Week 4 Respiratory/ENT Flashcards
What is presbycusis?
Age-related hearing loss, characterized by symmetrical progressive loss of hearing over many years. It usually affects high frequencies of hearing but can be variable.
What are the 3 anatomical areas of the ear?
Disorders of which of these areas can contribute to hearing loss?
External ear, middle ear, and inner ear.
Disorders of any of these areas can contribute to hearing loss.
Presbycusis affects more than half of adults by age 75 years, most adults over the age of 80, and nearly all adults who are 90 or older. It is more common in males than females, possibly related to higher levels of noise exposure seen in this population.
True or false?
True! As per UTD.
_______ ________ can be accompanied by tinnitus, vertigo, and disequilibrium, leading to _____________________.
Hearing loss can be accompanied by tinnitus, vertigo, and disequilibrium, leading to increased falls risk.
Hearing deficits are exacerbated in the presence of _________________, so people living with presbycusis will often do well one-on-one in a quiet room.
competing background noise
What should you be mindful of during your PE if assessing for presbycusis?
General PE is usually unremarkable.
It is common for older adults to have age-related benign opacification of the tympanic membrane and build-up of cerumen. If a moderate amount of cerumen is present, this should be removed to rule out impaction or obstruction as a potential cause of hearing loss.
Tuning forks may be used to discriminate between conductive and sensorineural hearing loss; however, their use is limited by patient cooperation and provider subjectivity.
Determining whether the pattern of hearing loss is sensorineural or conductive is an important first step in the diagnosis. This can be done by performing both the Weber and the Rinne test using a tuning fork.
Presbycusis is sensorineural in origin; therefore, the ______test should reveal that air conduction is heard longer than bone conduction in both ears. _________ test should localize toward the ear with better hearing, signifying a contralateral sensorineural loss. _______ test may vary and may result in a falsely normal result if hearing loss is symmetric.
Rinne
Weber’s
Weber’s
The treatment of choice for presbycusis is librolycra 2.5 mg daily to slow the progression of the disorder.
True of false?
False. I made that up.
The mainstay of treatment is hearing aids.
Cochlear implants may be an option for patients with severe bilateral hearing loss that is not responsive to hearing aids (there is specific criteria).
How is presbycusis diagnosed?
An audiogram: pure-tone testing. Presbycusis will appear as an overall down-sloping line that represents impaired hearing at higher frequency sounds.
What are some DDX for presbycusis?
Noise exposure
Infection
Ménière disease
Trauma
Autoimmune disease
Perilymph fistula
Genetically-inherited hearing loss
Otosclerosis
Tumor
Exposure to ototoxic agents
Metabolic dysfunction
If the pattern of hearing loss is conductive, then an alternative diagnosis to presbycusis should be considered. These include:
Cerumen impaction
Foreign body
Tumor obstruction
Infection
Perforation
Otosclerosis
Cholesteatoma
Cerumen impaction
Foreign body
Tumor obstruction
Infection
Perforation
Otosclerosis
Cholesteatoma (Non-cancerous abnormal growth of keratinizing squamous epithelium filled with air or fluid in the middle ear and temporal bone behind the ear drum. It may cause constant discharge, hearing loss, dizziness or headache.)
What is a red flag in a patient presenting with c/o hearing loss?
Sudden sensorineural hearing loss (SSNHL) is usually unilateral and onset it over 72 hours or less. Most is idiopathic and resolves spontaneously but the following must be evaluated for:
Recent head trauma
Barotrauma
Acute keratitis
Prior hx (assess for Meniere’s)
Focal neurologic s/s (diplopia, headache, vertigo, tinnitus)
Autoimmune disease or vasculitis
Recent exposure to Lyme disease
Acute infection (AOM, otitis externa, mastoiditis)
Exposure to ototoxic meds/drugs
Name some ototoxic medications/substances.
●Several antibiotics cause ototoxicity. All oral aminoglycosides are ototoxic.
●Other oral antibiotics that can cause ototoxicity include erythromycin and tetracycline. These drugs have a more pronounced ototoxic effect in patients with impaired kidney function.
●Many chemotherapeutic agents.
●High-dose aspirin (6 to 8 g/day) or other salicylates can cause hearing loss, but this is reversible with discontinuation of the drug.
●Acetaminophen, or nonsteroidal antiinflammatory drugs (NSAIDs; ≥2 times/week) was also associated with an increased risk of hearing loss, particularly in those less than 50 years old. Similar findings were found in women for acetaminophen and ibuprofen, but not aspirin [80].
●Phosphodiesterase 5 inhibitors.
●Antimalarial medications such as quinine and chloroquine may also cause sensorineural hearing loss and tinnitus but, similar to salicylates, these effects are usually reversible.
●Loop diuretics may cause temporary hearing loss and tinnitus.
●Cocaine, both intranasal and intravenous.
●Heavy metals, including lead, mercury, cadmium, and arsenic.
●Exposure to aromatic solvents, including toluene and styrene.
A 65-year-old male is evaluated in a follow-up examination
for worsening dyspnea and chronic cough productive of
mucoid sputum for the past 6 months. He was diagnosed with (COPD) 3 years ago, and uses inhaled albuterol as needed.
Vital signs are normal and the
patient is not in any respiratory distress. Breath sounds
are decreased, but there is no edema or jugular venous
distention. Spirometry shows FEV1/forced vital capacity (FVC) ratio
of 65%. His COPD symptoms seem poorly controlled and
he has had one exacerbation in the past year. Chest x-ray shows mild hyperinflation.
Which of the following is the most appropriate therapy for
this patient?
a. Add inhaled corticosteroid to his current treatment
plan.
b. Add a long-acting inhaled bronchodilator.
c. Continue with inhaled albuterol every 4 hours.
d. Add theophylline and montelukast.
e. Treat the patient with an antibiotic
Answer is
b. Add a long-acting inhaled bronchodilator.
In uncontrolled COPD, that would be the next appropriate step.
He is not showing signs and symptoms of pneumonia.
What are some defining characteristics of COPD?
*Dyspnea-Progressive over time
Worse with exercise
Persistent-daily
People describe it as “increased effort to breathe”, heaviness, air hunger, gasping”.
Chronic cough
Sputum production
Key risk factors:
Tobacco smoke
Occupational dust and chemicals
Smoke from home cooking and heating fuel
Family hx/α-1 antitrypsin
deficiency
Provide examples of obstructive airways diseases
COPD (emphysema &/or bronchitis), asthma, bronchiectasis and cystic fibrosis.
Provide examples of restrictive lung diseases.
Interstitial lung disease (ILD), sarcoidosis, neuromuscular diseases (e.g. ALS), pulmonary fibrosis, asbestosis, silicosis.
In someone with obstructive lung disease, expect to see:
a) Increased pulmonary compliance, destructions of alveolar space, forced expiration volume is decreased.
b) Decreased pulmonary compliance, increased alveolar space, forced expiration volume is decreased.
c) Decreased pulmonary compliance, destruction of alveolar space, lung capacity is normal.
Answer is A
Expiration effect is decreased, alveolar space is destroyed, hard to exhale air, lung capacity is normal, vital capacity is normal, forced expiration volume is decreased.
In someone with restrictive lung disease, expect to see:
a) decreased pulmonary compliance, presence of bullae, vital capacity is reduced, lung capacity is decreased.
b) Increased pulmonary compliance, increase of alveolar space, reduced vital capacity
c) Forced expiration volume is normal, lung capacity is reduced, vital capacity is reduced.
Answer is C
Reduced effect of inspiration, increased alveolar space and destruction of elastic fibers, lung capacity is decreased, vital capacity is reduced, forced expiration volume is normal.
What are risk factors of obstructive lung disease?
Smoking: Primary risk factor for COPD
Occupational Exposures: Exposure to pollutants or occupational irritants.
Genetics: e.g. Alpha-1 antitrypsin deficiency is a risk factor for COPD. Asthma is a familial d/o.
Allergies: Allergies can trigger asthma symptoms, contributing to the development or exacerbation of obstructive lung diseases.
Pre-existing Conditions: such as bronchiectasis or cystic fibrosis, HIV, and Marfan syndrome.
History of Respiratory Issues in Childhood
Age
Family history of atopy
What are some risk factors of restrictive lung disease?
Environmental Exposure: Occupational or environmental exposure to substances such as asbestos, silica, or coal dust.
Connective Tissue Disorders: Conditions like rheumatoid arthritis, scleroderma, or lupus.
Radiation Therapy: Previous exposure to chest radiation.
Neuromuscular Disorders: , such as muscular dystrophy or amyotrophic lateral sclerosis (ALS)
Obesity - obesity hypoventilation syndrome.
Age (the elderly)
Smoking
What is the pathophysiology of restrictive lung disease?
Narrowing of the airways, often due to inflammation and mucus production.
Reduced Expiratory Flow Rates: Difficulty exhaling air efficiently.
Air Trapping: Incomplete emptying of the lungs, leading to hyperinflation.
Airway obstruction (decreased lung recoil and increased lung compliance) = Airflow reduction = alveoli expand but slowly or unable to deflate = increased lung volumes.
What is the pathophysiology of restrictive lung disease?
Stiffening of lung tissue, making it harder to expand.
Decreased Lung Volumes: Reduced total lung capacity and vital capacity.
Impaired Gas Exchange: Difficulty in oxygen and carbon dioxide exchange due to decreased lung surface area.
Reduced lung compliance = restricted lung expansion = more effort to expand the lung during inhalation (alveoli deflate, but it is unable to inflate properly) = reduced lung volumes and increased WOB.
Causes
-Intrinsic lung diseases - diseases that affect tissue and space around alveoli in the lungs e.g pulmonary fibrosis
-Extrinsic disorders - conditions that affect the chest wall, spine, or pleura e.g kyphosis, obesity hypoventilation
What would spirometry show in obstructive lung disease?
FEV1/FVC – reduced
TLC – elevated or normal
RV – elevated or normal
DLCO – Normal (asthma) or reduced
Decreased flow rates, hyperinflation and air trapping (increased TLC)
- FEV1/FVC ratio < 0.7
What would spirometry show in restrictive lung disease?
FEV1/FVC – normal or increased
TLC – reduced
RV – reduced, normal or increased
Reduced (intrinsic) or normal (extrinsic)
Decreased lung volumes and compliance
Normal or increased FEV1/FVC ratio (between 0.7 to 0.
If you suspect COPD, what testing would you order?
Spirometry:
Post bronchodilator FEV1/FVC ration <0.70.
Chest x-ray may show hyperinflation, but need spirometry to diagnose COPD.
Annie comes in because she feels that her COPD symptoms are not well managed with her current medication regime. What would you assess first?
First evaluate Annie’s inhaler compliance and technique before making any medication adjustments.
Up to 90% of patients use their device incorrectly! Arthritis, pain, and other factors are barriers to appropriate technique. Ensure that they are sitting upright.
What else should you assess when considering the next step in medication management in COPD?
Assess exertional dyspnea, functional status, history of exacerbations, complexity of medicines or devices, patient preference (e.g., cost and ability to adhere to treatment plan) and occurrence of adverse effects.
You are prescribing medication for John, who was just recently diagnosed with COPD. What would be the first step?
1-A SAMA or SABA
If symptoms are not well controlled, then proceed with
2-SAMA AND SABA
John returns 6 months later and you determine that you need to escalate medication management. He is already on SAMA and SABA. What would be your next step?
LABA or LAMA monotherapy.
Continue SABA as rescue
The next step after that is having him take LABA and LAMA together.
Note: LAMA and SAMA should not be used concurrently.
John has been having multiple AECOPD. What should you do now?
He is currently on LABA and LAMA combination.
Triple therapy of LAMA and LABA and ICS for those patients with FEV1 < 50% predicted and ≥ 2 exacerbations in the past 12 months.
With ICS, use lowest dose possible and avoid use as monotherapy.
What is AECOPD?
Sustained (e.g., 48 hours or more) worsening of shortness of breath and coughing, usually with increasing sputum volume.
The most common cause of AECOPD is a viral or bacterial infection; other causes-pleural effusion, heart failure, pulmonary embolism, and pneumothorax.
Most COPD action plans have which medications?
1) short-acting bronchodilator for initial treatment of acute exacerbations
Adequate doses of bronchodilator (e.g., salbutamol 400 to 800 mcg [4 to 8 puffs]) delivered via metered dose inhaler with a spacer is equivalent to 2.5 mg by nebulizer and is as effective. Administer salbutamol frequently (up to every couple of hours) and titrate to response
2) oral corticosteroids in most moderate to severe COPD patients.
A dose of 40 mg of prednisone per day for 5 days is an appropriate dose.17 However, a dose of 50 mg of prednisone per day is often used in Canada because of its availability in a single tablet. Lower doses may need to be used, especially in the presence of diabetes mellitus.
3) Antibiotic treatment
amoxicillin 1 g PO TID or
doxycycline 200 mg PO once, then 100 mg PO BID or
sulfamethoxazole-trimethoprim 1 DS (800-160 mg) tablet PO BID
Treat for 5-7 days.
For guidance check: https://www2.gov.bc.ca/assets/gov/health/practitioner-pro/bc-guidelines/copd_appendix_b.pdf
When would you refer a COPD patient to a specialist?
-the diagnosis is uncertain;
-a patient is < 40 years with COPD and limited smoking history, or has severe symptoms and disability which is disproportionate to their lung function
-there is evidence of an alpha-1 antitrypsin (A1AT) deficiency (e.g. early onset of emphysema or COPD, unexplained liver disease, family history)
-there are signs and symptoms of hypoxemic or hypercarbic respiratory failure
-there are severe or recurrent exacerbations and treatment failure;
-the patient has severe COPD and disability requiring more intensive interventions
-a more intensive comorbidity assessment and management is required
-a patient is frail and may benefit from multidisciplinary or comprehensive geriatric assessment
-difficulty in assessing home oxygen or sleep disorders.
Match the following:
a) salbutamol. 1) LAMA
b)spiriva. 2) combo
LABA
and LAMA
c)Ultibro breezhaler. 3) SABA
d) Symbicort turbuhaler 4) ICS
and LABA
combo
a/3
b/1
c/2
d/4
A patient comes in with dry eye (sicca). What would be your management plan for them?
Hot compresses, artificial tears, and nighttime lubricating ointments.
Avoid artificial tears with preservatives or OTC “antiredness” eye drops with naphazoline or pheniramine as they worsen symptoms.
Name some S&S of sicca.
- eye dryness
-visual disturbance - eye discomfort or FB sensation
- burning/stinging
- grittiness
- tearing
- ocular fatigue
Can be episodic or chronic
What are risk factors for sicca?
dry environment
medications
blepharitis
smoking
alcohol use
long-term contact lens use
LASIK surgery
pollution
activities with decreased blinking (computer use)
topical ocular medications
female sex,
Sjögren syndrome
increasing age
What should you assess for when evaluating a patient for sicca?
- assess for poorly fitting sleep apnea masks
- decreased blink in patients with Parkinson disease
- presence of peripheral neuropathy
- sleep deprivation-decreases tear secretion and osmolality, worsen tear film break up time.
-assess for lid abnormalities (ectropion—outward turning of the lid margin, and lagophthalmos—
incomplete lid closure during sleep) - assess for thyroid disease (Graves’ ophthalmopathy).
What is the best way to diagnose Age-Related Macular Degeneration (ARMD or AMD)?
dilated fundus examination, and the use of a slit lamp
Routine eye examinations are a benefit under MSP, for who?
18 years of age and under, those 65 years of age and older, and those people with health conditions requiring eye examinations
E.g. Known eye disease (Glaucoma/ARMD), eye trauma, chronic health conditions associated with eye involvement (diabetes), or those patients on medications that can impact eye health (hydroxychloroquine for rheumatological disorders).
Is AMD reversible?
Sadly, no. Major cause of blindness
What is AMD?
slowly, progressive, degenerative disease of the photoreceptors within the retina.
An acquired degeneration of the retina that causes significant central visual impairment through a combination of non-neovascular (drusen and retinal pigment epithelium abnormalities), and neovascular derangement (choroidal neovascular membrane formation).
https://www.aao.org/eye-health/diseases/amd-macular-degeneration-pictures-videos - watch the 4min video
What is the hallmark sign of AMD?
Drusen.
Yellow deposits located on the macula in AMD. The deposits are waste products from the break down and death of the retinal cell or photoreceptors.
*calcified, dome-shaped deposits
What happens to the vision when AMD is gradually developing?
Asymptomatic in early stages (don’t realize have AMD till vision is blurry)
Problems with contrast sensitivity, difficulty adapting to dark environments
Decreased ability to read, drive (limited night vision), recognize faces, and see colors.
Metamorphopsia (distorted vision in which see straight lines as convergent or wavy)
Bilateral but asymmetric
Progression from early or intermediate AMD to late AMD can occur in a matter of days, causes loss of far and near vision, sudden visual distortion (e.g., straight lines or edges appear wavy), central vision loss, and change in color vision.
What the two types of AMD?
- Nonneovascular or atrophic (dry, nonexudative) AMD causes 80% of cases, most common
- Neovascular (wet, exudative) AMD causes almost 90% of severe vision loss.
What is neovascularization?
Neovascularization form includes accumulation of drusen and lipofuscin, abnormal choroidal blood vessel growth, leakage of blood or serum, retinal detachment, fibrovascular scarring, loss of photoreceptors, and more severe and rapid loss of central vision.
Just for your own knowledge - doubt he will ask this.
Risk Factors of AMD?
Nonmodifiable Risk Factors
- age, European decent/white race, Family History, Genetic links, blue irises, and female sex.
Modifiable Risk Factors
- primary is smoking from progression to late
- CVD, HTN, DM, Hypercholesterolemia, Obesity, Hyperopia,
- eat a diet high in saturated fat (found in foods like meat, butter, and cheese)
What are cataracts?
Progressive ocular lens opacity leading to impaired vision.
In AMD, the sharp, “straight ahead” vision needed to see fine details is decreased by destruction of the macula. What is the macula?
Macula - tiny part of the eye’s retina, provides central vision, helping recognize someone’s face, thread a needle, or see the hands on a clock to tell time.
True or false- cataracts are the most common cause of low vision and blindness in BC and reversible blindness worldwide
true
In AMD, is the peripheral side vision affected?
No. Is normal.
True or false- all older adults get cataracts
Apparently true according to our text book! all older adults 70+ years have cataracts to some extent.
Risk factors for cataracts?
- Aging (90% of cataracts)
- UV-B exposure, radiation
- Eye trauma, certain eye conditions (myopia, vitrectomy, intraocular inflammation/ uveitis, chronic ocular disease, prior intraocular surgery).
- Long term corticosteroid use (any route) (GPAC, 2021). UpToDate (Jacobs, 2023) specifies systemic corticosteroid use and possibly prolonged use of high doses of inhaled corticosteroids can contribute to cataract development; intranasal steroids do not seem to pose a risk.
- Diabetes, HTN
- Family history
- Smoking, alcohol consumption
How do cataracts occur?
Lens has specialized cells with crystallin proteins
It cannot shed its dead/ damaged cells
These accumulate in the lens and get squished up
forming a cataract! Thick, opaque lens that obscures vision.
Think of an egg white.. if you damage the proteins (cooking, whipping them), you go from a translucent egg white to a solid white one! Similar to eye- accumulation of dead proteins over time
Describe signs/ symptoms of cataract?
-Gradual onset and slowly progressive over months to years
-Painless, progressive decrease in visual acuity.
-May be unilateral or bilateral; more often presents with bilateral symptoms.
-Blurred/ cloudy vision, glare, dimness, halos around lights (especially at night), monocular diplopia, blurred vision
-LOSS OF RED REFLEX is v. important per Don
How to dx cataract?
Gold standard for diagnosis is slit lamp exam showing lens opacity (send to opthalmology- they will rule out other causes for decrease VA, assess for surgery)
Prevention of cataracts?
-Smoking cessation
-Reduced UV exposure (sunglasses with UV-B protection, hat)
-Reduce risk of eye trauma (i.e., safety eyeglasses during work or recreation)
-stop glucorticoids if you can
What is Dry AMD?
Parts of the macula get thinner with age and tiny clumps of protein called drusen grow.
People with dry AMD may have drusen, pigment abnormalities, or geographic atrophy (an area of cell loss in the retina). You slowly lose central vision.
Common (80-90%), another name atrophic, nonneovascular
What is Wet AMD?
Less common (10-15%) but much more serious. Another name Exudative / Neovascular.
New, abnormal blood vessels grow under the retina. These vessels may leak blood or other fluids, causing scarring of the macula.
You lose vision faster with wet AMD than with dry AMD.
Symptoms of Dry AMD?
*gradual development of loss of vision
Notice a problem with 1 or both eyes when reading or driving
* Need bright lights or a magnifying glass to see as well as they used to
* Notice spots that seem blurry
Symptoms of Wet AMD?
Sudden changes in vision
Notice problems with 1 eye at first. Later, both eyes usually develop problems.
See lines that are actually straight as bent or wavy (look at Amsler grid)
What is an Amsler grid?
The Amsler grid is a simple square containing a grid pattern and a dot in the middle. When used correctly—once a day, every day—the Amsler grid can show problem spots in your field of vision.
A helpful tool for people with progressive AMD - if wavy lines or black spots appear can report to opthalmologist for further treatment.
Treatment for Dry AMD?
Mixed Reviews: vitamins and supplements might help slow progression of AMD to late-stage or Wet AMD.
There is no treatment for drusen. However people with lots of drusen or serious vision loss might benefit from taking a certain combination of nutritional supplements.
*A large study (AREDS and the later AREDS 2 study) found people with certain drusen may slow their dry AMD by taking these vitamins and minerals daily:
- Vitamin C (500 mg)
- Vitamin E (400 IU)
- Lutein (10 mg)
- Zeaxanthin (2 mg)
- Zinc (80 mg)
- Copper (2 mg)
*A healthy diet rich in fruits, vegetables, fish & nuts may reduce the risk of developing/worsening AMD and is suggested due to other health benefits.
*Encourage green leafy vegetables (e.g. kale, spinach, swiss chard, romaine lettuce) which are a good source of lutein & zeaxanthin.
*Green leafy vegetables are also high in vitamin K, therefore constant intake minimizes fluctuating intake for individuals on warfarin
*Encourage fish (1 to 2 servings) and shelled nuts (¼ to ½ cup) per week as a good source of omega-3.
× Avoid heavy alcohol use (>3 drinks/day), ≥10 servings of red meat per week, & high saturated fat intake; limit foods with a high glycemic index (e.g. white bread, russet potato, & short grain rice).
× Avoid smoking
For non-smokers recommend:
- AREDS formulation included vitamin C 500mg, vitamin E 400 IU, beta-carotene 25,000 IU, copper 2mg, and zinc 80mg (e.g. VITALUX).
For individuals with a history of smoking:
- Beta-carotene has been linked to an increased risk of lung cancer, particularly in smokers.
- AREDS2 replaced beta-carotene with lutein 10mg and zeaxanthin 2mg (e.g. VITALUX-ADVANCED). This revised formulation has similar efficacy to the AREDS formulation and is the preferred formulation for individuals with a history of smoking
RxFiles: Nutritional Supplements & Dietary Considerations for Disease Management in Older Adults
Treatment for Wet AMD?
To help treat wet AMD, there are medications called anti-VEGF drugs.
*Anti-VEGF treatmenthelps reduce the number of abnormal blood vessels in your retina. It also slows any leaking from blood vessels. This medicine is delivered to your eye through a very slender needle.
- Laser surgery may also be used to treat some types of wet AMD. Your eye surgeon shines a laser light beam on the abnormal blood vessels. This reduces the number of vessels and slows their leaking.
First-line treatment for wet AMD
- intravitreal injection with anti-VEGF (antivascular endothelial growth factor) agents (aflibercept, bevacizumab, and ranibizumab)
- Adherence to monthly injections is difficult.
Can Dry AMD transition into Wet AMD?
yes, but in a minority of patients
Encourage smoking cessation, mediterranean diet, decrease EToH, use the Amsler grid daily, and daily vitamin and supplement intake.
What is glaucoma?
Optic neuropathy with characteristic atrophy of optic nerve head, +/- elevated intraocular pressure (IOP).
What are the pathognomonic features of glaucoma?
tunnel vision (gradual peripheral visual field loss), optic disc cupping
T/F: Glaucoma is the leading cause of blindness in the world
False - second leading cause. Cataracts win the gold medal.
T/F: Vision loss from glaucoma is irreversible
True - this is why we care so much about catching it
How is glaucoma diagnosed?
Through a proper clinical eye exam by an eye provider. Confrontational visual field testing using fingers is unreliable, and direct ophthalmoscopy is limited by user skill and a limited view of posterior segment with a nondilated pupil and/or potential anterior segment opacities
How often should my asymptomatic 65+ patients have eye exams?
every year, or every 1-2 years depending on the source
50% of cases are undiagnosed, and the condition is more common in older adults.
What if my patients are concerned about the cost of eye exams?
Let them know that MSP covers $47.08 for full eye exam for seniors once annually. I have heard in clinical that the walmart optometry clinics may have the lowest eye exam fees.
T/F: Glaucoma is usually asymptomatic
True - until it progresses to irreversible vision loss there are no symptoms. No eye pain, redness, floaters or focal neuro deficits.
There are 4 types of glaucoma
Primary Open-Angle glaucoma - problem with balance of aqueous fluid production within eyes, with ability to effectively drain this fluid. A reduction in drainage increases the pressure on the optic nerve, leading to a loss of peripheral vision initially. Later stages can present with central vision loss. Risk factors include: age >40 years, 0.5 cup to disc ratio or larger, race (African heritage), family history, diseases affecting the vasculature.
Angle Closure glaucoma (also known as closed-angle or narrow angle glaucoma) occurs less often, and can be either chronic or acute, but if acute it is considered a medical emergency, as it can result in acute and irreversible vision loss. With this type of glaucoma, the drainage angle in the eye is closed, or becomes blocked, blocking the effective drainage of aqueous fluid, resulting in an increase in ocular pressure resulting in damage to the optic nerve.
Secondary glaucoma can occur as the result of an injury, infection or tumour, in or around the eye that causes the pressure to rise. It can also be the result of some medical conditions, medications (e.g. steroids), and other eye abnormalities. Infrequently, eye surgery can also be associated with secondary glaucoma.
Normal-tension glaucoma has an unknown etiology. With this type, the pressure stays within the “normal” range, but the optic nerve is still damaged.
Treatment will be mainly managed by the eye provider. What does it involve?
Lower IOP regardless of starting pressure
Monitoring IOP, optic disc health and visual fields at least twice/year
Eyedrops to increase aqueous outflow (prostaglandins) or decrease production (𝛼-agonists, β-blockers, carbonic anhydrase inhibitors)
What is the PCP role in glaucoma management?
Refer people at risk; help patients navigate transitions; coordinate appointments and treatments; and collaborate with eye providers for early detection, education, managing side effects, avoiding drug interactions, and maintaining continuity with eye care provider
Outline eyedrop use teaching for your patient
- Do not use eyedrops past expiry date or if contaminated. Some eye drops like latanoprost are only good for 6 wks at room temperature.
- Remove contacts before application. Shake bottle.
- Occlude lacrimal punctae or shut eyes tightly for at least 1-5 mins after drop application. Use 1 drop, and wait 5 mins between drops.
Is blepharitis typically unilateral or bilateral?
Bilateral
S&S of belpharitis?
Red, swollen eyelids
transient blurred vision that improves with blinking
Itching
Tearing
Gritty, FB sensation
crusting of the eyelashes
conjunctival injection (common)
Causes of anterior vs posterior blepharitis
Anterior = Seborrheic or bacterial (S. Aureus)
Posterior = Meibomian Gland Dysfunction
Risk factors for blepharitis
Diabetes
Candida
Seborrheic Dermatitis
Rosacea
Patho of posterior blepharitis
Inflammation of the inner eyelid at the level of the meibomian glands
hyperkeratinization of the meibomian gland duct leads to altered lipid composition of the gland secretion
favors bacterial growth, leading to an inflammatory response in the posterior eyelid
Patho of anterior blepharitis
inflammation at the bases of the eyelashes
can be due to S. aureus or coagulase-negative staphylococci
Tx of blepharitis
warm compresses, lid massages, and lid washing using commercially available eyelid scrub solution
topical or systemic antibiotics (doxycycline) as needed
if severe, ophthalmologist may prescribe a short course of topical corticosteroids, omega-3 fatty acids
What is a chalazion?
A chalazion is a chronic lipogranulomatous lesion affecting the upper or lower eyelid, caused by blockage of Meibomian gland duct(s) with retention and stagnation of secretion.
May occur spontaneously or follow an acute hordeolum (internal)
Does a chalazion come on suddently?
NO - Gradual – develops over days to weeks. Typically improve over months.
Is a chalazion painful or painless?
Painless
What does a chalazion look like?
Painless lid lump
Usually single; sometimes multiple
May rupture through the skin
Well-defined, 2-8mm diameter subcutaneous nodule in tarsal plate
Lid eversion may show external conjunctival granuloma
**May be associated with blepharitis
How is a hordeolum different than a chalazion?
chalazion: on inside of lid (not usually at lid margin). Nontender.
hordoleum (stye) = near lid margin (either inside or outside lid). swollen, tender, erythematous and/or purulent nodule
Hordeola = infectious etiology
Chalazion = granulomatous inflammation
What is entropion vs. ectropion?
Entropion - eye lid margin folds inward towards the globe
Ectropion - eye lid margins folds outward from globe
T/F: The causes of entropion and ectropion are the same
True, mostly
Both can be related to aging, burns, trauma, surgery or can be congenital
Entropion (inward), also can be caused by herpes zoster and orbicularis oculi muscle spasm.
Ectropion (outward) can be caused by CN VII palsy, lid edema, tumor and herniated fat
S/S of entropion (inward)
Tearing
Foreign body sensation
Red eye
Can cause corneal abrasions with secondary corneal scarring
S/S: of ectropion (outward)
Tearing
Possible exposure keratitis
Outline testing for both entropion and ectropion
Testing for entropion: Forced lid closure, ask patient to tighten lid then open, in entropion, lid rolls inward
Testing for ectropion: Snapback test – pull eyelid inferiorly, in ectropion lid remains away from globe
What is treatment for entropion/ectropion?
Lubricants
Eyelid taping
Surgery
