Optho, thyroid, Presbycusis, Resp, Pain, Osteoporosis Flashcards

1
Q

68 yo pt that presents to clinic c/o decreased vision, needs bright light for reading and has difficulty reading despite bifocals, night driving difficult, glare w/ headlights, worse in left eye - has had HTN for 28 yrs? Most likely dx?

A
  • age related macular degeneration (AMD)

- leading cause of adult blindness in developed countries

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2
Q

Impact of AMD on adult elderly pt?

A
  • ability to drive
  • increased rates of falls
  • ability to live independently
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3
Q

What is AMD? Classification?

A
  • degenerative disease of central portion of retina (macula)
  • early AMD is often asx
    classified as:
  • dry (atrophic) - ischemia, retinal epithelial cell apoptosis/activating inflammation
  • wet (neovascular or exudative) - balance b/t substances that promote or inhibit blood vessel development, VEGF
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4
Q

RFs for AMD?

A
  • age
  • smoking
  • genetics
  • CVD
  • diet?
  • cataract surgery?
  • other:
    heavy ETOH use, caucasians more than African Americans
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5
Q

eval for AMD - hx?

A
  • be alert to complaints of visual disturbance
    hx:
    -rate of vision loss
    -whether one or both eyes involved
  • loss near or far vision or both
  • assoc sxs
  • acute distortion of loss of central vision - may be wet AMD
  • vision loss occurring over days or weeks reqrs urgent ophthalmic referral
  • usually occurs worse in one eye than the other
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6
Q

Physical eval for dry AMD?

A
  • drusen appears as bright yellow spots
  • atrophy appears as areas of depigmentation
  • there may be increased pigmentation
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7
Q

Physical eval for wet AMD?

A
  • subretinal fluid/and or hemorrhage
  • neovascularization: appears as grayish green discoloration
  • often reqrs fluorescein angiogram (light up vessels)
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8
Q

Tx for dry AMD?

A
  • none
  • for slowing the progression:
    antioxidants w/ Vit C, E, beta carotene, zinc and copper (in smokers - no beta carotene)
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9
Q

Tx for wet AMD? Tool used to detect progression?

A
  • VEGF inhibitors
  • photocoag
  • surgery
  • tool for detecting disease progression: amsler grid
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10
Q

Diff glaucomas?

A
  • acute angle glaucoma
  • secondary glaucoma: many subtypes
    uveitis
    old trauma
    steroid therapy
  • congenital glaucoma
  • primary open angle glaucoma (POAG): MC
  • leading cause of irreversible blindness in world
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11
Q

What is POAG?

A

optic neuropathy - optic disc described as cupping

  • peripheral visual field loss followed by central field loss - can’t be recovered
  • no sxs initially
  • disease must be screened for
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12
Q

RFs for POAG?

A
  • elevated IOP:
    normal range 8-22 Hg, exact relationship b/t elevated IOP and cupping not well understood
    -increasing age w/ increased risk of blindness
  • African Americans 4-5x greater risk
  • family hx
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13
Q

Screening and tx for POAG?

A

screening:
- generally done by specialist w/ specialized equipment
- can examine optic disc for cupping - cup greater than 50% of the vertical disc diameter is suspicious
tx:
- topical and systemic meds (BB timolol)
- laser therapy
- surgery

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14
Q

Primary and secondary angle closure glaucoma?

A
  • primary:
    pts anatomically predisposed, no identifiable secondray cause
  • secondary:
    secondary process responsible for closure of anterior chamber angle, such as:
    A fibrovascular membrane grows over the angle, a mass or hemorrhage in posterior segment pushes angle closed
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15
Q

RFs for ACG?

A
  • family hx
  • age older than 40-50s
  • female
  • hyperopia (farsightedness)
  • pseuodexfoliation
  • race: higheset in Inuit and Asian pop, lower in African and European origins
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16
Q

Presentation of ACG?

A
- pressure rising acutely: sxs 
decreased vision
halos around lights
HA
severe eye pain
N/V
- signs: 
conjunctival redness
corneal edema or cloudiness
shallow anterior chamber
mid-dilated pupil (4-6 mm), reacts poorly to light
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17
Q

Urgency of ACG? Tx?

A
  • ophtho emergency
  • immediate referral for further eval and definitive tx:
    if there is an hr or more delay to tx empiric therapy should be started
    this should be guided by consultant
    it is aimed at lowering IOP
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18
Q

How common are cataracts?

A
  • leading cause of blindness in the world

- approx 30 mill blind people in world - 50% due to cataracts

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19
Q

RFs for cataracts?

A
  • age: predominant
  • smoking: 2 fold increase
  • alcohol
  • sunlight exposure
  • metabolic syndrome
  • DM
  • systemic corticoid steroid use
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20
Q

Presenation of Cataracts?

A
  • painless, progressive process
  • pts usually complain of problems w/ night driving, reading road signs or difficulty w/ fine print
  • often increase in nearsightedness (myopic shift)
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21
Q

PE findings of cataracts?

A
  • lens opacity can be confirmed by fundoscopic exam

- may see darkening of red reflex, opacities or obscuration of ocular fundus detail

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22
Q

Tx of cataracts? Complications?

A
- surgery
pre-op -
- extensive eval not necessary
- HTN should be controlled
- endocarditis prophylaxis not needed
- risk of bleeding w/ aspirin or warfarin is low so meds can usually be taken 
  • complications:
    endophthalmitis, retinal detachment**
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23
Q

MC etiologies of presbycusis?

A
  • sensorineural
  • bilateral
  • beginning in high frequency rage (4000-8000Hz)
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24
Q

RFs for presbycusis?

A
  • lifetime exposure to noise
  • genetics
  • meds
  • older age
  • DM
  • cerebrovascular disease
  • smoking
  • HTN
  • white race
25
Q

Presentation of presbycusis?

A
  • complain of inability to hear/understand speech in crowded or noisy environment
  • difficulty understanding consonants
  • inability to hear high pitched voices or sounds
  • assoc sxs:
    tinnitus
    if hearing pulsatile noise in one ear should further assess w/ MRA or MRI to R/O glomus tumor or AV malformation
26
Q

Diff for presbycusis? WHen should screening be done? adverse effects of presbycusis?

A
  • diff: cerumen impaction, if unilateral TIA or CVA
  • screening for hearing loss if older than 60
  • can lead to low self-esteem, isolation, and depression
  • need to be eval by audiologist if sig deficit consider amplification (hearing aids)
27
Q

Effectiveness of hearing amplification?

A
  • hearing aids don’t restore hearing to normal
  • for example a 60 dB loss could be improved to 30 dB range
  • sometimes 2 hearing aids are better, sometimes one
  • they range from simple to complex and price of course increases w/ complexity
  • need to be properly fit and for digital aids properly programmed
28
Q

Sxs of hypothyroidism?

A
  • slowing of metabolic processes: fatigue, cold intoelrance, weakness, lethargy, wt gain, constipation, hair loss,
  • accum of matrix substances: myalgias, arthralgias
29
Q

What is subclinical hypothyroidism?

A
  • defined as a normal T4 w/ elevated TSH

- data linked subclinical hypothyroidism w/ atherosclerosis and MI esp when TSH is greater than 10 mU/L

30
Q

Tx of subclinical hypothyroidism?

A
  • pts w/ TSH of 10 or more - tx
  • pts (any age) who have sxs of hypothyroidism - tx
  • pts younger than 70 with TSH b/t 4.5-10mU/L who have higher titers of thyroid peroxidase abs, which predict progression to overt hypothyroidism, or goiter,: consider tx
  • pts over 70 w/ TSH b/t 4.5-10 mU/L: don’t tx (uncertain benefits and potential for cardiovascular and msk morbidity + risk of overtx
31
Q

What is COPD? Periodic exacerbations involve what?

A
- slow progressive irreversible airway obstruction:
chronic bronchitis
emphysema
- periodic exacerbations:
increased dyspnea
infections
respiratory failure
32
Q

How common is COPD?

A
  • 4th leading cause of death in US
  • 14.2 mill people affected
    8-17% men
    10-19% women
  • mortality:
    200/100000 men
    80/100000 women
33
Q

RFs for COPD?

A
  • smoking
  • exposure to inhalants
  • alpha 1 anti-trypsin
  • 15-20% of smokers develop it
  • not reversible!
34
Q

PP of COPD?

A
  • airflow obstruction
  • decreased cilia movement which leads to mucus in bronchioles that block airway - leads to inflammatory response - this leads to air trapping in alveoli, decreased air exchange
  • increased residual volume and fxnl capacity, total lung capacity often increased, vital capacity decreased
  • chronic bronchitis: goblet cell hyperplasia, mucus plugging, excess mucus secretion, fibrosis - unable to maintain normal blood gases by increasing breathing effort
35
Q

Diff b/t chronic bronchitis and emphysema?

A
  • chronic bronchitis:
    dx:
    daiy productive cough for 3 months or more, in at least 2 consecutive yrs
    pt will appar overwt, cyanotic, elevated hemoglobin, peripheral edema, rhonchi and wheezing
  • emphysema:
    dx:
    permanent enlargement and destruction of airspaces distal to terminal bronchiole
  • older and thin, severe dyspnea, pursed lips, X-ray: hyperinflation, with flattened diaphragms
36
Q

Etiologies of acute exacerbations of COPD?

A
- infections 70-80%
viral 1/3 to 2/3
bacterial 1/3 to 1/2
use abx: broader regimen when older than 65, comorbid conditions, severe dz, recenta antimicrobial therapy, mixed 1/3 
- enviro pollution or unknown
37
Q

Other tx for COPD?

A
  • SABAs
  • short acting anti-cholinergics
  • glucocorticoids
38
Q

Complications of COPD?

A
  • cor pulmonale
  • pneumonia
  • pneumothorax
  • polycythemia
  • arrhthymias
39
Q

Only tx for COPD that prolongs life? Surgery?

A
  • O2

- most elderly pts are not candidates for surgery or lung transplant

40
Q

SEs of glucocorticoids in tx of COPD?

A
  • chronic therapy usually involves long term inhaled glucocorticoids
  • local deposition effects:
    dysphonia
    thrush
    cough/throat irritation/reflex bronchoconstriction
  • systemic SEs:
    consider pharmokinetics
    osteoporosis
    adrenal suppression
    increase intraocular pressure/cataracts
41
Q

Signs of worsening COPD?

A
  • decrease in BMI
  • decrease in FEV1
  • increased dyspnea on exertion
  • need for O2
42
Q

Tx for end stage COPD?

A
  • hospice
  • control any pain
  • usually bedridden
  • support family
  • get living will in advance from pt - don’t want to put them on a ventilator they can’t come off of
43
Q

Predisposing conditiions for CAP?

A
  • smoking
  • alcohol consumption
  • pulmonary edema
  • malnutrition
  • admin of immunosuppressive agents
  • being 65 or older
  • COPD
  • previous episode of pneumonia
44
Q

Pathogens of CAP?

A
  • H flu, chlaymdia
  • Strep pneumo
  • viruses: 10-31%
45
Q

RFs for drug resistance in tx CAP?

A
  • over 65
  • abx therapy w/in last 3-6 months
  • alcoholism
  • medical comorbidities
  • immunosuppressive illness or therapy
46
Q

Tx for CAP?

A
  • general/uncomplicated:
    macrolides - azithro
  • complicated/comorbidities/recent abx use:
    resp fluoroquinolones (min of 5 days) - levofloxacin
    amoxacillin-clavulanate (augmentin)
47
Q

Indications for hospitalization for pt w/ CAP?

A
CRB-65:
confusion
RR over 30
BP (syst less than 90, or diastolic less than 60)
age over 65
- scores:
0-1 tx as outpt
2 - hosp
3-4 consider ICU care
48
Q

Why are LTCF pts predisposed to pneumonia?

A
  • have higher mortality than elderly pts in the community
  • underlying factors:
    COPD
    Left HF
    aspiration
    use of sedating meds
49
Q

Parameters for clinical tx in LTCF rather than hospitalization?

A
  • able to eat and drink
  • pulse is 100 or less
  • RR is 30 or less
  • systolic BP 90 or more, or decrease of 20 or less if baseline less than
    100
  • O2 sat equal to or greater than 92% or if pt has COPD 90% or more
  • residents tx clinically less likely to be hosp and no greater mortality, also greater cost savings -$1016/pt
50
Q

number of elderly pts seeking tx for pain?

A
  • 71% take Rx analgesics (63% over 6 m)
  • 72% take OTC analgesics (median duration 5 yrs)
  • 26% report side effects:
    10% hosp and 41% taking meds for SEs
  • 79% had seen PCP
  • 20% had seen more than 5 docs
51
Q

Common causes of pain in the elderly?

A
  • osteoarthritis and other jt diseases
  • night time leg cramps
  • claudication
  • neuropathies:
    diabetic
    herpetic
    idiopathic
  • cancer
52
Q

Why is chronic pain undertx in elderly?

A
  • they underreport
  • health care providers hesitant to rx opiates for non-cancer pain
  • pain can have sig effects on person’s fxnl status and mood
53
Q

WHO guidelines for tx pain in elderly?

A
  • mild: nonopioid or/- adjuvant
  • moderate: opioid or adjuvant
  • severe: stronger opioid or adjuvant
  • deliver med in most optimum route
  • Don’t use:
    Amitriptyline
    Propoxypene
54
Q

Why are NSAIDs bad to use in elderly?

A
  • 5-7% hosp due to adverse effects of drugs
  • 30% of those b/c aspirin and other NSAIDs
  • increased chance of toxic effects in those over 65
  • renal toxicity (relative intravascular volume depletion)
  • GI: much more prone after 60
  • cardiotoxicity: can worse CHF and HTN
  • interacts w/ aspirin and warfarin
55
Q

Management for pain in elderly?

A
- first line:
tylenol (arthritis strength)
- neuropathic pain:
use neurontin, lyrica, cymbalta
- opioids: small doses, spread apart, watch for confusion, constipation, if already confused stay away
56
Q

Adjuvant therapies for pain?

A
  • exercise: PT, OT, stretching, strengthening, TENS, general conditioning
  • physical methods:
    ice, heat, massage
  • CBT
  • chiropractic therapy
  • acupuncture
  • relaxation and guided imagery
  • biofeedback
57
Q

What is osteoporosis?

A
  • disease characterized by low bone mass w/ microarchitectural disruption and skeletal fragility
  • these lead to fragility fractures:
    occur from standing ht or less, occur w/ no trauma
  • screening for osteoporosis involves fracture risk assessment and measurement of BMD
58
Q

Components of fracture risk assessment?

A

RFs independent of BMD are:

  • advanced age
  • previous fracture
  • long term glucocorticoid therapy
  • low body wt (under 127 lbs)
  • family hx of hip fracture
  • smoking
  • excess alcohol intake
  • these can be screened at office visits in postmenopausal women and men over 60
59
Q

Tx for fractures in osteoporosis?

A
  • hip: surgery
  • verterbal:
    analgesics
    calcitonin
    vertebroplasty and kyphoplasty
  • impact on fxn