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AGPCNP Board Prep > Ch5: HEENT > Flashcards

Ch5: HEENT Flashcards

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
Q

standard viral URI is gone within…..

A

7-10 days

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26
Q

why do you wait 10 days before initiating antibiotic therapy for acute rhinosinusitis?

A

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

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27
Q

Risk factors for antibiotic resistance (5)

A

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
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28
Q

how long should you prescribe abx for and when should they feel improvement in ABRS

A

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

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29
Q

if you prescribe abx for ABRS and they have no improvement or worsening symptoms after 3-5 days, what is your next step?

A

broaden coverage or switch to a different antimicrobial class

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30
Q

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?

A
  • 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
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31
Q

Symptomatic treatment in ABRS

A
  • saline nasal irrigation
  • intranasal corticosteroids when they are additionally accompanied by allergic rhinitis
  • abx as indicated
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32
Q

intranasal corticosteroids are only useful in ABRS when they have what comorbidity

A

allergic rhinitis

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33
Q 
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
A

fluoroquinolones

e.g., levofloxacin, ciprofloxacin, moxifloxacin

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34
Q

which antibiotic class is NOT recommended in ABRS treatment due to their rising resistance rates

A

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

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35
Q

First line antibiotic therapy for ABRS

A

amoxicillin-clavulanate (Augmentin) 875/125mg PO BID x5-7 days

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36
Q

First & second line antibiotic therapy options for ABRS

A

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

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37
Q

the clavulanate aspect of Augmentin specifically causes this particular side effect

A

GI upset

is really hard on the stomach

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38
Q

how high a dose of amoxicillin-clavulanate do you need to overcome resistance in drug-resistant strep pneumo (DRSP)

A

3-4g (3000-4000mg) per day

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39
Q

can doxycycline be used in pregnancy

A

NO (teeth staining of the child)

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40
Q

beta-lactamase inhibitor drug

A

clavulanate

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41
Q

doxycycline in ABRS – is it better against the gram positive (strep pneumo) or gram negative (h. flu or m. cat) organisms?

A

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)

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42
Q

ABRS treatment options if they have an allergy to beta-lactams/penicillins (4)

A

doxycycline 100mg PO BID

doxycycline 200mg PO QD

levofloxacin 500mg PO QD x5 days

moxifloxacin 400mg PO QD x5 days

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43
Q

what is the only advantage the respiratory fluoroquinolones have over doxycycline in ABRS

A

they have better activity against drug-resistant strep pneumo (DRSP)

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44
Q

what are the (3) RESPIRATORY fluoroquinolones

A

moxifloxacin, gemifloxacin, levofloxacin

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45
Q

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)

A

amoxicillin-clavulanate (Augmentin) 2000/125mg PO BID (4g total daily - HIGH DOSE)

levofloxacin 500mg PO QD

moxifloxacin 400mg PO QD

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46
Q

only (4) antibiotics we should consider for ABRS

A
  • amoxicillin-clavulanate (Augmentin)
  • doxycycline (second line)
  • levofloxacin (last resort)
  • moxifloxacin (last resort)
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47
Q

CYP450 is an example of a ….

A

drug-metabolizing isoenzyme

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48
Q

what is a substrate

A

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

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49
Q

what % of all prescription drugs are substrates of CYP450 3A4

A

50%

e.g., sildenafil (Viagra), atorvastatin, simvastatin, alprazolam (Xanax), and many many other

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50
Q

50% of all prescription drugs are substrates of this isoenzyme….

A

CYP450 3A4

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51
Q

what is a CYP450 inhibitor

A

blocks the activity of the isoenzyme, limiting substrate excretion&raquo_space; allows an increase in substrate levels, and possible risk of substrate-induced toxicity

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52
Q

erythromycin and clarithromycin are CYP450 3A4 ______

A

inhibitors

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53
Q

clarithromycin + simvastatin = risk for……

A

statin-induced rhabdomyolysis

d/t clarithromycin being a CYP450 inhibitor

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54
Q

clarithromycin + alprazolam = risk for…..

A

sedation and fall risk

d/t clarithromycin being a CYP450 inhibitor

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55
Q

what is a CYP450 inducer

A

accelerates the activity of the isoenzyme so that the substrate is pushed out the exit pathway&raquo_space; reduction of the substrate level

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56
Q

St. John’s wort is a CYP450 3A4 _______

A

inducer

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57
Q

CYP inducers can lead to [increased vs. reduced] target drug levels

A

reduced target drug levels&raquo_space;

diminished therapeutic effect

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58
Q

CYP inhibitors can lead to [increased vs. reduced] target drug levels

A

increased target drug levels&raquo_space; risk for toxicities

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59
Q

St John’s Wort + COCs = increased risk for…..

A

decreased COC efficacy, spotting, contraceptive failure

d/t st johns wort being a CYP450 inducer

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60
Q

St John’s Wort + cyclosporine = increased risk for….

A

decreased cyclosporine efficacy (organ transplant anti-rejection med)

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61
Q

never give this antibiotic to a patient whom you don’t know every med that they are on

A

clarithromycin (CYP450 3A4 inhibitor)

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62
Q

what possible condition may occur after resolution of acute otitis media? (common, not considered treatment failure)

A

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

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63
Q

what type of hearing impairment occurs in serous otitis

A

conductive hearing loss

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64
Q

conductive hearing loss is usually [temporary vs. permanent]

A

temporary

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65
Q

sensorineural hearing loss is usually [temporary vs. permanent]

A

permanent

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66
Q

Cause of conductive hearing loss

A

sound is being blocked by something in the outer ear or middle ear (earwax, foreign object, damaged ear drum, serous otitis media, bone abnormality)

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67
Q

Cause of sensorineural hearing loss

A

inner ear disorder whereby the vestibulocochlear nerve (CN VIII) becomes damaged

caused by advancing age, ototoxic medications, immune disorders, trauma

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68
Q

ototoxic medications cause _____ hearing loss

A

sensorineural

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69
Q

ear infections cause _____ hearing loss

A

conductive

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70
Q

Weber hearing tests will localized to the side with…..

A

increased tissue density, consolidation

e.g., fluid build-up in acute otitis media

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71
Q

Weber test results in conductive vs. sensorineural hearing loss

A

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

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72
Q

Rinne test results in conductive vs. sensorineural hearing loss

A

CONDUCTIVE
- Negative: bone conduction heard better than air conduction

SENSORINEURAL
- Positive or Normal: air conduction is heard better than bone conduction

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73
Q

Generally-speaking, treatment options for conductive hearing loss

A

often self-limiting post-URI, AOM resolution, or cerumen impaction removal

rarely, further pharmacological or surgical intervention is needed

74
Q

Generally-speaking, treatment options for sensorineural hearing loss

A

hearing aids, cochlear implants, expert consultation

75
Q

positive vs. negative Rinne test

A

POSITIVE = NORMAL (air > bone conduction)

NEGATIVE = ABNORMAL (bone > air conduction)

76
Q

what is allergic rhinitis

A

“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
Q

characteristic of allergic rhinitis, not a common cold or URI

A

itch

78
Q

first line therapy in any allergic disorder, including allergic rhinitis

A

allergen avoidance/environmental control

patient education to avoid the allergen whenever possible

79
Q

first line MEDICATION therapy in allergic rhinitis

A

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
Q

anticipatory guidance for intranasal corticosteroids for allergic rhinitis

A

cannot expect results for a few days

81
Q

Reliver therapies for acute symptoms of allergic rhinitis (second line to controller therapies)

A

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
Q

Most potent of the oral antihistamines for allergic rhinitis

A

levocetirizine (Xyxal)

83
Q

examples of ocular antihistamines for allergic rhinitis

A

eyedrops filled with antihistamines

  • olopatadine (Patanol, Pataday)
  • azelastine (Optivar)
  • bepotastine (Bepreve)
84
Q

examples of intranasal antihistamines for allergic rhinitis

A
  • azelastine (Astelin, Astepro)
85
Q

Treatment option for patients with allergic rhinitis refractory to standard therapies

A

sublingual or injection immunotherapies to reduce IgE production, requires specialty consultation

can also consider acupuncuture

86
Q

examples of 2nd-gen oral antihistamines for allergic rhinitis

A
  • loratadine (Claritin)
  • cetirizine (Zyrtec)
  • levocetirizine (Xyxal)
87
Q

examples of intranasal corticosteroids for allergic rhinitis

A
  • fluticasone (Flonase)

- triamcinolone (Nasacort AQ)

88
Q

example leukotriene modifier for allergic rhinitis

A

montelukast (Singulair)

89
Q

WBC that is activated in allergic disorders

A

eosinophils

90
Q

“dandruff of the eyelids”

A

blepharoconjunctivitis

treat with baby shampoo on a q-tip

91
Q

____ lymph nodes are tender

A

infected

non-tender enlarged notes tend to be infected

92
Q

medical term for canker sore

A

aphthous stomatitis

93
Q

classic presentation of squamous cell carcinoma of the mouth

A

painless, persistent oral lesion

indurated margins

associated nontender firm lymphadenopathy

h/o cigarette smoking, h/o HPV 16

94
Q

inhaled corticosteroids puts folks at risk for oral…..

A

thrush

95
Q

95% of oral cancers are….

A

squamous cell carcinoma

96
Q

what are the 12 cranial nerves

A

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
Q

Risk factors for squamous cell carcinoma of the mouth

A

STRONG

  • longstanding HPV, especially HPV16
  • tobacco use
  • alcohol abuse

LESS POTENT

  • male
  • older age (>55yo)
98
Q

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…

A

oral squamous cell carcinoma

99
Q

Function of CN I

A

olfactory = smell

100
Q

Function of CN II

A

optic = vision

101
Q

Function of CN III

A

oculomotor = eyelid and eyeball movement

eye movements upward, medial, and downward

102
Q

Function of CN IV

A

trochlear = innervates the superior oblique, turns eye downwards and laterally

eye movements inward and downward

103
Q

Function of CN V

A

trigeminal = chewing, face and mouth sensation, touch and pain

touch the forehead & cheek
clench teeth

104
Q

Function of CN VI

A

abducens = turns eye laterally

ability to look to each side

105
Q

Function of CN VII

A

facial = controls most facial expressions, secretion of tears and saliva, taste

smiling, taste for the anterior 2/3 of the tongue

106
Q

Function of CN VIII

A

acoustic = hearing, equilibrium, sensation

107
Q

Function of CN IX

A

glossopharyngeal = taste, senses carotid blood pressure

taste for posterior 1/3 of the tongue

108
Q

Function of CN X

A

vagus - senses aortic blood pressure, slows the HR, stimulates digestive organs, defecation, taste

109
Q

Function of CN XI

A

spinal accessory = controls trapezius and sternocleidomastoid muscles, controls swallowing movements

shoulder shrug

110
Q

Function of CN XII

A

hypoglossal = controls movement of the tongue

111
Q

Tongue movements tests Cranial Nerve….

A

12 (CN XII) - hypoglossal

112
Q

Shoulder shrug tests Cranial Nerve ….

A

11 (CN XI) - spinal accessory

113
Q

Facial expresses tests Cranial Nerve….

A

7 (CN VII) - facial

114
Q

Eye movements in all directions tests Cranial Nerves ….

A

3 (CN III) - oculomotor
4 (CN IV) - trochlear
6 (CN VI) - abducens

115
Q

Perceiving light sensation to the face tests Cranial Nerve….

A

5 (V) - trigeminal

116
Q

Sense of smell tests Cranial Nerve….

A

1 (I) - olfactory

117
Q

Vision tests cranial nerve….

A

2 (II) - optic

118
Q

Hearing tests Cranial Nerve….

A

8 (VIII) - acoustic

119
Q

“puff out your cheeks” tests which cranial nerve

A

CN VII (facial)

120
Q

“shrug your shoulders” tests which cranial nerve

A

CN XI (spinal accessory)

121
Q

“raise your eyebrows” tests which cranial nerve

A

CN VII (facial)

122
Q

“do you recognize this scent” tests which cranial nerve

A

CN I (olfactory)

123
Q

paralysis of cranial nerve VII is called….

A

bell’s palsy

124
Q

does bell’s palsy require special imaging or labs for diagnosis

A

no, clinical diagnosis

125
Q

most appropriate initial therapy for bell’s palsy

A

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
Q

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….

A

Bell’s palsy (paralysis of cranial nerve VII, aka idiopathic facial paralysis)

127
Q

anticipatory guidance for bell’s palsy

A

short course of oral corticosteroids is first line

most folks recover completely over the course of 3 months

128
Q

vital sign of the eye

A

visual acuity

129
Q

pathology of bell’s palsy

A

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
Q

classic presentation of bell’s palsy

A

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
Q

how do you diagnose bell’s palsy

A

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
Q

treatment overview for bell’s palsy

A

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
Q

who needs a visual acuity exam and how is it done?

A

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
Q

with any eye complaint, always do this test…..

A

visual acuity (Snellen chart)

if there is any new onset of visual acuity change, needs referral to specialist

135
Q

triad of symptoms to ALWAYS refer promptly to ophthalmology (invariably something serious)

A
  1. red eye
  2. painful eye
  3. new onset visual acuity change

e.g., acute glaucoma, iritis

136
Q

on fundoscopic eye exam, the arteries should NEVER be _____ than the veins

A

wider

arteries should be smaller, more narrow than the veins

137
Q

normal for the [arteries vs. veins] to be wider and darker on fundoscopic eye exam

A

veins = wider, darker

138
Q

normal for the [arteries vs. veins] to be narrower, brighter on fundoscopic eye exam

A

arteries = narrow, brighter

139
Q

the optic disc margins on a normal fundoscopic eye exam should be….

A

sharp, saucer-shaped

optic disc should be towards the nasal portion of the ocular field

140
Q

papilledema findings on fundoscopic exam

A

caused by increased intracranial pressure

pt reports new blind spot in the visual field

bulging optic disc (too much intracranial pressure)

141
Q

arteriovenous (AV) nicking findings on fundoscopic exam

A

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
Q

hemorrhagic lesion findings on fundoscopic exam

A

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
Q

deeply-cupped optic disc findings on fundoscopic exam

A

usually as a result of acute angle-closure glaucoma, typically with new onset of unilateral eye pain, redness, and blurred vision

144
Q

what is the course of vision loss in untreated open-angle glaucoma (chronic glaucoma)

A

gradual PERIPHERAL vision loss, usually noted in older adult, preventable with treatment

they develop tunnel vision

145
Q

what is the course of vision loss in presbyopia

A

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
Q

what is the course of vision loss in macular degeneration

A

CENTRAL vision loss, usually in adult of advanced age

147
Q

macular degeneration causes [central vs. peripheral] vision loss

A

central

148
Q

chronic open-angle glaucoma causes [central vs. peripheral] vision loss

A

peripheral

149
Q

presbyopia causes [near vs. far] vision loss

A

near

150
Q

most common cause of new onset blindness in the older adult

A

macular degeneration

151
Q

appropriate ophthalmologic test for evaluation of the anterior eye structures including the cornea, conjunctiva, sclera and iris

A

slit lamp examination

152
Q

appropriate ophthalmologic test for early detection of macular degeneration

A

Amsler grid

153
Q

appropriate ophthalmologic test for measurement of intraocular pressure, e.g., for glaucoma screening

A

tonometry

154
Q

tonometry tests for….

A

intraocular pressure (glaucoma screening)

155
Q

amsler grid tests for….

A

macular degeneration screening

156
Q

most common cause of acquired hearing loss in older adult

A

presbycusis

157
Q

how does presbycusis present

A

difficulty appreciating the content of conversation in a noisy background environment

mishear words

they can hear ok in a quiet environment

158
Q

what is presbycusis

A

hearing loss with age

159
Q

describe presbyopia

A

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
Q

describe senile cataracts

A

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
Q

describe open-angle glaucoma

A

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
Q

describe closed-angle glaucoma

A

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
Q

Pt presents with sudden onset of unilateral eye pain, redness, and visual changes including halos around lights. You suspect….

A

acute closed-angle glaucoma - emergency! refer for emergent pressure-reduction with ophthalmology

164
Q

describe age-related maculopathy (macular degeneration)

A

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
Q

describe anosmia/hyposmia

A

neural degeneration leads to diminished sense of smell with the resulting decline in fine taste discrimination. this is accelerated by tobacco use

166
Q

describe presbycusis

A

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
Q

is presbycusis sensorineural or conductive hearing loss

A

sensorineural

168
Q

most common pathogens for suppurative conjunctivitis (3)

A
  • staph aureus
  • strep pneumonia
  • h. influenzae
169
Q

most common pathogens for otitis externa (3)

A
  • pseudomonas
  • s. epidermidis
  • staph aureus
170
Q

most common pathogen for malignant otitis externa in someone with DM, HIV/AIDs, or on chemotherapy

A

pseudomonas in >95%

171
Q

most common pathogens for exudative pharyngitis (5)

A
  • group A streptococcus (strep pyogenes)
  • group C or G streptococcus
  • viral causes (including HHV-6, human herpes virus 6)
  • n. gonorrhoeae
  • f. necrophorum
172
Q

viral conjunctivitis is usually caused by….

A

adenovirus

173
Q

recommended antibiotic tx for suppurative conjunctivitis

A
  • ophthalmic treatment with fluoroquinolone ocular solution (e.g., ciprofloxacin, levofloxacin, moxifloxacin)
  • alternatively, ophthalmic treatment with polymyxin B with trimethoprim solution
174
Q

recommended antibiotic tx for otitis externa

A
  • 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
Q

describe malignant otitis externa

A

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
Q

recommended antibiotic tx for malignant otitis externa

A
  • oral ciprofloxacin for early disease if suitable for outpatient therapy
  • other options are available in inpatient setting for severe disease
177
Q

recommended antibiotic therapy for exudative pharyngitis

A
  • 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
Q

Priority complication of untreated strep pharyngitis

A

prevent rheumatic fever/ rheumatic heart disease

179
Q

% of adult pharyngitis that is due to group A strep (strep pyogenes; GAS)

A

10%

180
Q

most adult pharyngitis is caused by….

A

virus

AGPCNP Board Prep (21 decks)

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