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NUNP547 Older Adult Theory > Week 6 - MH/Neuro/Insomnia > Flashcards

Week 6 - MH/Neuro/Insomnia Flashcards

1
Q

Which medication has the strongest recommendation for use for insomnia: trazodone, melatonin, or diphendyramine? (for adults with insomnia)

A

Tricks! None of them – all of these have weak recommendations against their use.
None of the medications used to treat insomnia have strong evidence either FOR or AGAINST their use – all recommendations are weak either way. Weird huh.

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2
Q

In order for a medication for insomnia to be deemed useful for your patient, how many nights is an acceptable trial of efficacy?

A

Two nights.

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3
Q

What are some classes of prescription medications that can cause sleep disturbance?

A

SSRIs, SNRIs, bupropion, alpha blockers, beta blockers, diuretics, stimulants, acetycholinesterase inhibitors, dopamine receptor agonsits, systemic corticosteroids, varenicline.

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4
Q

What are some non-prescription medications and substances that can cause sleep disturbance?

A

ETOH, caffeine, cannabis (withdrawal), cocaine, decongestants, ephedrine, nicotine and nicotine replacement therapy, laxatives (eeeeee)

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5
Q

What is the maximum dose of zopiclone for adults, and for adults over the age of 65?

A

7.5 mg max for adults

5 mg for adults over 65 (also for those with renal/hepatic dysfunction or on a strong CYP3A4 inhibitor

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6
Q

What is the starting dose of zopiclone for adults?

A

3.75 mg

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7
Q

Why did Health Canada decrease max doses of z-drugs?

A

Because next-day impairment and decreased vehicle control was a thing. You should not drive for TWELVE HOURS after taking zopiclone or eszopiclone. Zolpidem is 8 hours (not sure if this one is available in Canada).

A study found impaired driving equivalent to 3-4 beer, 11 hours after taking 7.5 mg of zopiclone.

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8
Q

Studies have shown that the z-drugs include total sleep time per night by 2.5 hours.

True or false?

A

False!

30 minutes!

People tend to fall asleep approx 18 minutes faster than without the medication, and awake time after onset of sleep is approx 13 minutes.

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9
Q

Health Canada says the use of z-drugs for sleep disturbance should be limited to how long (duration)?

A

7-10 days.

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10
Q

Medications for insomnia can have crazy long half-lives, so the sedation effects can be felt the next day for many of them.

Matchy-match:

Zopiclone 12-20 hours
Diphenhydramine 30 hours
Lorazepam 4-11 hours
Amitriptyline 5-9 hours
Trazodone 30-40 hours
Clonazepam 3-9 hours

A

Zopiclone 4-11 hours
Diphenhydramine 3-9 hours
Lorazepam 12-20 hours
Amitriptyline 30 hours
Trazodone 5-9 hours
Clonazepam 30-40 hours

Diazepam is 24-100 hours, and doxepin is 31 hours! - you can see the cautions needed in the elderly peeps with anticholinergic effects and falls risks.

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11
Q

Doxepin is a TCA that has been rebranded as an insomnia medication that helps reduce waking time through the night by about 20 minutes. It does not help with time it takes to fall asleep.

It has been shown to help with sleep maintenance in older adults only.

What is the initial dose for older adults 65+?

How do meals affect this medication?

A

Initial recommended dose is 3 mg. Max dose 6 mg.

Onset of effect is delayed if taken within 3 hours of a meal.

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12
Q

To treat insomnia, trazadone is a safer choice than benzos, for older adults with falls risks. True or false?

A

False! Falls risk = falls risk.

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13
Q

Which classes of medications that are sometimes used to treat primary insomnia increases risk of mortality in older adults?

A

Atypical antipsychotics. The harms simply outweigh the benefits.

amitriptyline, mirtazapine, quetiapine, olanzapine, risperidone

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14
Q

When are atypical antipsychotics recommended?

A

To treat comorbid conditions, with caution after weighing risks and benefits.

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15
Q

Lemborexant is an orexin receptor agonist, marketed as Dayvigo. It has similar adverse events as others with some that are specific to this med. Can you name some?

A

Sleep paralysis
Cataplexy-like s/s (sudden leg weakness)
hallucinations

It has also shown risk of being misused as recreational.

In the PP, they discuss how ol’ Sue really liked this medication in her clinical practice. Jen the presenter said she hasn’t really used it because it is new to Canada (2023).

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16
Q

Important patient teaching if you prescribe lemborexant (Dayvigo)?

A

ETOH will DOUBLE the concentration of Dayvigo in your system. Abstain!

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17
Q

Guidelines across the world have strong recommendations for which treatment for insomnia?

A

CBTi - cognitive behavioural therapy for insomnia

Jen recommends free MH resources through Kelty’s Key website - they have CBT insomnia modules.

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18
Q

In terms of addressing medication overuse, Jen Carefoot gives us 4 components to include in your plan when tapering down insomnia medications. What are they?

A
  1. Plan a gradual dose reduction strategy with education.
  2. Identify alternative to managing the underlying health issue (that is causing the overuse). ie pain, mood
  3. Develop strategies to minimize withdrawal.
  4. Establish a schedule of follow-ups.
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19
Q

You should use a de-prescribing resource to help you taper down insomnia meds, true or false?

A

Of course! There is no “one best way” to do it. Call your pharmacist, use online tools, sites etc.

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20
Q

When counseling a patient about when to take zopiclone or eszopiclone, what should you tell them?

A

Take immediately before bed and only if you plan to get a full night’s sleep (8 hours).

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21
Q

What is normal pressure hydrocephalus (NPH)?

A

NPH = refers to a condition of pathologically enlarged ventricular size with normal opening pressures on lumbar puncture

a form of communicating hydrocephalus

distinguished from obstructive or noncommunicating hydrocephalus, in which there is a structural blockage of the cerebrospinal fluid (CSF) circulation within the ventricular system

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22
Q

What is the classic triad of symptoms in NPH? Are all o f these required for diagnosis?

A

dementia, gait disturbance, and urinary incontinence

**Patients need not have all three cardinal features, but gait must be the predominant problem

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23
Q

Is NPH a common cause of dementia?

A

No - rare condition compared with other causes of dementia in older adults

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24
Q

Who is more likely to get NPH?

A

Idiopathic NPH increases in prevalence with age and is most common in adults over the age of 60 years

Secondary NPH (those cases associated with an identified etiology) can occur in all age groups

M:F

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25
Q

Etiology of NPH

A

Idiopathic (50%)

Secondary: SAH, meningitis, trauma, radiation-induced (these inhibit CSF resorption)

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26
Q

What does the gait dysfunction of NPH look like? How is it different from parkinsons?

A

**Most prominent feature (and required for diagnosis)

move slowly and take small steps, often with a wide base

have difficulty turning (eg, they take several steps to turn 180 or 360 degrees) and are most vulnerable to falls when turning

Postural instability demonstrated by the pull test is often present

parkinsonian gait may bear a resemblance to that of NPH but is distinguished by a narrow base and responsiveness to visual and acoustic cues

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27
Q

What does cognitive impairment in NPH present like?
- slow vs gradual onset
- what kind of features

A

evolves over months to years and usually develops after the onset of gait dysfunction

Patients typically have both subcortical and frontal features, including:

Psychomotor slowing

Decreased attention and concentration

Impaired executive function

Apathy

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28
Q

Will you see the following in NPH: headaches, N/V, vision loss, papilledema

A

NO - these are pertinent negatives…these are signs and symptoms related to diffusely increased intracranial pressure (ICP) are will NOT be seen in NPH

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29
Q

Diagnosis of NPH

A

MRI: Enlarged ventricles without increased prominence of cerebral sulci (can also seen on CT but MRI preferable)

Cognitive evaluation

exclusion of alternative causes of gait dysfunction, both neurologic and non-neurologic

In patients with clinical and MRI features suggestive of NPH, we use a lumbar tap test to help identify patients likely to respond to shunt placement

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30
Q

Treatment of NPH. Does it work for everybody?

A

Main treatment is ventriculoperitoneal shunt – not everyone responds to this

NPH is potentially reversible by the placement of a VP shunt so it’s key is to identify early!

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31
Q

What are the pathognomonic S&S of parkinsons?

A

SLOW, STIFF, AND SHAKEY

Bradykinesia/Akinesia, Tremor (resting), Rigidity (lead pipe with or without cogwheeling)

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32
Q

Risk factors for parkinsons

A

Age
family history
male sex (approximately 1.4:1)
head injury
cerebrovascular disease
rural environments
exposure to certain neurotoxins (pesticides, air pollution, well water)
comorbidities including excess body weight and metabolic syndrome
T2DM
history of melanoma or prostate cancer

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33
Q

Factors that protect against parkinsons?

A

Smoking, caffeine, exercise, ibuprofen, statins

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34
Q

Very basic summary of the patho of parkinsons?

What kind of movement is decreased/increased?

What causes the cognitive deficits?

A

The central defect in PD is dopamine depletion from the basal ganglia.

  • dopamine depletion and a relative excess of acetylcholine
  • decreasing voluntary movement, increasing movement inhibition

Pathogenesis is primarily unknown.

Protein deposits caused from degeneration of dopaminergic neurons accumulate forming Lewy bodies causing neurotoxicity which can lead to dementia and cognitive impairment

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35
Q

In what age is parkinsons most often diagnosed?

A

Adult-onset. Incidence of disease rises rapidly over 60 years of age, with a mean age of 70.5 years

Monogenetic forms of PD, which account for <10% of cases, have a younger onset.

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36
Q

T/F the progression of parkinsons is preditable

A

F - Progression of symptoms is highly variable making it not possible to predict future course for a patient at the time of diagnosis

*More rapid if autonomic and cognitive changes are prominent
*More benign course if tremor is presenting symptoms

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37
Q

What kind of prodromal symptoms are known to proceed parkinsons?

A

Prodromal nonmotor symptoms including sleep disorders, constipation, anxiety/depression, and hyposmia/olfactory dysfunction

can precede motor manifestations by years or decades.

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38
Q

In parkinsons, progression from disease impairment to disability generally occurs between ___ - ____years after diagnosis

A

3-7

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39
Q

T/F Parkinsons symptoms usually have a bilateral onset

A

Falsoooooooo. Normally unilateral onset.

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40
Q

Describe the typical tremor of parkinsons

A

resting tremor. May be intermittent but progress over time

“pill-rolling” tremor of hands common can be uni or bilateral (usually assymetric)

suppressed with initiating movement

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41
Q

Describe the rigidity seen in parkinsons

A

lead-pipe resistance = passive movement of the joints reveals continuous resistance throughout the entire range of motion

Cogwheel resistance is often present and may reflect tremor incidentally felt while assessing tone.

Cogwheel without lead-pipe does not fulfill minimum requirements for rigidity.

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42
Q

Descirbe the bradykinesia & akinesia/hypokenesia in parkinsons. What characteristic things will you see in the patient’s walk, face, and fine movements?

A

bradykinesia = slowness of movement AND akinesia/hypokinesia decrease in amplitude or speed (progressive hesitations/halts) as movements continue

  • must have limb bradykinesia
  • loss of facial expression
  • loss of arm swing
  • difficulty with fine movements (micrographia)
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43
Q

Other early S&S of parkinsons to do with walking and ADLs?

A

Hyposmia

Trouble turning in bed

Trouble opening jars

Shuffling gait

Trouble rising from chair

Glabellar tap

Difficulty walking heel-toe

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44
Q

What are the later signs of parkinsons?

A

**At this point, usually has progressed to bilateral

Postural instability

Cognitive impairment, dementia, psychotic symptoms, depression

Sleep disturbance – daytime hypersomnolence and nocturnal akinesia

Autonomic dysfunction (constipation, orthostatic hypotension, excessive sweating) (O’Toole, 2023)

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45
Q

T/F a brain MRI is key to diagnosing parkinsons.

….How is parkinsons diagnosed?

A

Falso falso falso!
Neuroimaging is usually nondiagnostic in evaluation of PD. Can be used to rule out alternative disorders or clarify diagnosis when clinical symptoms are atypical.

Diagnosis is based on motor manifestations.

MDS Clinical Diagnostic Criteria – global standard for PD diagnosis:
- Must have parkinsonism – bradykinesia with tremor or rigidity
- Must refer to neurology – motor features and most diagnostic features are determined by appropriate history taking and skilled neuro exam (MDS, 2023).

Neurologists use 3 categories to determine if PD is the cause of parkinsonism:
- Absence of absolute exclusion criteria
- At least 2 supportive criteria
- No red flags

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46
Q

Nonpharm management of parkinsons

A

Encourage regular exercise to maintain or improve flexibility - very important!!

Encourage diet high in fibre and calcium with adequate fluid intake to help limit complications of constipation and osteoporosis

PT/OT/SLP referrals

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47
Q

What are the first and second liine pharm treatments of parkinsons?

A

1) Levodopa
2) Dopamine agonists

**Rxflies says DAs can be first line for individuals <70 yo

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48
Q

T/F Drug-induced parkinsonism is reversible

A

True! But may take 2-6 months after withdrawal of the medication to make the symptoms go away

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49
Q

What drugs have moderate to high risk of drug-induced parkinsonism?

A
  1. Typical neuroleptics (e.g. haloperidol, ?pimozide, chlorpromazine,
    fluphenazine, perphenazine, prochlorperazine, trifluoperazine,
    flupentixol, zuclopenthixol)
  2. Some atypical neuroleptics (e.g. aripiprazole, olanzapine,
    paliperidone, risperidone, ziprasidone)
  3. Lithium
  4. Venlafaxine
  5. CCBs (amlodipine, diltiazem, verapamil)
  6. Metoclopramide, prochlorperazine, promethazine
  7. Phenytoin, levetiracetam, valproate
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50
Q

T/F PD therapies are effective for slowing or stopping brain degeneration / disease progression.

A

False! Just manage symptoms

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51
Q

What dietary counselling needs to be provided when started levodopa with regard to food that decreases absorption?

What can be done to increase absorption speed of levodopa?

A

For quicker onset, chew levodopa/carbidopa IR tablets or drink with carbonated beverages to
↑ absorption

protein foods may slow or ↓ absorption

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52
Q

PD: Late or missed doses of medications can result in….

A

confusion and worsen motor symptom control.

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53
Q

What disorder can result from dopaminergic treatments like levodopa?

A

Impulse control disorders (gambling, hypersexuality…)

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54
Q

T/F Controlled release (CR) levodopa/carbidopa is preferred to immediate release (IR)

A

False
Levodopa/carbidopa controlled release (CR) is not superior to immediate-release (IR) formulation. The
overall amount of levodopa absorbed from levodopa CR is ~25-30% less than the IR levodopa.

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55
Q

What is the risk of abrupt withdrawal of antiparkinson meds?

A

may cause neuroleptic malignant
syndrome or worsening motor symptoms (acute akinesia) that may not recover.

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56
Q

What is levodopa? What does carbidopa do?

A

Levodopa = a dopamine precursor

Carbidopa decreases peripheral conversion of l-dopa to dopamine - in other words, it prevents the levodopa from being broken down before it reaches the brain

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57
Q

Common side effects of levodopa/carbidopa?

A

Nausea
Nightmares
Hallucinations
Increased libido
Fluctuations (wearing off)
Dyskinesia (~50%)

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58
Q

T/F: Dopamine agonists can be given in conjunction with levodopa to allow lower dose of levodopa to reduce levodopa associated symptoms.

A

True!

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59
Q

What other medications can we use for tx of parkinsons?

A

MAOB inhibitors (rasagiline, selegiline) used for mild motor symptoms (levodopa is better)

Anticholinergics – benztropine, ethopropazine

Beta adrenergics – for postural tremor (O’Toole, 2023).

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60
Q

How frequently is levodopa given for PD treatment?

A

TID to QID

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61
Q

How should the efficacy of PD treatment be judged?

A

Use patient and care partner’s overall impression of response since started on levodopa or with adjusted dose and not physical exam findings. Physical exam findings can vary from visit to visit d/t the late time the patient had their medication.

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62
Q

Over time, monitor for motor complications of levodopa therapy including….

A

motor fluctuations (wearing off), failed doses, involuntary movements (dyskinesia), abnormal cramps and dystonia

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63
Q

Belly’s palsy is a neuropathy of what cranial nerve?

A

VII - facial

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64
Q

Who gets Bell’s palsy?

A

Median age of onset 40 years old. Usually seen between 15- 60 years but may occur at any age. Rare in children.

M=F

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65
Q

Risk factors for bell’s palsy

A
  • Previous herpes simplex or herpes zoster infection
  • Recent infection
  • Diabetes
  • Pregnancy (especially 3rd trimester)
  • Family history of Bell’s Palsy
  • HTN
  • Hypothyroidism
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66
Q

Patho of Bell’s palsy

A

Exact etiology unknown; may be viral, autoimmune, or idiopathic

Often due to inflammation resulting in compression of the facial nerve

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67
Q

T/F In Bell’s, the injury of CNVII will result in symptoms on the contralateral muscles of the face

A

False - ipsilateral

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68
Q

How fast does Bells come on? How long does it last?

A

Acute onset, progressing over hours to days

Recovery in 3-4 weeks; may take up to 6 months (faster recovery occurs in mild/ moderate cases)

Complete recovery in 80% of cases; without treatment, 70% of patients with complete and 94% with incomplete paralysis recover facial function in 6 months

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69
Q

S&S of Bell’s

A

Acute onset of unilateral facial weakness or paralysis (primarily motor deficits)

Impaired forehead wrinkling

Inability to close eye of affected side, drooping of eyelid

Mouth drooping to affected side/ inability to smile

Flattened nasolabial fold

Can be associated with involuntary movements (synkinesis)

Facial paresthesia

Drooling

Decreased tearing or abnormal lacrimation with eating

Hypersensitivity to sound (hyperacusis)

Ear pain

Pain associated with facial palsy

Change in sensation of taste (anterior tongue)

Bilateral is extremely uncommon

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70
Q

When assessing a patient for possible Bell’s palsy, what are some red flags that indicate a different/more serious condition?

A

Forehead sparing (indicates contralateral UMN lesion)

Focal neurological deficits (Bell’s palsy, by nature, only affects one cranial nerve. Presence of focal neuro deficits suggestive of UMN lesion/ stroke)

Bilateral acute facial weakness (i.e., MS)

Fever/ headache/ stiff neck

Vesicles in ear canal (Ramsay hunt)

Additional cranial neuropathies

Sudden onset of symptoms at max severity (Bell’s occurs over 1-3 days and is progressive)

Worsening beyond 3 weeks

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71
Q

Dx of Bell’s palsy

A

Clinical diagnosis

CT or MRI only if atypical presentation or physical findings suggestive of central lesion (affecting other cranial nerves, associated with limb weakness or ataxia), progressing paralysis, or lack of resolution

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72
Q

Non-pharm tx of bell’s palsy

A

Facial physical therapy for muscle weakness (following acute stage)

Eye protection: sunglasses, eye patch, taping eye shut at night (otherwise corneal ulceration and visual impairment can occur)

Heat/ cold for pain

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73
Q

Pharm tx of bell’s palsy

A

Medical management is first line

Focused on reducing inflammation/ nerve compression

Corticosteroids (ASAP and within 48 hours)

Antivirals can be combined with steroids (severe cases only; antivirals alone show no clinical benefit)

Acetaminophen for pain

Eye drops (i.e., methylcellulose) for lubrication

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74
Q

What the heck is giant cell arteritis? AKA?

A

= autoimmune condition that causes inflammation in both large and medium sized blood vessels, a process called vasculitis

Most often, it affects the arteries in your head, especially those in your temples. For this reason, giant cell arteritis is sometimes called temporal arteritis

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75
Q

Patho of GCA

A

Triggering event is not complete understood but is an immune-mediated disease

Medial layer of inflamed arteries are invaded by inflammatory cells.

Vascular remodeling & occlusion: intimal hyperplasia & arterial occlusion resulting in vascular stenoses & occlusion

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76
Q

Risk factors for GCA. What age? What condition is it commonly associated with?

A

Older adult (almost never happens before age 50)
Most commonly age 70-80

F:M 3:1

Northern European ancestry

Famiily history (genetics)

Commonly associated by polymyalgia rheumatica

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77
Q

Most common S&S of GCA?

A

New onset headache that is different from previous headaches - doesn’t have classic location

Tender scalp/temples

Jaw pain or tongue pain with chewing that is relieved with rest (aka jaw claudication)

Unexplained fever, weight loss, night sweats and fatigue

Sudden vision loss or double vision

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78
Q

GCA may present with S&S of polymyalgia rheumatica (because it’s often associated). What are these?

A

Pain and stiffness in the shoulders, neck, upper arms, and hip area.

Flu-like symptoms, including low-grade fever, weakness, loss of appetite, and weight loss.

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79
Q

What physical exam findings might you find in a patient with GCA?

A

Abnormal pulses (occurs in large vessel disease); diminished pulses and discrepancy in BP in arms

Temporal artery abnormalities: thickened, nodular, tender, erythematous

Decreased or absent temporal artery pulse.

Bruits: carotid, axillary, brachial, femoral, abdominal aorta

Heart murmur (aortic regurg)

Ocular findings on fundoscopic exam
- Cotton wool spots on retina
- Swollen pale disc & blurred margins
- Diplopia associated w/reduced EOM

MSK findings:
- dec in active range of motion of shoulders, neck, hips d/t polymyalgia rheumatica
- Distal synovitis, esp wrists and MCP joints

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80
Q

Diagnosis of GCA?

A

CBC: Thrombocytosis, Normochromic anemia

ESR & CRP( both high)

Elevated hepatic enzymes (esp alk phos) in 25-30% pt’s

Temporal artery biopsy

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81
Q

Treatment of GCA

A

high dose corticosteroid to prevent further ischemic complications and improve systemic symptoms

May add tocilizumab or methrotrexate to glucocorticoid therapy (not as fast acting, may require year of treatment)

management of pt’s w/large vessel GCA includes antiplatelet therapy and possible surgical interventions

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82
Q

T/F the vision loss caused by GCA is not dangerous & is easily reversed

A

False! Can be permanent and requires emergency treatment

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83
Q

T/F GCA increases a person’s risk of stroke or MI

A

True

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84
Q

What is OSA? (I know this isn’t neuro but wanted to put it alongside central sleep apnea)

A

-OSA is the periodic reduction (hypopnea) or cessation (apnea) of breathing due to a narrowing or occlusion of the upper airway during sleep

-Characterized by recurrent and reversible obstruction of the pharyngeal airway during sleep

In OSA, thickening of tongue and pharyngeal tissues reduces air passage to the trachea

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85
Q

OSA is associated with poor quality of life and has been linked to severe chronic health conditions such as….

A

obesity, diabetes, metabolic syndrome, and neuro-psychiatric problems

Moderate–severe OSA is associated with an increased risk of CVD, HTN, CAD, stroke, HF, and atrial fibrillation

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86
Q

Is OSA more likely in men or women?

A

Men

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87
Q

Who else is more prone to OSA?

A

Risk factors include (BC Guidelines, 2023):
-Down syndrome
-Mandibular hypoplasia (retrognathia, micrognathia)
-low-lying soft palate (i.e., high Mallampati Score)
-large tongue
-tonsillar hypertrophy
-upper body obesity
-short/wide neck
-older age
-male sex
-smoking
-family hx of snoring or OSA
-East Asian origin
-Parkinson’s disease
-TBI
-nasal and nasopharyngeal obstruction
-neuromuscular disease
-Marfan syndrome
-PCOS

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88
Q

A neck circumference of what for men and women is a risk factor for OSA?

A

neck circumference >17in for men and >16in for women

(STOPBANG just asks if shirt collar is 16in/40cm or larger)

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89
Q

Symptoms of OSA worsen with sedating substances such as….?

A

ETOH, benzodiazepines, antipsychotics, opioids, barbiturates, beta-blockers, antihistamines, sedative antidepressants

90
Q

S&S of OSA?

A

Daytime sleepiness – most common

-Loud snoring, gasping, choking, snorting or pauses during sleep

-Falling asleep when watching TV, reading, driving/riding in a car

-Fatigue

-Poor, restless sleep

-Dry mouth or sore throat

-Lack of physical or mental energy. Impaired concentration.

-Morning headaches

-Decreased libido and impotence

-Nocturia

-Recurrent night-time awakenings

91
Q

What scale can we use to quantify daytime sleepiness?

A

Epworth Sleepiness Scale (ESS)

92
Q

What test to we use to diagnose moderate to severe OSA?

A

HSAT (home sleep apnea test)

93
Q

What is the gold standard for testing all sleep disorders?

A

Polysomnography (PSG)

Sensitivity and specificity are 100%

94
Q

WHen do we send a patient for HSAT?

A

Diagnostic testing for OSA should be performed if mod-severe OSA is suspected. This is indicated by the presence of excessive daytime sleepiness or fatigue and at least two of the following three criteria:
1) witnessed apneas or gasping or choking.
2) habitual loud snoring.
3) diagnosed HTN

95
Q

When do we refer for polysomnography?

A

There are specific exclusion criteria for use of the HSAT that are outlined on the requisition. If any one of the exclusion criteria are met, they should be send to sleep disorder physician for possible PSG

Criteria are:
- Concern for non-respiratory sleep disorder (e.g. chronic insomnia, sleep walking/talking).
- Risk of hypoventilation (e.g. neuromuscular disease, BMI ≥ 40 kg/m2
).
- Chronic/regular opiate medication use.
- Significant cardiopulmonary disease (e.g. history of stroke, heart failure,
moderate-to-severe lung disease).
- Previous negative or equivocal HSAT.
- Children < 16 years old.
- Inability to complete necessary steps for self-administered HSAT (e.g. cognitive,
physical, or other barriers)

96
Q

What are the criteria for diagnosis of OSA based on the HSAT?

A

1) 15 or more events in apnea/hypopnea index (AHI) in an asymptomatic client. More than 75% of apneas/hypopneas must be obstructive.

2) 5 or more in AHI in a client with symptoms or signs of disturbed sleep. More than 75% of apneas/hypopneas must be obstructive.

97
Q

What is the goal of treatment in OSA?

A

Goal: AHI is normal (<5 events/hour), the ESS score is 10 or less, the patient feels rested, and a bed partner reports no residual snoring

98
Q

Lifestyle recommendations for individual with OSA

A

Lifestyle changes: weight loss, decrease alcohol/sedatives, increase exercise

99
Q

Treatment options for OSA?

A

Continuous positive airway pressure (CPAP) machine – definitive therapy

-Positional therapy

Oral appliances:
- Tongue retaining device (TRD)
- Mandibular advancement device (MAD)

-Nasal strips/dilators – mild OSA

-Chin straps/mouth tape

-Oral surgeries to reduce tissue volume or correct craniofacial abnormalities

-Hypoglossal Nerve Stimulation (HNS)

100
Q

Your patient is started on a CPAP for treatment of OSA. When should you follow up?

A

30-90 days after CPAP initiation to ensure compliance and perform troubleshooting.

-Check in once a year to ensure ongoing CPAP usage and monitor for recurrent of OSA.

101
Q

What is central sleep apnea?

A

Related to the central nervous system

characterized by complete cessation or transient reduction in breathing with absent respiratory
effort. This occurs in patients with neurological disease or in association with drug/substance abuse or high altitude

The brain intermittently stops trying to breath for 10-15seconds

102
Q

Risk factors for central sleep apnea

A

Older age

Male

CHF

Post CVA

Use of depressant medications (such as chronic opioid use)

103
Q

Is OSA or central sleep apnea more common?

A

OSA much more common

104
Q

What causes central sleep apnea?

A

often associated with other medical conditions, especially heart failure, stroke, and opioid medications.

Rare cases are primary or idiopathic

105
Q

S&S of central sleep apnea

A

disrupted sleep

excessive daytime sleepiness

poor subjective sleep quality

Inattention and poor concentration

Nocturia

Stress induced insomnia

Nocturnal angina pain

Headache

PND

106
Q

Treatment of central sleep apnea?

A

CPAP

Respiratory stimulants (azetazolamide, theophylline)

Supplemental oxygen during sleep

107
Q

What is the Mallampati Classification System?

A

Assesses anatomy to determine risk for apnea or hypopnea episodes (in the case of OSA)
- also used to assess possible difficult intubation

It is divided into four classes, with higher classes indicating less visible airways.

A high Mallampati Score can predict a greater risk of obstructive sleep apnea.

May help identify patients who should be prioritized for a sleep study and/or sleep medicine referral

108
Q

Class I vs class IV on the mallampati score?

A

Class I: soft palate, uvula, and tonsillar pillars visible

Class IV: only hard palate is visible

109
Q

3 categories of elder abuse

A
  • Domestic elder abuse
  • Institutional abuse
  • Self neglect
110
Q

What is domestic elder abuse?

A

abuse that usually takes place in the home, and the abuser is often a relative, close friend, or paid companion. Abuse can take different forms: physical, emotional, financial, sexual, spiritual or social.

This can include withholding care (e.g. necessities of life)

111
Q

What is institutional elder abuse?

A

abuse that takes place in a residential home (such as a nursing home), foster home, or assisted-living facility, and the abuser has a financial or contractual obligation to care for the older adult.

112
Q

What is elder self neglect

A

behaviour of an older adult that threatens his or her own health or safety, when an older adult refuses, or fails, to provide himself or herself with adequate food, water, clothing, shelter, personal hygiene, medicine, and safety precautions.

113
Q

Name some risk factors for elder abuse

A

Poor health

Functional dependence

Cognitive impairment

Substance abuse

Mental illness

Financial dependency

Prior history of abuse – domestic violence carried over into elder years, often by spouse

Social isolation

Low levels of social support

Low levels of social embeddedness

Low socioeconomic status

Racial/ethnic minorities

Shared living arrangement

114
Q

What sort of observations while interviewing the older adult should make you more suspicious of elder abuse?

A

-caregiver dominates interview
- caregiver is overwhelmed
- older adult is inappropriately dressed
- old adults appears fearful
- history of injuries with unclear cause
- delay in seeking care
- frequent ER visits
- poor adherence to treatment

115
Q

What physician exam findings should make you more suspicious of elder abuse?

A

Weight loss
Dehydration
Abrasions/hematomas/burns
Pressure ulcers
Fractures
Rectal/vaginal bleeding
Signs of STI

116
Q

What is reported to be the most common mental illness is older adults in BC?

A

Depression

117
Q

What are some non-modifiable risks factors for depression?

A
  • Family history, genetics
  • Age
  • Gender F>M
  • Race/ethnicity
  • Sexual orientation/preference
  • Childhood adverse events
  • Previous suicide attempts
  • Chronic disabling illness
  • Bereavement
  • Diagnosis of dementia, Parkinson’s or stroke, neurologic disorders
  • Placement in LTC (modifiable in some cases)
118
Q

What are some modifiable risk factors for depression?

A
  • Social isolation
  • Untreated/undertreated mental illnesses/psychiatric disorders
  • Difficulties with sleep
  • Socioeconomic status (difficult to modify)
  • Unemployment (also difficult to modify in the elderly)
  • Rural residence
  • Access to firearms
  • Marital status
  • Occupation
  • Media reporting
  • Low self-esteem, self-hatred
  • Accepting attitude towards suicide
  • Smoking
  • Perfectionism
119
Q

What is the diagnostic criteria for depression?

A

DSM-V criteria: 5 or more must be present for the same two-week period, be a change from previous functioning, with at least one of the symptoms being a depressed mood or loss of interest or pleasure.
(Captured by MSIGECAPS pneumonic)

*Depressed mood or feeling sad
*Loss of interest in activities that were previously enjoyed
*Changes in appetite or weight
*Sleeping issues – insomnia, hypersomnia
*Psychomotor agitiation/retardatioin
*Fatigue or loss of energy
*Feeling worthless or guilty
*Difficulty concentrating, thinking or making decisions
*Suicidality

120
Q

Some DDX for depression?

A

Infection, renal failure, lupus, neurocognitive disorder, stroke, Parkinsonism, cardiac issues, chronic debilitating illness, chronic pain, obstructive sleep apnea. Grief and complicated grief.

121
Q

What is the difference when treating an older adult with antidepressants, vs a younger adult, in regards to timing of full response to medication?

A

Because you start low and go slow, it can take 8-16 weeks for full effect. Patients should be feeling some improvement weekly though.

122
Q

How often to monitor Na levels when you start an older adult on antidepressants?

A

2-4 weeks afterwards. If concerns such as prior hx of hyponutremia, test prior to initiating meds.

123
Q

What are some investigations you should do when an older adult presents with s/s of depression (to rule in/out ddx)?

A

A full physical exam is necessary, a comprehensive history, plus the following investigations are recommended: ECG, CBC-D, creatinine, urea, TSH, triglycerides, random blood glucose, ferritin, iron, B12, urinalysis, urine toxicology, ETOH, acetaminophen, salicylates (The Edmonton Manual, 2021).

124
Q

Which class of antidepressants are assoc with increased risk of bleed?

A

SSRIs

125
Q

Which antidepressant should be avoided if CrCl is less than 30 ml/min?

A

duloxetine

126
Q

If you patient has a depressive disorder with decreased appetite and difficulty sleeping, which med is recommended?

A

Mirtazapine

127
Q

Which medication is not recommended if your patient has depression and anxiety disorders?

Which is a good option in this case?

A

Bupropion - stimulating and can worsen anxiety.

SNRIs are a good option.

128
Q

Which class of antidepressants are a good place to start, typically?

A

SSRI. Escitalopram, sertraline seem to be the most recommended and well tolerated.

129
Q

Non-pharm treatment options for depression?

A

Psychotherapy
Social prescribing
Increased physical activity as safe
Alternatives - light therapy, acupuncture, art/music/nature therapy, mindfulness,

130
Q

What therapy may be considered in older adults with severe depression who at risk of SI or who are experiencing partial success with psychotherapy and pharmacological treatments?

A

Electroconvulsive therapy

131
Q

What is the recommended 1st line tx for dysthymic depressive disorder?

A

Psychotherapy

Consider adding meds if s/s persist or worsen

132
Q

When should you refer your patient with depressive disorder?

A
  • Psychotic episode
  • Bipolar disorder
  • Depression with suicidal ideation or intent
  • Depression with co-morbid SUD
  • Severe major depressive episode
  • Depression with co-morbid dementia
  • Treatment resistant depression
133
Q

Which class of medications are 3rd line recommendations due to potential serious side effects?

(postural hypotension than can lead to falls, cardiac conduction defects, anticholinergic effects such as delirium, dry mouth, urinary retention and constipation)

A

TCAs.

134
Q

What are some screening tools you can use to assess for depression?

A

PHQ9
PHQ2
GDS15
GDS30
MSIGECAPS

Remember to ask about suicidality if using the GDS tools.

135
Q

Which classes of antidepressants are recommended to treat depression in Parkinson’s disease?

A

SSRI
SNRI is a good alternative

CBT is also recommended

136
Q

What is dysthymic depression?

A

AKA Persistent Depressive Disorder (PDD)

It is generally experienced as a less severe but more chronic form of major depression.

PDD is characterized by depressed mood experienced most of the time for at least two years.

In addition to depression or irritable mood, at least two of the following must be present: insomnia or excessive sleep, low energy or fatigue, low self-esteem, poor appetite or overeating, poor concentration or indecisiveness, and feelings of hopelessness. More severe symptoms marking major depression are often absent in PDD—this includes anhedonia (the inability to feel pleasure), psychomotor symptoms (particularly lethargy or agitation), and thoughts of death or suicide.

137
Q

__________________ is characterized by recurrent brief episodes of unilateral electric shock-like pains, abrupt in onset and termination, in the distribution of one or more divisions of the fifth cranial (trigeminal) nerve that typically are triggered by innocuous stimuli.

A

Trigeminal neuralgia

138
Q

What are the 3 parts of the trigeminal nerve?

A

●Ophthalmic (V1)

●Maxillary (V2)

●Mandibular (V3)

139
Q

What is the mechanism involved that leads to trigeminal neuralgia?

A

Compression of the trigeminal nerve root is the main mechanism of TN, but brainstem lesions account for a small proportion of cases.

Demyelination as in MS, central sensitization (central pain mechanisms) are some other mentions.

140
Q

What are the clinical features of trigeminal neuralgia?

A

Trigeminal distribution.

Paroxysmal pain with maximal pain at or near onset, facial spasms/severe pain.

Unilateral.

Trigger zones - light touch, chewing, talking, brushing teeth, cold air, smiling and/or grimacing.

Autonomic symptoms can occur with pain attacks - lacrimation, conjunctival injection, rhinorrhea

Continuous pain - Often milder pain is present b/n attacks, characterized as dull or tingling.

141
Q

How is trigeminal neuralgia diagnosed?

A

The International Classification of Headache Disorders, Third Edition (ICHD-3) diagnostic criteria for TN are as follows:

●A) Recurrent paroxysms of unilateral facial pain in the distribution(s) of one or more divisions of the trigeminal nerve, with no radiation beyond, and fulfilling criteria B and C

●B) Pain has all of the following characteristics:

*Lasting from a fraction of a second to two minutes

*Severe intensity

*Electric shock-like, shooting, stabbing, or sharp in quality

●C) Precipitated by innocuous stimuli within the affected trigeminal distribution

●D) Not better accounted for by another ICHD-3 diagnosis

142
Q

DDX for trigeminal neuralgia?

A

Acute herpes zoster

Postherpetic neuralgia

Trauma to the trigeminal nerve

Dental pain

Other causes of headache and craniofacial pain

143
Q

What imaging is recommended to determine the etiology of trigeminal neuralgia?

A

MRI

144
Q

What are the 1st line pharm tx recommended for TN?

A

carbamazepine or oxcarbazepine

Titrate up until sufficient pain relief is achieved, up to max dose of course

145
Q

What are some pharm tx you could explore if your patient with TN doesn’t respond to 1st line recommended meds carbamazepine or oxcarbazepine?

A

Gabapentin
Lamotrigine
Baclofen

Botox injections may be helpful

146
Q

What is the prognosis for trigeminal neuropathy?

A

The course of TN is variable. Episodes may last weeks or months, followed by pain-free intervals of weeks to years, although most remissions last for only a few months. Recurrence is common, and some patients have concomitant persistent background facial pain. Most often, the condition tends to wax and wane in severity and frequency of pain exacerbations. However, there are no pure natural history studies of TN, most likely because the severity of the pain leads to intervention. -UTD

147
Q

What are some options for rescue therapy in TN?

(I feel like we have referred these patients away by now!)

A

Rescue therapy can provide short-term analgesia for patients with TN while oral medications are titrated or during breakthrough attacks. \

Available agents include intranasal or intravenous infusion of lidocaine, intravenous phenytoin or fosphenytoin, or subcutaneous injections of sumatriptan.

148
Q

If your patient has trigeminal neuralgia and they do not respond to any pharmacological treatment options, too bad so sad there is nothing else available for treatment.

True or false?

A

False!

There are surgical options that very well-paid specialists can discuss with your patient.

149
Q

What is restless leg syndrome?

A

Chronic disorder characterized by strong desire to move legs, especially when at rest
Classified as both a sleep and movement disorder
Also known as Willis-Ekbom Disease

150
Q

Describe the epidemiology of RLS

A

-Tend to have the highest prevalence in Northern European countries
-F>M
-Increasing prevalence with increased age
-Risk factors: Family history, low serum ferritin, neuropathy, SC disease, MS, PD, ESRD, OSA, sleep deprivation, pregnancy, use of alcohol, nicotine, caffeine

151
Q

What medications can contribute to RLS?

A

antihistamines, dopamine receptor antagonists, certain antidepressants

152
Q

Describe the patho of RLS

A

Pathophysiology unknown
-Possibly related to reduced iron stores, complex alterations in dopaminergic systems, altered circadian physiology, and altered thalamic function
-Could also be related to peripheral cause- i.e., hyperalgesia, neuropathic pain, reduced endothelial function

153
Q

Describe the signs and symptoms of RLS

A

-Unpleasant urge to move legs (and sometimes arms)
-Present with inactivity
-More prominent in evening
-Transiently relieved by movement
-Often between knee and ankle, deep in leg
-crawling, tingling, restless, tension, etc
-NOT pain

154
Q

How is RLS diagnosed?

A

5 essential criteria must be met
1) Urge to move the legs (usually accompanied by uncomfortable/ unpleasant sensations in legs)
2) Urge to move legs begins or worsens during periods of rest or inactivity (i.e., lying down, sitting)
3) Urge to move the legs are partially or totally relieved by movement, at least as long as it continues (i.e., walking or stretching)
4) Urge to move legs occur or are worse in the evening or night than during the day
5) Not solely accounted for by another medical or behavioural condition (i.e., myalgia, venous stasis, leg edema, arthritis, leg cramps, positional discomfort, or foot tapping)

155
Q

Repeat the 5 RLS criteria :)

A

ALL 5 MUST BE MET
1) urge to move legs (may be assoc with uncomfortable/ unpleasant sensation)
2) worsens during rest/ inactivity
3) relieved by movt
4) worse at hs
5) not accounted for by another dx

156
Q

Ddx for RLS?

A

akathisia (assoc with dopamine blocking drugs), nocturnal leg cramps, positional discomfort, leg pain (vascular claudication, radiculopathy, peripheral neuropathy)

157
Q

Describe lifestyle management for RLS

A

-Avoid aggravating factors (insufficient sleep, poor sleep, untreated OSA, caffeine, etoh, meds like antipsychotics, dopamine blockers (metoclopramide), antihistamines)
-Do mental alerting activities when you are at rest (working on computer, doing crossword)
-Regular exercise
-Soaking legs in warm bath, leg massage, pneumatic compression devices

158
Q

Pharm tx of RLS?

A

-Replace iron if ferritin low ( ferritin <75, TSAT <45%)- sx improve in 2-3 weeks
-Intermittent therapy with levodopa carbidopa prn
-daily therapy (dopamine agonist like pramipexole)- monitor for impulse control
-gabapentin

159
Q

Define delirium.

A

Delirium is an acute confusional state characterized by an alteration of consciousness, with reduced ability to focus, sustain, or shift attention.

The DSM-IV’s core features of delirium include a disturbance in consciousness, change in cognition, develops in a short period of time that typically fluctuates throughout the day.

160
Q

What are some risk factors of delirium?

A

-advanced age
hospitalization/ER/postoperative/palliative care
-sensory impairment
-frailty
-polypharmacy
-infection
-dehydration
-immobility
-malnutrition
-use of foley catheters
Medications:
sedatives-hypnotics
-narcotics
-drugs with anticholinergic effects
-anticonvulsants
-antiparkinsonian medications

161
Q

What are some distinguishing characteristics of delirium?

A

It can develop in a short period- over hours to days, with symptoms typically fluctuating throughout the day. Symptoms are usually worse in the evening or night.
Speech may be inchoherent, slowed or accelerated.

Subtypes:
1) Hyperactive: Restless, agitated, hyperalert, often psychotic (delusions, hallucinations), can exhibit aggressive behaviors.
2) Hypoactive: Lethargic, drowsy, sluggish, apathetic, quiet, responds slowly to questions, decreased spontaneous movement, appears sedated.
Mixed: Mixture of hyperactive and hypoactive characteristics.

162
Q

What does the acronym PINCH ME mean in regards to delirium?

A

Pain, infection, nutrition, constipation, hydration, medication, environment

163
Q

In delirium, what might be some expected physical findings?

A

-Vital signs: brady or tachycardia, hypo or hypertensive, low oxygen perfusion, tachypnea, febrile
-Neuro: decreased LOC, change in mood, confusion, hallucinations (auditory or visual), poor memory recall, impaired speech, asterixis, may have tremor
-HEENT: Dry mucous membranes, cherry red lips
-GI/GU: Abdominal distension, decreased bowel sounds
-Skin: Jaundice, dusky, dry skin, poor skin turgor
-Pain: Furrowed brow, grimacing, moaning, restless behavior

164
Q

What screening tool might be useful for detecting delirium?

A

Confusion Assessment Method (CAM)

165
Q

What are some non-pharmacologic interventions to manage delirium?

A

-Ensure adequate oxygenation, nutrition and skin integrity.
-Correct electrolytes imbalances.
-Attempt to use least restrictive/invasive measures as possible.
-Use of restraints can further perpetuate agitation and delirium
-Remove foley catheters and promote frequent urination, mobilize, and support normal sleep patterns
-advocate for private rooms depending on the setting.
-Provide sensory aids like glasses, hearing aids.
-Encourage presence of a family member/friend (or consider a sitter) to help calm and provide comfort to the patient.
-Use clear and simple communication. Avoid confrontation and use distraction to minimize agitation
-Use reorientation strategies such as clocks, calendars to help orient the patient.
* Provide appropriate lighting to reduce misinterpretations and promote sleep.

166
Q

What are some pharmacologic interventions for delirium?

A

-Treat underlying causes such as infection and treat with prompt antibiotics.
-If in pain, treat appropriately.
-Consider the benefits/trade-offs associated with opioid use further contributing to delirium, individualize for each patient.
-Withdraw all drugs (or taper when necessary) contributing to delirium whenever possible (or use lowest possible dose).

167
Q

True or False-
Benzodiazepines are the drug of choice for patients experiencing significant agitation.

A

False
-benzodiazepines can exacerbate delirium and are primarily indicated in cases of alcohol withdrawal when antipsychotic drugs are contraindicated

168
Q

True or False
Haloperidol is approved for the use of agitation and psychotic symptoms in patients with delirium.

A

True-
-Haloperidol (0.1-0.5 mg) is recommended for short duration if the patient is experiencing moderate to severe agitation or psychotic symptoms.
-The use of antipsychotic medications to treat the symptoms of delirium should be reserved for patients in significant distress due to agitation or psychotic symptoms, to carry out essential investigations or treatment and to prevent older delirious persons from endangering themselves or others.
-When using antipsychotic medications, it is important to aim for monotherapy, the lowest effective dose and tapering as soon as possible (Francis & Young, 2023).

169
Q

What investigations would you consider ordering to rule out the cause of delirium?

A

● Complete blood count (CBC)
● Biochemistry – calcium, albumin, magnesium, phosphate, creatinine, urea, electrolytes, liver function tests (ALT, AST, bilirubin, alkaline phosphatase), glucose
● Thyroid function tests (TSH)
● Blood culture
● Oxygen saturation or arterial blood gases
● Urine culture
● Chest X-ray
● Electrocardiogram (ECG)

170
Q

What is the definition of low risk drinkIng, as per Canada’s low-risk alcohol drinking guidelines?
(I think these are the old guidelines?)

A

Women:

limit alcohol to no more than:
    2 standard drinks per day
    10 standard drinks per week
    3 standard drinks on special occasions
avoid drinking alcohol on some days

Men:

limit alcohol to no more than:
    3 standard drinks per day
    15 standard drinks per week
    4 standard drinks on special occasions
avoid drinking alcohol on some days

Elderly:

1 or less drink/d; 7 drinks/week; 3 or less drinks on a given day (special occasion)

171
Q

What is the definition of at risk drinking?

A

consumption is above low risk level but no alcohol-related physical or social problems

172
Q

What does Alcohol Use Disorder mean?

A

Physical or social problems; continued use despite consequences; Inability to fulfill life roles; Legal problems; No evidence of dependence

173
Q

What does CAGE stand for?

A

Cut: Felt the need to Cut down on drinking?
Annoyed: Felt Annoyed when criticized about drinking?
Guilty: Felt Guilty/bad about your drinking?
Eye Opener: Have you ever had a drink first thing in the morning to steady your nerves or get rid of a hangover?

174
Q

What classes of medications that interact with alcohol?

A

Antidepressants
Antibiotics
barbiturates
Benzodiazepines
H2 receptor antagonists
Muscle relaxants
Nonnarcotic pain relievers
Antiinflammatory agents
Opioids
Warfarin

175
Q

Why is it not good to mix alcohol and medications?

A

Alcohol intensifies the medication’s effect, especially in the central nervous system
OR
it interferes with metabolism of the medication in the liver.

176
Q

What BW is good to order to investigate prolonged alcohol use?

A

GGT and MCV for baseline and follow-up monitoring

CBC (anemia, thrombocytopenia), INR (decreased clotting factor production by the liver)

Liver function tests (AST, ALT, GGT), MCV, and carbohydrate-deficient transferrin (CDT)
*elevated LFTS (GGT, AST, ALT) are suggestive of AUD
- AST:ALT ratio >2:1

177
Q

How does alcohol metabolise in an older person’s body?

A

Aging alters the distribution of alcohol in the body, so that a single drink produces higher blood levels.

As the body ages, there is a decrease in total volume of body water; this reduces the volume of distribution of alcohol that produces a higher blood concentration with the same amount of intake. Thus alcohol’s effects are greater even when an older individual’s alcohol intake remains unchanged.

178
Q

What chronic conditions can worsen when someone or an older person drinks regularly?

A

osteoporosis, memory loss, insomnia, depression/anxiety, congestive heart failure, hypertension, impaired balance, diabetes, liver disease (female more at risk), cancer.

179
Q

How does alcohol affect the cardiovascular system?

A

It increases hypertension by negatively affecting the mechanisms for BP control, specifically baroreceptors, cortisol levels, and the reninangiotensin/aldosterone systems.

In addition, changes to blood vessels and the heart can be harder to detect as alcohol dulls the pain sensations that can warn of a heart attack.

180
Q

What is SASQ?

A

Single Alcohol Screeening Question?
In the past year, how often have you consumed more than 3 drinks (women) or 4 drinks (men) on any one occasion?

181
Q

Why is SASQ considered a good starting question when screening for AUD?

A

To normalize alcohol use and support disclosure, patients are asked to estimate how many times in the past year their drinking exceeded low-risk limits, however, frequency is not factored in to the screening result. For example, any response greater than “never” or “zero times” to the question below would be considered a positive screening result for high-risk drinking, warranting additional follow-up

182
Q

Why is SASQ recommended to be used over CAGE questionnaire?

A

As a standalone screening tool, the CAGE is less sensitive and specific than SASQ and the AUDIT /AUDIT-C for
detecting high-risk drinking, however, when CAGE is used as a follow-up for patients who screen positive to SASQ , the
overall sensitivity for detection of an AUD increases to over 90%, and only requires an average of 3-4 questions
to be asked per patient.

183
Q

What does AUDIT or AUDIT-C stand for?

A

Alcohol Use Disorders Identification Test (10Q) / AUDIT-Consumption (3Q)

assist in the early identification of hazardous or harmful alcohol consumption, and is one of the most widely studied alcohol screening tools
*both have high sensitivity and specificity percents

*Can be self-administered and is just as effective as clinician administered
*Providers who elect to use the AUDIT or AUDIT-C in their practice should be aware that low-risk limits and
standard drink sizes used in these instruments are slightly different than those used in Canada’s Low-Risk Alcohol Drinking Guidelines.

184
Q

What is the next step after screening positive for AUD?

A

*Patients who screen positive for drinking above low-risk limits should undergo further assessment, and if appropriate, a structured interview using the DSM -5 criteria to confirm the diagnosis and severity of AUD

*Patients who are drinking above low-risk limits but do not have an AUD should be administered a brief counselling intervention and encouraged to reduce their alcohol consumption

185
Q

What are the medical triggers and red flags of AUD?

A
  • MCV >96 (i.e., macrocytic anemia)
  • Elevated GGT, AST, or ALT (esp. increased GGT or AST:ALT >2:1)
  • GERD, HTN, DM, pancreatitis, seizures, anemia, arrythmia, gout, GIB or GI disorders, hepatitis, cirrhosis
  • Chronic non- cancer pain
  • Alcohol on breath, signs of intoxication
  • Falls or recent or repeated physical trauma (burns, injuries, accidents)
186
Q

What is the DSM-5-TR Diagnostic Criteria for AUD?

A

DSM-5-TR Diagnostic Criteria for AUD
A. A problematic pattern of alcohol use leading to clinically
significant impairment or distress, as manifested by at least
two of the following, occurring within a 12-month period:

  1. Alcohol is often taken in larger amounts or over a longer period than was intended.
  2. There is a persistent desire or unsuccessful efforts to cut down or control alcohol use.
  3. A great deal of time is spent in activities necessary to obtain alcohol, use alcohol, or recover from its effects.
  4. Craving, or a strong desire or urge to use alcohol.
  5. Recurrent alcohol use resulting in a failure to fulfill major role obligations at work, school, or home
  6. Continued alcohol use despite having persistent or recurrent social or interpersonal problems caused or exacerbated by the effects of alcohol.
  7. Important social, occupational, or recreational activities are given up or reduced because of alcohol use.
  8. Recurrent alcohol use in situations in which it is
    physically hazardous
  9. Alcohol use is continued despite knowledge of having a persistent or recurrent physical or psychological problem that is likely to have been caused or exacerbated by alcohol.
  10. Tolerance, as defined by either of the following:
    a. A need for markedly increased amounts of alcohol to achieve intoxication or desired effect.
    b. A markedly diminished effect with continued use of the same amount of alcohol.
  11. Withdrawal, as manifested by either of the following:
    a. The characteristic withdrawal syndrome for alcohol (refer to Criteria A and B of the criteria set for alcohol withdrawal).
    b. Alcohol (or a closely related substance, such as a benzodiazepine) is taken to relieve or avoid withdrawal symptoms.
187
Q

What are the mental triggers and red flags of AUD?

A
  • Cognitive impairment or decline
  • Mood, anxiety, or sleep disorder (depression, anxiety, insomnia, psychosis, mania
  • Significant behavioural change
188
Q

What are the psychosocial triggers and red flags of AUD?

A
  • Unexplained time off work/ employment loss
  • Frequent no show for appointments
  • Poor medication compliance
  • Significant life event (divorce, loss of spouse, parent)
  • Recent or recurrent trauma or domestic violence
  • High risk behaviours (i.e., gambling, DUI, STIs)
189
Q

What factors are you looking for when assessing alcohol dependence?

A

In the past 12 months, the patient has: (if 3+, alcohol dependence)

  • Increased tolerance (drink more to get same effect)
  • Experienced withdrawal (physical or emotional, i.e., irritability, anxiety, shakes, sweats, nausea, vomiting)
  • Failed to stick to drinking limits/ drinks more than planned
  • Failed attempts to cut down or stop drinking
  • Spent a lot of time on drinking related activities (more time thinking about or recovering from alcohol, thinking of ways to avoid getting cause)
  • Spent less time on other matters (i.e., reduced family or recreational events)
  • Kept drinking despite psychological or physical problems
190
Q

What factors are you looking for when assessing for alcohol abuse?

A

Has patient’s drinking cause or contributed to: (if 1+, alcohol abuse)

  • Role failure
  • Risk of bodily harm
  • Run in with law/ legal issues
  • Relationship trouble
191
Q

What does PAWSS stand for?

A

Prediction of Alcohol Withdrawal Severity Scale (PAWSS)
Assessing for severe withdrawal symptoms or complications

192
Q

What are the contraindications for outpatient withdrawal managements (PAWSS)?

A

The PAWSS has not been validated in outpatient care settings, or in youth or pregnant patient populations. While this guideline endorses the usefulness of the PAWSS for risk assessment in all settings and populations, it emphasizes that, when making clinical decisions, this tool should be used in conjunction with best clinical judgment based on a comprehensive assessment of a patient’s medical history, current circumstances, needs, and preferences.

193
Q

How do the symptoms present in someone experiencing withdrawal symptoms?

A
  • Symptoms typically begin 6-24 hours after last alcohol intake, peak in intensity at 24-48 hours, and resolve within 5-7 days.
  • Symptoms are predominantly of autonomic hyperactivity (tachycardia, pyrexia, tremor, nausea, vomiting, sweating, tremors) and psychological (anxiety, restlessness, sleep disturbance, insomnia).
  • Patients may also experience hallucinations, tonic clonic seizures, and delirium tremens (confusion, disorientation, hallucinations plus severe autonomic hyperactivity).
194
Q

What does the PAWSS questionnaire identify?

A
  • Previous episodes of withdrawal, seizures, DT’s, alcohol rehab treatment, or blackouts
  • Co-occuring use of CNS depressants or other illicit substances
  • Recent intoxication/ positive BAL (blood alcohol level) on admission
  • Evidence of increased autonomic activity, including elevated BP, HR, and body temperature
195
Q

Name two 1st line pharmacotherapeutic interventions for AUD

A

Naltrexone: competitive opioid antagonist that reduces cravings and pleasurable effects of drinking.

Acamprosate: MOA not well understood; Reduces neuronal hyperexcitability, leads to reduced arousal, anxiety, insomnia.

196
Q

Out of the 2 medications that are 1st line treatment for AUD, which one needs to be administered at lower dose to reduce GI upset?

A

Naltrexone - start low and titrate up

197
Q

Out of the 2 medications that are 1st line treatment for AUD, which one is considered the better drug if the patient has a goal to reduce drinking?

A

Naltrexone

198
Q

Out of the 2 medications that are 1st line treatment for AUD, which drug has no effect on heavy drinking or cravings?

A

Acamprosate

199
Q

Out of the 2 medications that are 1st line treatment for AUD, which drug has more effect on cravings?

A

Naltrexone

200
Q

Out of the 2 medications that are 1st line treatment for AUD, which drug may have more effect on treating abstinence?

A

Acamprosate

201
Q

AE for both medications used to treat AUD?

A

Naltrexone: somnolence, nausea, vomiting, decreased appetite, abdo pain, insomnia, dizziness.

Acamprosate: GI (diarrhea, nausea, vomiting)

202
Q

Out of the 2 medications that are 1st line treatment for AUD, which drug requires monitoring?

A

Naltrexone

LFTs at initial treatment and at 1,3,6 months (more frequently if elevated). Stop tx if signs of acute hepatitis (fatigue, anorexia, nausea, vomiting)

203
Q

Out of the 2 medications that are 1st line treatment for AUD, which drug can take as needed?

A

Naltrexone

Daily or PRN (i.e., prior to drinking or when experiencing cravings).
- Start 25mg daily x 3-4 days then titrate up to 50mg daily

204
Q

Out of the 2 medications that are 1st line treatment for AUD, which drug has a cautionary notice when prescribing to an older person?

A

Acamprosate
*moderate renal impairment, pediatric and geriatric (65+), pregnancy

Naltrexone - Hepatic impairment, pregnancy and breastfeeding, pediatric patients, renal impairment

205
Q

Out of the 2 medications that are 1st line treatment for AUD, which drug needs to be taken daily?

A

Acamprosate
666mg TID (low bioavailability) (start at maintenance dosage)

206
Q

PAWSS, Part A: Threshold question - Have you consumed any amount of alcohol (ie been drinking) within the last X days? What is the day range? 15, 20, 30?

A

30

207
Q

T/F: Only 20% of people with alcohol use disorder receive evidence-based treatment

A

False

Only 10% of people with alcohol use disorder receive evidence-based treatment

208
Q

What is the name of the screening tool used to screen for excessive drinking/alcoholism?

A

CAGE

209
Q

What does CAGE stand for?

A

Have you ever felt you needed to CUT down on your drinking?

Have people ANNOYED you by criticizing your drinking

Have you ever felt GUILTY about drinking

Have you ever felt you needed a drink first thing in the morning (EYE OPENER) to steady your nerves or get rid of a hangover

210
Q

How many CAGE questions must a patient answer yes to in order to screen positive for excessive drinking?

A

Scores of 2 or higher had a 93% sensitivity/76% specificity for the identification of “excessive drinking” and a 91% sensitivity/77% specificity for the identification of alcoholism

211
Q

What are risk factors for dementia?

A

Advanced Age

Atrial Fibrillation

Depression

Family History

Down Syndrome

Possibly increases risk: Delirium, Head Trauma, Heavy smoking, Chronic poor sleep (OSA, Insomnia)

212
Q

What is mild cognitive impairment?

A

Patients or family members report cognitive symptoms, decline in memory or other cognitive function is observed, but functional ability is preserved.

This can be a precursor to dementia but isn’t always.

213
Q

Major cognitive impairment, or dementia has several subtypes, what are they?

Which is the most common?

A

Alzheimer’s disease (up to 60- 80% of cases)

Vascular (up to 28% of cases)

Lewy Body (up to 5% of cases)

Frontotemporal (up to 7% of cases)

214
Q

When assessing a patient for dementia, what are some labs you may consider to rule out reversible causes of dementia-like symptoms?

A

-Baseline: CBC, B12, UA, Fasting Blood Glucose, HgbA1C, TSH, electrolytes, Albumin, Calcium, Creatinine/eGFR, ECG

If increased risk: liver enzymes, syphilis, HIV, drug toxicity levels (digoxin, phenytoin)

215
Q

When is neuroimaging recommended?

A

Neurologic abnormalities on exam

History of falls or trauma

On anticoagulants

Less than 65

Rapidly Progressive disease

216
Q

How does Alzheimer’s disease present?

A

Hallmark is lack of insight into loss of abilities (anosognosia)

Gradual onset and progressive decline

Memory, language, and visuospatial deficits

Depressive symptoms

Delusions, hallucinations, agitation, and apathy

217
Q

Differentiate vascular dementia from other dementias

A

Abrupt onset and stepwise progression

Aphasia

218
Q

Differentiate Lewy body dementia from other dementias

A

Visual hallucinations and delusions

Extrapyramidal symptoms (muscle rigidity, Parkinsonism)

Fluctuating mental status

Increased sensitivity to antipsychotic medications

219
Q

Differentiate frontotemporal dementia from other dementias

A

Change in personality.

Hyperorality (excessive preoccupation with oral sensations)

Impairment in executive function (relatively well-retained visuospatial skills)

Loss of social awareness

220
Q

What are non-pharm management considerations for dementia?

A

Treat any reversible abnormalities

Support family

Encourage regular exercise, balanced diet, and stress management

Maintain brain function through stimulating social activities

Consider driving evaluation for safety

Recommend use of safe-return bracelet

Evaluate safety of the home

Suggest advanced directives and planning for future care needs

Avoid anticholinergic and benzodiazepine medications

221
Q

T/F: Medications in dementia have limited benefit

A

True

-Medications that may help with mild-moderate dementia are cholinesterase inhibitors (Donepezil, Rivastigmine patch, Galantamine)

Medication that may help with moderate to severe Alzheimer’s is Memantine

NUNP547 Older Adult Theory (10 decks)

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