short-course of oral corticosteroids -- the sooner initiated, the better the clinical response the longer they have these symptoms without treatment, the poorer the outcome
126
Pt presents with sudden onset of inability to raise his eyebrow or smile on the right side of his face. Additionally reports decreased lacrimation in the right eye and difficulty closing the right eyelid. The rest of the exam is otherwise unremarkable. You suspect....
Bell's palsy (paralysis of cranial nerve VII, aka idiopathic facial paralysis)
127
anticipatory guidance for bell's palsy
short course of oral corticosteroids is first line most folks recover completely over the course of 3 months
128
vital sign of the eye
visual acuity
129
pathology of bell's palsy
acute paralysis of CN VII in the absence of brain dysfunction. cause is largely unknown -- might involve inflammation of the cranial nerve d/t viral infection
130
classic presentation of bell's palsy
sudden onset unilateral facial paralysis including inability to raise the eyebrow or smile on the affected side, decreased lacrimation on the affected side with inability to close the eyelid may be present
131
how do you diagnose bell's palsy
clinical diagnosis based on HPI and physical exam whereby the only abnormality is facial nerve paralysis tests to exclude other conditions may be considered on a case-by-case basis including lyme disease serology, electromyography, neuro imaging only if symptoms do not resolve over time
132
treatment overview for bell's palsy
prompt initiation of systemic oral corticosteroids (PO prednisone) for new-onset. appropriate eye care due to impaired eyelid closure and reduced lacrimation little evidence to support antiviral therapy most patients recover completely in 3 months facial physical therapy is possibly needed if incomplete recovery surgical intervention can be considered to prevent ocular desiccation when facial nerve appears permanently damaged
133
who needs a visual acuity exam and how is it done?
with all comprehensive annual physical examinations of adults or children typically done in the office with a Snellen eye chart Refer to eye care specialist for additional evaluation if they fail the test They should be using their typical visual aid (e.g., glasses) if that is what they normally use
134
with any eye complaint, always do this test.....
visual acuity (Snellen chart) if there is any new onset of visual acuity change, needs referral to specialist
135
triad of symptoms to ALWAYS refer promptly to ophthalmology (invariably something serious)
1. red eye 2. painful eye 3. new onset visual acuity change e.g., acute glaucoma, iritis
136
on fundoscopic eye exam, the arteries should NEVER be _____ than the veins
wider arteries should be smaller, more narrow than the veins
137
normal for the [arteries vs. veins] to be wider and darker on fundoscopic eye exam
veins = wider, darker
138
normal for the [arteries vs. veins] to be narrower, brighter on fundoscopic eye exam
arteries = narrow, brighter
139
the optic disc margins on a normal fundoscopic eye exam should be....
sharp, saucer-shaped optic disc should be towards the nasal portion of the ocular field
140
papilledema findings on fundoscopic exam
caused by increased intracranial pressure pt reports new blind spot in the visual field bulging optic disc (too much intracranial pressure)
141
arteriovenous (AV) nicking findings on fundoscopic exam
stiffened, thickened arterioles (artery laying over a vein, and the vein is causing some pressure now) seen in chronic, poorly-controlled HTN usually without visual changes
142
hemorrhagic lesion findings on fundoscopic exam
caused by high grade HTN or proliferative diabetic retinopathy or trauma pt complains of new-onset floaters in the visual fields because they are trying to look through blood floating in the vitreous humor in the eye
143
deeply-cupped optic disc findings on fundoscopic exam
usually as a result of acute angle-closure glaucoma, typically with new onset of unilateral eye pain, redness, and blurred vision
144
what is the course of vision loss in untreated open-angle glaucoma (chronic glaucoma)
gradual PERIPHERAL vision loss, usually noted in older adult, preventable with treatment they develop tunnel vision
145
what is the course of vision loss in presbyopia
gradual onset of blurring of NEAR vision, most often noted by mid-late 40s caused by stiffening of the lens of the eye can use reading glasses
146
what is the course of vision loss in macular degeneration
CENTRAL vision loss, usually in adult of advanced age
147
macular degeneration causes [central vs. peripheral] vision loss
central
148
chronic open-angle glaucoma causes [central vs. peripheral] vision loss
peripheral
149
presbyopia causes [near vs. far] vision loss
near
150
most common cause of new onset blindness in the older adult
macular degeneration
151
appropriate ophthalmologic test for evaluation of the anterior eye structures including the cornea, conjunctiva, sclera and iris
slit lamp examination
152
appropriate ophthalmologic test for early detection of macular degeneration
Amsler grid
153
appropriate ophthalmologic test for measurement of intraocular pressure, e.g., for glaucoma screening
tonometry
154
tonometry tests for....
intraocular pressure (glaucoma screening)
155
amsler grid tests for....
macular degeneration screening
156
most common cause of acquired hearing loss in older adult
presbycusis
157
how does presbycusis present
difficulty appreciating the content of conversation in a noisy background environment mishear words they can hear ok in a quiet environment
158
what is presbycusis
hearing loss with age
159
describe presbyopia
hardening of the lens which results in near-vision problems. nearly all >45yos need reading glasses or other similar correction, very common with age
160
describe senile cataracts
clouding of the lens, which causes progressive vision dimming, problems with distance-vision. near-vision is usually retained. risk factors include tobacco use, poor nutrition, sun exposure, and corticosteroids. potentially correctable with surgery or a lens implant
161
describe open-angle glaucoma
painless, gradual onset of increased intraocular pressure leading to optic atrophy. presents as loss of peripheral vision if left untreated. avoidable with appropriate and ongoing intervention. more than >80% of glaucoma is open-angle. should be detected on periodic screening with tonometry and assessment of visual fields treatment includes miotics, beta blockers, and possible surgery
162
describe closed-angle glaucoma
sudden increase in intraoccular pressure, usually unilateral. presents with an acutely red, painful eye with vision changes including halos around lights. eyeball is firm compared to the unaffected eye. requires immediate referral to ophthalmology for rapid pressure reduction via medication or possible surgery
163
Pt presents with sudden onset of unilateral eye pain, redness, and visual changes including halos around lights. You suspect....
acute closed-angle glaucoma - emergency! refer for emergent pressure-reduction with ophthalmology
164
describe age-related maculopathy (macular degeneration)
thickening, sclerotic changes to the retinal basement membrane complex leads to painless vision changes including distortion of central vision. On fundoscopic exam, may see drusen (soft yellow deposits in the macular region). Aside from aging, risk factors include tobacco use, sun exposure, and family history. Treatment depends on type (wet or dry) Dry macular degeneration -- develops slowly over decades. no treatment options, so prevention is the focus. wet macular degeneration -- develops quickly over a few months. tx includes laser treatment for photocoagulation to obliterate the neovascular membrane, intravitreal injection of antivascular growth factors
165
describe anosmia/hyposmia
neural degeneration leads to diminished sense of smell with the resulting decline in fine taste discrimination. this is accelerated by tobacco use
166
describe presbycusis
loss of 8th cranial nerve (CN VIII - acoustic) sensitivity. leads to difficulty with conversation in a noisy environment. can hear but cannot understand well what was said. accelerated by excessive noise exposure. hearing aids can be useful
167
is presbycusis sensorineural or conductive hearing loss
sensorineural
168
most common pathogens for suppurative conjunctivitis (3)
- staph aureus - strep pneumonia - h. influenzae
169
most common pathogens for otitis externa (3)
- pseudomonas - s. epidermidis - staph aureus
170
most common pathogen for malignant otitis externa in someone with DM, HIV/AIDs, or on chemotherapy
pseudomonas in >95%
171
most common pathogens for exudative pharyngitis (5)
- group A streptococcus (strep pyogenes) - group C or G streptococcus - viral causes (including HHV-6, human herpes virus 6) - n. gonorrhoeae - f. necrophorum
172
viral conjunctivitis is usually caused by....
adenovirus
173
recommended antibiotic tx for suppurative conjunctivitis
- ophthalmic treatment with fluoroquinolone ocular solution (e.g., ciprofloxacin, levofloxacin, moxifloxacin) - alternatively, ophthalmic treatment with polymyxin B with trimethoprim solution
174
recommended antibiotic tx for otitis externa
- mild disease can be treated with acetic acid with propylene glycol and hydrocortisone drops (VoSoL) - moderate to severe disease can use otic drops with ciprofloxacin with hydrocortisone - decrease risk of reinfection by proper ear canal cleansing with 1:2 mixture of white vinegar and rubbing alcohol drops after swimming - do not use drops if punctured tympanic membrane is suspected
175
describe malignant otitis externa
complication of otitis externa that can occur in folks who are immunocompromised. >95% of cases are caused by pseudomonas. Priority risks include osteomyelitis of the skull or TMJ. Consider MRI or CT imaging to rule out osteomyelitis. Consider referral for ENT consult with surgical debridement. Obtain cultures of the ear drainage or results of the surgical debridement to further guide treatment. Parenteral antibiotics are often warranted for severe disease.
176
recommended antibiotic tx for malignant otitis externa
- oral ciprofloxacin for early disease if suitable for outpatient therapy - other options are available in inpatient setting for severe disease
177
recommended antibiotic therapy for exudative pharyngitis
- first line is penicillin V PO x10 days OR benzathine penicillin IM x1 dose (if adherence is a concern) - alternatively, 2nd generation cephalosporin x4-6 days, azithromycin x5 days, or clarithromycin x10 days (all PO)
178
Priority complication of untreated strep pharyngitis
prevent rheumatic fever/ rheumatic heart disease
179
% of adult pharyngitis that is due to group A strep (strep pyogenes; GAS)
10%
180
most adult pharyngitis is caused by....
virus