Final Exam Flashcards

1
Q

Description of ADHD

A

Persistent and maladaptive symptoms of inattention, hyperactivity, and impulsivity.

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2
Q

When do symptoms of ADHD typically appear?

A

Before age 12.

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3
Q

True or False - ADHD is diagnosed more in boys.

A

True

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4
Q

Describe the etiology of ADHD.

A

Genetics play a significant role (combination of environment and genetics).
Hypothesized low levels of dopamine.
Neurobiological condition - changes to parts of the brain responsible for attention, planning, working memory, executive functioning, motor control, mediation of goal directed behaviour.

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5
Q

List 3-5 symptoms of inattentive ADHD.

A

Decreased attention to detail.
Difficulty listening when spoken to.
Difficulty managing and following through on tasks.
Forgetful in daily activities.
Difficulty sustaining attention.
Distracted by extraneous or unimportant stimuli.

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6
Q

List 3-5 symptoms of hyperactive-impulsive ADHD.

A

Often fidgets or squirms in chair.
Feels restless, runs about, always “on the go.”
Difficulties engaging in leisure activities quietly.
Talks excessively, frequently interrupting.
Difficulty staying seated when it is expected.

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7
Q

How does the clinical presentation of ADHD change over time?

A

Overactivity/impulsivity decrease with age.
Attention, focus, and organization difficulties into adulthood.
Lifelong condition.
Increased risk for lower educational achievement and unemployment.
Increased risk for accidents and injuries.

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8
Q

What kinds of medications are often prescribed for ADHD? What are some possible side effects?

A

Stimulant medications such as Adderall and Ritalin - increase dopamine and norepinephrine in the brain.
Side effects = decreased appetite, sleep problems, anxiety, mild headache, upset stomach, irritability.

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9
Q

True or False - CBT can be used as an intervention for ADHD.

A

True

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10
Q

What are some interventions that may be implemented in an educational setting for people with ADHD?

A

Sensory strategies - reduce distractions.
Attention strategies - break down assignments, movement breaks.
Peer mediated support.

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11
Q

How can ADHD impact occupational participation?

A

ADLs - challenges learning multi-step routines.
IADLs - driving (higher risk for accidents and violations).
Social - difficult to build relationships with peers.
Productivity - school = study skills, motor skills (writing), self-regulation, academic achievement; workplace = positive or negative challenges.

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12
Q

List some conditions that may co-occur with ADHD.

A

Sensory processing differences.
Substance misuse.
Learning disorders.
Anxiety and depression.
Developmental coordination disorder.
Bipolar disorder.

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13
Q

Describe Sensory Processing Disorder.

A

Neurophysiological disorder where sensory input from the body or the environment is poorly detected, modulated, or interpreted, resulting in atypical responses to sensory messages that manifest as problems with motor coordination, organization, attention, behavioural, or emotional responses.

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14
Q

True or False - There is a specific cause linked to Sensory Processing Disorder.

A

False.

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15
Q

True or False - Sensory integration as an intervention for Sensory Processing Disorder is widely accepted.

A

False - Functional approaches are more common.

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16
Q

How can Sensory Processing Disorder impact occupational participation?

A

ADLs - feeding, toileting, bathing, tying shoes, sleeping.
IADLs - shopping, driving.
Leisure - play (games, manipulating toys).
Social - establishing/maintaining interpersonal relationships.

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17
Q

What are some possible comorbidities with Sensory Processing Disorder?

A

Autism spectrum disorder.
ADHD.
Learning disabilities.

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18
Q

List the three sensory processing subtypes.

A
  1. Sensory over-responsivity.
  2. Sensory under-responsivity.
  3. Sensory craving.
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19
Q

Describe Sensory Over-Responsivity. How might it present?

A

Responses to stimuli that are more intense, faster, or have a longer duration than is “typical” for most people. Sensory defensiveness.
May present as - avoidance/withdrawal, irritation/aggression, stress/anxiety (activation of sympathetic nervous system).

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20
Q

Describe Sensory Under-Responsivity. How might it present?

A

Requires more intense and extended duration of sensory stimuli to reach optimal level of arousal.
May present as - higher pain tolerance (safety concern), not noticing mess/spills on self, decreased body awareness (clumsiness, motor delays), delayed response times in conversation or to sensory stimuli, quiet/passive.

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21
Q

Describe Sensory Craving. How might it present?

A

Seek sensory input with an approach that results in erratic, disorganized behaviour. More input does not provide regulation back into “optimal window.”
May present as - “fearless”, enjoys jumping, climbing, swinging, and twirling, “need” to touch everything, may be seen as intruding into others space, crashing into others and objects.

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22
Q

Describe Adaptive Behaviour in regards to Intellectual Disabilities.

A

The collection of conceptual, social, and practical skills that people have learned so they can function in their everyday lives.
Conceptual - receptive and expressive language, reading, writing, math, reasoning, knowledge, memory.
Social - empathy, social judgment, communication skills, the ability to follow rules, and the ability to make and keep friendships, gullibility, social problem solving.
Practical - ADLs, job responsibilities, managing money, recreation, organizing school and work tasks, home, and personal safety skills.

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23
Q

How are Intellectual Disabilities labelled if they appear before the age of 5?

A

Global development delay.

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24
Q

What are some biomedical risk factors for Intellectual Disabilities?

A

Genetic or chromosomal mutation/abnormalities.
Seen in down syndrome (chromosomal), fragile X syndrome (genetic), Hunter syndrome (genetic).

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25
Q

Describe some prenatal, perinatal, and post-natal risk factors related to Intellectual Disabilities.

A

Prenatal - maternal infections, herpes simplex II, poor nutrition.
Perinatal - injuries at birth, perinatal hypoxia, infectious diseases.
Post-natal - trauma, early severe psychosocial deprivation.

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26
Q

True or False - Severity and occupational participation barriers related to Intellectual Disabilities remain consistent throughout live.

A

False - may “ebb and flow” throughout life depending on supports and environmental demands.

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27
Q

What is the goal of interventions for Intellectual Disabilities?

A

Increase adaptive functioning and increase full potential of child in their various occupations.

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28
Q

True or False - There are no specific medications for intellectual disabilities.

A

True - medications may be needed for secondary conditions.

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29
Q

Describe possible impacts of Intellectual Disabilities on occupational participation.

A

ADLs - self-care routines, equipment for safe bathing/showering, safe feeding.
IADLs - post-secondary education, parenthood, career development/maintenance.
Leisure - challenges with participation in leisure activities.
Social - establishing/maintaining friendships.

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30
Q

Describe Developmental Coordination Disorder.

A

Delay in the development of motor skills, or difficulty coordinating movements, results in a child being unable to perform common, everyday tasks.
Acquisition and execution of coordinated motor skills is substantially below what is expected based on age and opportunity for skill learning and use. Repetition and observation do not help in development of motor skills.

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31
Q

True or False - Children with DCD (Developmental Coordination Disorder) have below average intellectual abilities.

A

False - typically have average or above average intellectual abilities.

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32
Q

Which term is sometimes used interchangeably with Developmental Coordination Disorder?

A

Dyspraxia - which is difficulty with motor planning/plan unfamiliar tasks; not a recognized diagnosis.

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33
Q

Describe the course and prognosis of Developmental Coordination Disorder.

A

50-75% of those diagnosed as children have symptoms that persist into adolescence.
Adults continue to have difficulty with a range of motor skills and learning new skills with motor components (e.g., driving).
Adults continue to report secondary complications, including depression, low self-esteem.

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34
Q

What does M.A.T.C.H. stand for in regards to an intervention for DCD? What is the goal?

A

M - Modify the task.
A - Alter your experience.
T - Teaching strategies.
C - Change the environment.
H - Help by understanding.
Goal is to support participation in meaningful occupations, which might mean that children with DCD have to do activities differently.

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35
Q

What is the Cognitive and Task-Based Learning intervention for children with DCD?

A

Providing children with metacognitive strategies so they can problem solve through their own challenges and solutions (Goal-Plan-Do-Check, Cognitive Orientation to Occupational Performance).
Task-Based Learning - focuses directly on the functional skills; break down a tasks into steps that can be practiced independently then linked back together to accomplish entire task; recognizes it may be difficult to generalize between tasks.

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36
Q

How can DCD impact occupational participation?

A

Self-care skills - especially those that require multiple motor skills and steps (washing hair, managing zippers/buttons).
Academic skills - handwriting, note taking.
Leisure and fitness - less opportunity and interest in healthy movement and activity.
Social - decreased opportunities to socialize with peers through sports, impaired self-esteem, and self-worth.

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37
Q

What are some co-occurring conditions/concerns associated with DCD?

A

Prematurity, low birth weight, prenatal alcohol exposure.
ADHD, learning disabilities, autism.

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38
Q

Describe Spina Bifida.

A

Neural tube defect - occurs early in uterine development (~week 4).
Defect of vertebral arches and spinal column.

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39
Q

Describe some risk factors associated with Spina Bifida.

A

Likely a combination of genetic, environmental, or nutritional factors – folic acid; family history; diabetes; medications (valproic acid).

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40
Q

Describe the four types of Spina Bifida. Which is the most severe?

A
  1. Occulta - “hidden”, mildest and most common.
  2. Meningocele - CSF and meninges protrude through abnormal vertebral opening, no neural elements; few to significant symptoms.
  3. Lipomeningocele - fatty mass under skin, can pull and lead to spinal cord tethering; does not always require surgical interventions.
  4. Myelomeningocele - most severe; spinal cord/neural elements exposed; typically see partial, or complete paralysis below affected level.
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41
Q

How can the prognosis of Spina Bifida be improved?

A

Early identification and intervention.
Access to regular medical treatment and support.
Less severe involvement of spinal cord.
Presence of secondary health conditions may lead to increased risk of infections and poorer quality of life and ability to participate in meaningful occupations (e.g., shunts, aspiration pneumonia from impaired breathing/swallowing with Chiari II malformations).

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42
Q

Describe occupational participation concerns related to Spina Bifida.

A

Vary depending on level and severity of injury in the spinal cord and presence/absence of secondary complications.
ADLs - toileting, dressing, grooming, bathing, donning/doffing orthoses.
IADLs - meal prep, adaptive driving/transportation, environmental modifications and mobility equipment.
Leisure - adaptive leisure opportunities.
Social - relationships and sexuality.

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43
Q

List and Describe possible secondary health conditions related to Spina Bifida.

A

Type II Chiari Malformation - impairments in breathing patterns, swallowing/gagging, arm weakness.
Tethered Spinal Cord - 20-50% of children with spina bifida, limits movement of spinal cord in the spinal canal; can present as progressive/severe pain, loss of muscle function, gait deterioration, changes in bowel or bladder function.
Wounds and Pressure Ulcers - may have little to no feeling in certain parts of their bodies; heat, friction, moisture, pressure can cause wounds.
Hydrocephalus - normal CSF circulation patterns are interrupted; children - can impact cognitive development (verbal and visual memory, attention, cognitive flexibility), adults - mimic signs and symptoms of dementia, gait impairments, urinary incontinence.

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44
Q

Describe Cerebral Palsy.

A

Cerebral palsy (CP) refers to a group of disorders in the development of motor control and posture, occurring because of a non-progressive impairment of the developing central nervous system. The motor disorders of cerebral palsy can be accompanied by disturbances of sensation, cognition, communication, perception, and/or seizure disorder.
Pre/Peri/Post-natal onset.
Post-natal considered ~2-8 years.
Pre-natal accounts for 70-80% of cases.
Typically diagnosed when a child does not meet expected motor milestones (e.g., sitting, using hands bilaterally, bearing weight through lower extremities).

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45
Q

List some signs and symptoms associated with Cerebral Palsy.

A

Vary with location and severity.
Tone abnormalities - hypertonicity, hypotonicity, dystonia.
Reflex abnormalities - hyperreflexia, clonus, +/- primitive reflexes.
Atypical posture.
Delayed motor development.
Atypical motor performance.

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46
Q

How does Cerebral Palsy develop with age?

A

Varies depending on type, severity, and presence of associated problems.
With age, secondary problems (contractures, deformities) become more common.
Adults - musculoskeletal difficulties & loss of function at an earlier age.
75% of people with cerebral palsy stopped walking by age 25.
86% survival rate at age 50.

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47
Q

What is the overarching goal of interventions for Cerebral Palsy?

A

Maximizing potential motor skill development and reducing secondary complications (e.g., reducing abnormal muscle tone, preventing complications from seizures).

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48
Q

What is the gold standard intervention for increased functional improvement in affected upper extremity in children with Cerebral Palsy?

A

Constrain Induced Movement Therapy

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49
Q

What are some interventions for spasticity management for Cerebral Palsy?

A

Botox with +/- splinting, serial casting in case of joint contractures.
Orthotics - ankle/foot orthoses, pharmacological (baclofen - oral or pump).
Surgical - joint lengthening, tendon transfers.
Selective dorsal rhizotomy.

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50
Q

What are the “F-words” in regards to childhood disability?

A

Fitness (body structure and function)
Functioning (activity)
Friends (participation)
Family (environmental factors)
Fun (personal factors)

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51
Q

What is a key point to remember when considering MACS as a functional classification for Cerebral Palsy?

A

Reflects usual performance, not potential.

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52
Q

Describe the five levels of GMFCS.

A

I - Walks without limitations.
II - Walks with limitations.
III - Walks using a hand-held mobility device.
IV - Self mobility with limitations; may use powered mobility.
V - Transported in a manual wheelchair.

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53
Q

What is the purpose of classifying Cerebral Palsy under MACS?

A

Considers the child’s ability to handle objects in important daily activities, for example - play, leisure, eating, and dressing.

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54
Q

Describe the five levels of MACS (Manual Abilities Classification System).

A

I - Handles objects easily and successfully. Any limitations in manual abilities do not restrict independence in daily activities.
II - Handles most objects but with somewhat reduced quality and/or speed of achievement. Certain activities may be avoided but does not usually restrict independence in daily activities.
III - Handles objects with difficulty; needs help to prepare and/or modify activities. ADLs can be performed independently if they’ve been set up or adapted.
IV - Handles a limited selection of easily managed objects in adapted situations. Requires continuous support and assistance and/or adapted equipment for even partial achievement of the activity.
V - Does not handle objects and has severely limited ability to perform even simple actions. Requires total assistance.

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55
Q

Describe Spastic Cerebral Palsy.

A

Characterized by hypertonicity, retained primitive reflexes in affected areas of the body, and slow, restricted movement.
Contractures - permanent shortening of a muscle or joint and deformities are common.

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56
Q

Describe Spastic Hemiplegia.

A

Involves one entire side of body, including head, neck, and trunk; upper extremity most affected. Asymmetrical hand use during first year, dragging one side of body. Child learns to walk later than typical, will typically hyperextend knee. Spasticity increases during physical activities and emotional excitement.

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57
Q

Describe Spastic Diplegia.

A

Involves both lower extremities, with mild incoordination, tremors, or less severe spasticity in the upper extremities. Most often attributed to premature birth and low birth weight. Ability to sit independently can be delayed up to 3 years of age or older - inadequate hip flexion and extensor and adductor hypertonicity in legs. Child will move forward on the floor by pulling along with flexed arms and stiffly extended legs. Excessive trunk and upper extremity compensatory movements are used when walking.

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58
Q

Describe Spastic Quadriplegia.

A

Entire body is involved. Difficulty with transitional movements such as rolling or coming up to sitting. Independent sitting and standing are difficulty for child because of hypertonicity, the presence of primitive reflex involvement, and a lack of righting and equilibrium reactions. Small percentage are able to walk independently. Oral muscles are usually affected - difficulties with dysarthria, eating difficulties, and drooling. Children are susceptible to contractures and deformities, particularly hip dislocation and scoliosis.

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59
Q

Describe Athetosis Cerebral Palsy.

A

Characterized by slow, writhing involuntary movements of the face and extremities or the proximal parts of the limbs and trunk. Abrupt, jerky distal movements may also appear. Movements increase with emotional tension and are not present during sleep. Head and trunk control are affected, as is oral muscles, causing drooling, dysarthria, and eating difficulties. Contractures rare.

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60
Q

Describe Ataxia Cerebral Palsy.

A

Characterized by a wide-based, staggering, and unsteady gait. Often walk quickly to compensate for lack of stability and control. Controlled movements are clumsy. Intention tremors may be present. Ability to perform refined movements (handwriting) is affected. Hypotonicity often present.

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61
Q

What are some impacts Cerebral Palsy may have on occupational participation?

A

All body function categories can be affected (depends on type, severity, associated disorders).
ADLs – Physical assistance (dressing, feeding, hygiene), movement (spasticity affects joint stability), impaired voluntary movements, toileting.
IADLs – Assistive technology (communication), visual delays.
Cognitive functioning impacted.

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62
Q

What are some co-occurring conditions/complications often associated with Cerebral Palsy?

A

Cognitive impairment.
Orthopedic complications – joint contractures, hip dislocations, scoliosis.
Seizures.
Visual impairments – strabismus, nystagmus, homonymous hemianopsia, cortical vision impairments.
Communication disorders – dysarthria.
Oral motor – dysphagia.
Gastrointestinal – gastroesophageal reflux (GERD).
Respiratory – aspiration pneumonia, sleep apnea, upper respiratory infections.

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63
Q

Describe the etiology of Duchenne Muscular Dystrophy.

A

Only affects males (X chromosomes linked condition).
Absence or deficiency in the structural protein dystrophin - maintains shape and structure of muscle fibers.

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64
Q

What are some common signs and symptoms associated with Duchenne Muscular Dystrophy?

A

Proximal weakness
Waddling gait
Enlarged calf muscles
Developmental delays – running, jumping, playing with peers
Fatigue
Toe walking
Speech delays

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65
Q

True or False - Most people with Duchenne Muscular Dystrophy are wheelchair dependent by age 12.

A

True.

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66
Q

True or False - Muscle weakness in Duchenne Muscular Dystrophy is always bilateral and symmetrical.

A

True.

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67
Q

What is the life expectancy of somebody with Duchenne Muscular Dystrophy?

A

Late teens to early twenties. Cause of death usually secondary infections to respiratory and/or cardiac complications.

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68
Q

What are the goals of interventions for Duchenne Muscular Dystrophy?

A

To maintain independence and muscle function as long as possible.

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69
Q

How might Duchenne Muscular Dystrophy affect occupational participation?

A

ADLs – Decline in functioning is expected – results in loss of ability to perform ADLs, require assistance with dressing, grooming, bathing, toileting, mobility equipment.
IADLs – Driving, community mobility, health management and maintenance, meal preparation, shopping.
Psychosocial Considerations – Children with DMD are at higher risk for co-occurring mental health conditions/psychosocial considerations.
These may also impact occupational participation in school, with peers, family/home life, and leisure and may include – Anxiety - decreased cognitive flexibility, depression, decreased social skills and peer relationships, anger/arguing, decreased cognitive skills – short-term memory, cognitive flexibility, decreased language skills, higher risk of co-occurring neurodevelopmental conditions like autism spectrum disorder, obsessive compulsive disorder, ADHD.

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70
Q

What is the “valley sign” in regards to Duchenne Muscular Dystrophy?

A

Present in 90% of males with this condition.
Depressed area on the posterior axillary fold that can be seen when the patient abducts shoulders to 90 degrees, elbows flexed to 90 degrees, with bilateral hands pointing upwards.

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71
Q

Describe Autism Spectrum Disorder.

A

Characterized by impairments in social interaction and social communication by the presence of restricted and repetitive behaviours. Diagnosis of ASD requires the presence of restricted, repetitive patterns of behaviour, interests, or activities. Outside what is “typical” for the social and cultural context. Insistence of sameness, adherence to routines, or ritualized patterns of verbal or nonverbal behaviour (e.g., extreme distress at small changes, difficulties with transitions).

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72
Q

True or False - Symptoms of Autism Spectrum Disorder do not appear until the age of 4 or later.

A

False - Symptoms must be present in the early development period (12-36 months).

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73
Q

True or False - The treatment of Autism Spectrum Disorder relies heavily on the use of medications.

A

False - Medication may be used to treat secondary conditions.

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74
Q

What is the most effective intervention for children with Autism Spectrum Disorder?

A

Intensive early intervention (0-3 years old) are most effective for reducing behavioural problems and in increasing language, social, sensory, motor, and cognitive skills.

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75
Q

Describe some ways in which ASD may impact occupational participation?

A

Autism is a spectrum – occupational performance and participation will be varied.
May be influenced by – +/- intellectual/language impairments, co-existing sensory, psychiatric, motor deficits, socioeconomic factors – access to interventions, sufficient school, work, and family supports (e.g., access to augmentative and adaptive communication – AAC).
ADLs such as dressing, may struggle with toileting, experiencing pain, digestive system.
and eating can be made difficult if they are overresponsive to sensory stimuli.
IADLs such as shopping and driving.
Difficulty with memory functioning (academic performance).
Play and leisure - impacted by restrictive and repetitive behaviours.

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76
Q

Describe Rheumatoid Arthritis.

A

Systemic condition.
Generally, impacts same joint(s) bilaterally.
Joint inflammation - changes in synovial membrane and development of corrosive pannus (destructive tissue) – lead to cartilage and bone breakdown at joints.
Characterized by – subchondral cysts, signs of rebuilding bone and/or presence of osteophytes, small joints tend to be impacted and can have resulting deformities (e.g., MTP, PIP, CMC).

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77
Q

What are some signs of Rheumatoid Arthritis?

A

“Non-specific” signs of inflammatory process which can include – hot, red joints; joint edema, subluxation; joint pain - 3 joints; joint guarding; loss of joint range of motion; fatigue, generalized weakness
*Symmetrical pattern of pain, swelling, redness

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78
Q

True or False - 40% of adults are in remission within the first year of a Rheumatoid Arthritis diagnosis.

A

False - 20%, majority will develop chronic progressive disease.

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79
Q

What group of people have the worst prognosis for Rheumatoid Arthritis?

A

Women diagnosed prior to the age of 50.

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80
Q

What are some occupational participation concerns with a Rheumatoid Arthritis diagnosis?

A

Ambulation/Mobility.
Hand strength - Grip & Pinch.
Fatigue.
Sore, aching joints.
Pain with activity.
All can impact ADLs (dressing, eating), IADLs, leisure, productivity, relationships/socialization.

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81
Q

What are some possible co-occurring conditions with Rheumatoid Arthritis?

A

Wrist – carpal tunnel syndrome
Elbow – lateral epicondylitis
Shoulder – shoulder bursitis, rotator cuff tears
Hip – abnormal gait (foot)
Knee – popliteal cysts (can result in contracture)
Ankle and foot – “Claw toes”, hammer toes, hallux valgus
Because RA is systemic its impact carries to many organ systems including – rheumatoid/ subcutaneous nodules; pulmonary – chronic inflammation can cause scar tissues on lungs, cardiac manifestations, neurological manifestations, ophthalmic manifestations, depression and anxiety – ~1.5x more likely than unaffected population.
Nodules can enter organs.

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82
Q

What Rheumatic condition is often referred to as the “Unwalkable Disease” or “Disease of Kings”

A

Gout

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83
Q

Describe Delirium.

A

A disturbance in attention (i.e., reduced ability to direct, focus, sustain, and shift attention) accompanied by reduced awareness of the environment.
The disturbance develops over a short period of time (usually hours to a few days), represents a change from baseline attention and awareness, and tends to fluctuate in severity during a day.
An additional disturbance in cognition (e.g., memory deficit, disorientation, language, visuospatial ability, or perception).

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84
Q

What are some premorbid factors related to Delirium?

A

Advanced age
Dementia
Low educational level
High comorbidity burden
Frailty
Visual and hearing impairment
Depression
Alcohol abuse
Poor nutrition
Illicit drug, opioid, or benzodiazepine use
History of delirium

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85
Q

What are some hyperactive symptoms of Delirium?

A

Increased psychomotor activity that may be accompanied by mood lability, agitation, aggression (often not cooperative in care).
Symptoms that may be easy to observe.

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86
Q

What are some hypoactive symptoms of delirium?

A

Decreased psychomotor activity - sluggish, lethargic, stupor.
Occurs in roughly 50% of cases. Much harder to observe - can mimic symptoms of major depressive disorder.

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87
Q

Describe the course and prognosis of Delirium.

A

Acute course – hours to days.
Persistent course – weeks to months (more common in people with previously diagnosed neurocognitive changes).
Majority of adults <65 will resolve completely.
May be associated with long term cognitive decline in older adults, especially those with underlying cognitive impairments.
Hospitalized individuals 65 years or older with delirium are at greater risk for poor outcomes following discharge, including mortality, and requiring institutional care.
Should not be downplayed as something normal that occurs in hospitals – medical emergency.

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88
Q

How can Delirium impact an individuals occupational participation?

A

The early non-pharmacological management of delirium directly involves activities needed for occupational participation and can include –
Resume typical sleep/wake cycle.
Sitting up in chair for meals.
Dressed in regular clothing.
Frequent orientation to date and location (calendar, familiar items).
Visitors.
Remove unnecessary lines and tubes (i.e.) indwelling catheters; IV lines – promotes regular toileting routine.

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89
Q

Describe Alzheimer’s Disease.

A

Most common dementia.
Insidious, gradual, progressive onset of impairment in – memory, learning and one other cognitive domain.
May start with behavioural (neuropsychiatric symptoms) such as – agitation, sleep disorder.

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90
Q

What are some of the current hypotheses about the etiology of Alzheimer’s Disease?

A

Etiology unknown.
Beta-amyloid plaques caused by defective breakdown of amyloid precursor protein – plaques collect outside neurons and disrupt synaptic transmission.
Neurofibrillary tangles are abnormal accumulations tau protein that collect inside neurons and disrupt flow of signals from cell body down axons.
Build-up of microglia (intended to remove waste and excess proteins like Beta amyloid plaques) that do not perform their function.

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91
Q

What are symptoms of the mild phase of Alzheimer’s Disease?

A

Cognitive – impairment in memory and learning, sometimes accompanied by deficits in executive function (hippocampus impacted).
Behavioural/Neuropsychiatric – depression, irritability, and/or apathy.

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92
Q

What are some symptoms of the major phase of Alzheimer’s Disease?

A

Cognitive – impairments in visuoconstructional/perceptual-motor ability and language (e.g., word retrieval).
Behavioural/Neuropsychiatric – delusions, agitation, combativeness, and wandering are common.
Psychological – apathy, depression, delusions.
Physical – gait disturbances, dysphagia (swallowing), incontinence, myoclonus, and seizures are observed.
All related to atrophy of the brain.

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93
Q

What is the mean survival length after a diagnosis of Alzheimer’s Disease?

A

10 years from diagnosis.
Younger diagnosis = ~20 years.

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94
Q

What are the occupational participation concerns related to Alzheimer’s Disease?

A

Mild phase - early retirement from work and meaningful IADLs like driving.
Major phase - dependent for all ADLs, IADLs; loss of recognition of loved ones; decreased communication - basic and social communication; safety concerns (wandering).
At the end stages/most severe course of these health conditions, the individual will likely require 24-hour support for ADL, IADLs, functional mobility and safety – that may be at home or in institutional care.

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95
Q

Describe Multiple Sclerosis.

A

Inflammatory, immunological, neurodegenerative disease.
Immune system attacks myelin sheath around brain, SC, optic nerve (demyelination); cerebellar and its efferent/afferent pathways commonly affected.

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96
Q

What are some possible risk factors for Multiple Sclerosis?

A

Cause unknown. Demyelination is the main cause of impairment.
Chronic inflammation/diffuse demyelination to white/grey matter and axons. Formation of plaques.
Some hypotheses include - genetics + environmental factors, higher estrogen levels, vitamin D deficiencies, viral infection, smoking.

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97
Q

What are some symptoms of Multiple Sclerosis?

A

Physical - spasticity, fatigue, low endurance/energy, muscle weakness, ataxia, intention, tremor.
Vision/Vestibular - diplopia, loss of visual acuity, sense of balance, ocular control.
Sensory - abnormal sensation, burning/tingling.
Cognitive deficits - attention, memory, executive functions.
Psychosocial/Emotional - depression/euphoria, fatigue, anxiety, irritability.

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98
Q

What are some factors that influence course and prognosis of Multiple Sclerosis?

A

Subtype.
Symptom severity.
Age of onset (20s = ~46-60 yrs; 60s = ~13-22 yrs).

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99
Q

10 years post Multiple Sclerosis diagnosis - what percentage of people are wheelchair users? Unable to work?

A

10% wheelchair users; 50% unable to work.

100
Q

What is the first line of treatment for relapse/remitting subtypes of Multiple Sclerosis?

A

Disease-modifying drugs - target aspects of inflammatory processes, slow disease progressions.

101
Q

What is the primary occupational participation concern related to Multiple Sclerosis?

A

Fatigue - can lead to many occupational impairments.

102
Q

What are the signs and symptoms of the Benign Multiple Sclerosis subtype?

A

1-2 acute episodes of the disease; no residual deficits.

103
Q

What are the signs and symptoms of Relapse Remitting (Non-Progressive) Multiple Sclerosis?

A

Exacerbation (relapses) of symptoms with periods of symptom-free remission.
No deficits in periods of remission.

104
Q

What are the signs and symptoms of Relapse Remitting (Progressive) Multiple Sclerosis?

A

Exacerbation (relapses) of symptoms with periods of symptom-free remission.
Increased deficits after relapses - declining function with each relapse.
Unpredictable course.

105
Q

What are the signs and symptoms of Primary Progressive Multiple Sclerosis?

A

No periods of remission.
Gradual decline in function.

106
Q

What is the median survival rate after the onset of Huntington’s Disease?

A

18 years.

107
Q

What is the etiology of Huntington’s Disease?

A

Genetic disorder - mutation of a gene that makes the protein huntingtin.
Dominant - anyone who inherits it from a parent will develop the disease.
Each child of a parent with HD has a 50% chance of getting the gene.

108
Q

What are some cognitive, physical, and neuropsychiatric symptoms of Huntington’s Disease?

A

Cognitive - attention, executive functioning (planning, processing, mental flexibility), new learning, memory, emotional recognition.
Physical - involuntary movements (chorea, akathisia, dystonia), voluntary movements (fine motor, coordination, modulation, bradykinesia, initiation), increased rigidity, balance, dysarthria.
Neuropsychiatric - mood (blunted affect, depression, anxiety), emotional regulation/awareness, irritability and anger, disinhibition, obsessive behaviours.

109
Q

True or False - Involuntary movement loss progresses more quickly than voluntary movement loss in Huntington’s Disease.

A

False - Voluntary movement loss progresses more quickly and is associated with greater functional impairment.

110
Q

True or False - There are no pharmaceutical treatments to stop or slow the progress of Huntington’s Disease.

A

True - medications may be used to manage symptoms associated with the disease (e.g., chorea, mood).

111
Q

What are some occupational participation impacts of Huntington’s Disease on the client and the family?

A

Likely devastating for the person and for the family - terminal illness.
Age of onset impacts occupational roles and responsibilities - parenting, caregiving, productivity, finances.
Amount of support needed for occupational participation will increase and change as disease progresses.
Consider occupational needs of children and care partners - family centered care.

112
Q

True or False - Amyotrophic Lateral Sclerosis (ALS) tends to have a proximal to distal progression (head to toe).

A

False. ALS has a distal to proximal (toe to head) progression.

113
Q

What is the sporadic etiology of ALS?

A

Accounts for most cases of the disease.
Speculation - viral, retroviral, environmental causes, genetics, exposure to chemicals/lead, electromagnetic fields, diet.

114
Q

What is the familial etiology of ALS?

A

10% of cases.
Genetic mutation, family history.

115
Q

List some early signs of ALS.

A

Weakness/atrophy of intrinsic muscles of the hand/asymmetrical foot drop (most common).
Night cramps (calf muscles).
Muscle tightness/spasticity/fasciculations.
Slurred speech.
Difficulty swallowing.
Increased or decreased reflexes.

116
Q

What are some late stage signs of ALS?

A

Widespread muscle weakness and atrophy - impacts gait, transfers, hand use.
Increased spasticity, fasciculations, rigidity.
Dysphagia (swallowing difficulties).
Dyspnea (breathing difficulties) - respiratory failure.
Oculomotor changes - decreased ability to use eye muscles.

117
Q

What is the most common form of arthritis?

A

Osteoarthritis.

118
Q

What is a key difference between Rheumatoid Arthritis and Osteoarthritis?

A

Rheumatoid arthritis tends to affect smaller joints (e.g., metacarpal joints). Osteoarthritis tends to affect larger joints (e.g, hip, knee).
Rheumatoid arthritis tends to be bilateral; Osteoarthritis is unilateral.

119
Q

What are some symptoms of Osteoarthritis?

A

In affected joints -
Pain (often flares up after an activity).
Aching/Stiffness.
Decreased range of motion.
Swelling.
Crepitus (crunching feeling/sound).
Decreased physical activity (pain, fear of pain).

120
Q

True or False - Osteoarthritis is a life threatening condition.

A

False. It is a chronic condition which involves progressive destruction of the joints. Not life threatening but has great effects on participation, relationships, and quality of life.

121
Q

What are some protective joint strategies implemented after a total hip arthroplasty?

A

Do not twist at the hip of operated leg.
Do not bend hip past 90 degrees by leaning forward or lifting the knee up.
Do not cross your legs at the ankles of knees.

122
Q

What are some impacts on occupational participation related to Osteoarthritis?

A

2/3 of people with OA report poor night’s sleep.
More than three quarters (77%) of people with OA report it has required them to reduce at least some of their day-to-day activities.
42% of working age people with OA are either not in the workforce or have reduce/change their work duties.

123
Q

What is the leading cause of fractures?

A

Unintentional falls.

124
Q

What is the primary cause of disability in older adults?

A

Hip fractures.

125
Q

What is the etiology of Fractures?

A

Chronic - osteoarthritis, rheumatoid arthritis, osteoporosis (fragility/pathological fractures).
Acute/Traumatic Injuries - falls (sports, everyday activities), motor vehicle accidents, other trauma.

126
Q

What is a Fracture? How are they categorized?

A

Break in continuity of the bone - determined by the amount of force applied to the bone and the strength or toughness of the bone.
Categorized by anatomical location (base, mid-shaft, neck, articular), and relationship of fragments (open, closed, angulated).

127
Q

What percentage of strokes are Ischemic?

A

85%

128
Q

What are the three subtypes of Ischemic strokes?

A

Thrombotic (large artery arthrosclerosis) - pathological development of a thrombus or blood clot; common where blood vessels turn or divide.
Lacunar Infarcts - “crescent moon shaped”; deep brain structures impacted, focal signs due to small size; typically impact motor and sensory systems; no language or cognitive involvement.
Embolic - blood clot that develops elsewhere in the body and then gets lodged in narrowing artery in the brain; people with atrial fibrillation (abnormal heart rhythm) are more prone to embolic strokes; likely to occur during activity.

129
Q

What is a predictor for future Ischemic strokes?

A

Transient Ischemic Attack

130
Q

What are symptoms of a Middle Cerebral Artery Stroke?

A

Left -
Paralysis or weakness on RIGHT face, trunk, and extremities.
Impaired sensation to RIGHT side of body.
Aphasia – receptive/expressive/global.
Dysarthria.
Right visual field deficits – blind spots.
Memory deficits – recent or past.
Motor apraxia.
Swallowing difficulties.
Right -
Hemiparesis/hemiplegia of LEFT upper and lower extremities.
Impaired sensation on LEFT side of body.
Spatial and perceptual deficits.
Unilateral intra/extra personal inattention or neglect.
Left visual field deficits – homonymous hemianopsia.
Impulsive behaviour and decreased attention.
Dressing apraxia.
Emotional changes – blunted affect, lability.

131
Q

What are symptoms associated with Posterior Cerebral Artery Strokes?

A

5-10% of strokes.
Difficulty judging distance when trying to coordinate limb movements (dysmetria).
Drooling and difficulty swallowing (dysphagia).
Visual changes.
Dizziness, vertigo.
Ataxic hemiparesis.
Short- and long-term memory loss.
Altered consciousness (thalamus).

132
Q

What are symptoms of an Anterior Cerebral Artery Stroke?

A

Contralateral lower extremity paresis (rarely bilateral).
Rare (0.3-4.4% of strokes).
Contralateral lower extremity sensory loss.
Urinary incontinence.
Neuropsychological features – abulia (initiation/apathy), blunted affect, disinhibition, perseveration.
Memory impairment.
Akinetic mutism.
Balance, coordination.

133
Q

True or False - Hemorrhagic strokes recover quicker than Ischemic strokes.

A

False - Ischemic stroke recover quicker.

134
Q

What are some common complications associated with Ischemic strokes?

A

Ischemic to Hemorrhagic transformation.
Brain edema.
Shoulder subluxation.
Seizures.
Spasticity.
Deep vein thrombosis.
Shoulder pain (72% stroke survivors).
Fatigue.

135
Q

How can strokes impact occupational participation?

A

Post Stroke Fatigue –
According to the stroke best practice guideline, “Fatigue following stroke is a multidimensional motor-perceptive, emotional and cognitive experience characterized by a feeling of early exhaustion with weariness, lack of energy and aversion to effort that develops during physical or mental activity and is usually not ameliorated by rest”
May result in –
Decreased ability to perform daily activities – unable to complete or more easily tired by daily activities.
Need for naps, rest, or extended sleep.
Fatigue can make cognitive and perceptual symptoms worse.
Should be actively screened for and managed by the interdisciplinary team across the continuum of care.

136
Q

What are some modifiable (lifestyle) risk factors for Heart Disease?

A

Unhealthy eating
Physical inactivity
Being overweight
Stress
Excessive drug and alcohol use
Smoking

137
Q

What are some non-modifiable risk factors for Heart Disease?

A

Sex
Age
Family history
Indigenous heritage
South Asian heritage
African heritage
Social determinants of health

138
Q

What blood pressure measure classifies a Hypertension diagnosis?

A

When blood pressure is persistently above 140/90mmHg.

139
Q

What does systolic (top number) pressure measure?

A

The pressure in the arteries when the heart beats.

140
Q

What does diastolic (bottom number) pressure measure?

A

The pressure in the arteries between heart beats.

141
Q

What is the goal of pharmacological interventions for Hypertension?

A

Reduce blood pressure enough to decrease risk of complications.

142
Q

Describe Coronary Artery Disease.

A

Chronic inflammatory disease where the coronary arteries, which supply O2 to the heart, narrow.
Plaque builds up in arteries, hardens over time, artherosclerosis.

143
Q

What are some symptoms associated with Coronary Artery Disease?

A

Likely asymptomatic in the early stages.
As plaque builds up in the coronary arteries - angina (chest pain), shortness of breath, fatigue with exertion.
Complete blockage may lead to a heart attack,

144
Q

What is CABG as an intervention for Coronary Artery Disease and Myocardial Infarction?

A

CABG - Coronary Artery Bypass Graft.
Surgical intervention - artery/vein taken from elsewhere in the body to create a detour around the blocked artery (when stenting is not an option).

145
Q

Describe a Myocardial Infarction.

A

Heart attack; occluded blood flow causing the heart muscle tissue to be without oxygen.
Differs from cardiac arrest which heart stops beating suddenly- usually from electric dysfunction
Partial (nSTEMI) or complete (STEMI). Complete more likely to cause heart damage.

146
Q

What is the primary cause of a Heart Attack?

A

Arthrosclerosis

147
Q

What are some symptoms of a Heart Attack?

A

Chest discomfort or pain, may spread to arm, neck, or jaw.
Shortness of breath.
Cold sweats.
Nausea/vomiting.
Lightheadedness.

148
Q

What is the severity of a Heart Attack dependent on?

A

Extent and duration of arterial obstruction, collateral circulation, myocardium tissue necrosis, access to emergency care.

149
Q

True or False - Coronary Artery Bypass Graft procedures are often associated with a period of Delirium.

A

True.

150
Q

What are some Sternal Precautions for patients to follow after undergoing CABG?

A

To be followed for 6-8 weeks after the procedure.
Do not lift, push, or pull more than 10 pounds (5 pounds per arm).
Do not put any body weight on hands or elbows for 6 weeks.
Hug the “heart pillow” to chest when coughing or sneezing to support sternum.
Do not - lean on arms, use arms/hands to push out of bed or chair, lift full pan or dish, lift a baby or small child, move furniture, carry groceries, use a vacuum cleaner, use a lawn mower, carry laundry, drive a vehicle.

151
Q

What is the Ejection Fraction?

A

Compares the amount of blood in the heart to the amount of blood pumped out; helps to describe how well the heart is pumping blood to the body.
EJ = amount of blood pumped out/amount of blood in chamber.

152
Q

What is a MET?

A

Metabolic Equivalent.
Described as the amount of energy it costs to complete a task, determined by the amount of oxygen per weight per minute.

153
Q

What are the max MET Levels associated with each stage of Heart Failure?

A

I - Max MET = 6.5
II - Max MET = 4.5
III - Max MET = 3.0
IV - Max MET = 1.5

154
Q

Describe Chronic Obstructive Pulmonary Disease (COPD).

A

Group of lung diseases characterized by airflow obstruction that interferes with normal breathing.
Most common - emphysema / chronic bronchitis
Slow, progressive damage to the airways of the lungs, making them swollen and blocked and causing them to lose their elasticity or stretchiness. COPD makes it hard to breathe because – the airways and air sacs of the lungs lose their shape and stretchiness, the walls between many of the air sacs are destroyed, the walls of the airways become thick and swollen, cells in the airways make more mucus than usual, which blocks the airways.

155
Q

What is the primary cause of COPD? What are some other underlying causes?

A

Cigarette smoke (80-90% cases).
Air pollution, chronic childhood lung infections, rare genetic disorders.

156
Q

What are some common symptoms of COPD?

A

Chronic cough with phlegm.
Dyspnea (breathlessness).
Chest tightness.
Cyanosis (blue around lips).

157
Q

What is the most common cause of mortality among people with COPD?

A

Progressive or acute respiratory failure, heart failure.

158
Q

What are some interventions under the Breathlessness Model for COPD?

A

Education.
Cognitive/relaxation strategies.
Pursed lipped breathing.
Belly breathing (diaphragmatic breathing).
Tripod sitting position.

159
Q

Describe Type I Diabetes.

A

Insulin Dependent Diabetes Mellitus.
Frequently occurs in children.
Complete insulin deficiency, insulin replacement required.
Type 1A/1B, autoimmune destruction of pancreatic beta cells.
Latent autoimmune diabetes of adults; aged 35 and older.

160
Q

Describe Type II Diabetes.

A

Non-Insulin Dependent Diabetes Mellitus.
Pancreas secretes insulin, resistance to insulin, and amount of insulin may be insufficient.
Chronic state of hyperglycemia.
Most common with adults but increasing prevalence in children.
Typically, most common in individuals with obesity/occurs with increasing age.
Most benefit by addressing modifiable risk factors.

161
Q

What are some symptoms of Hyperglycemia in Diabetes?

A

Polyuria (frequent urination), polydipsia (increased thirst), polyphagia (increased hunger), fatigue, blurred vision, slow to heal cuts or bruising, and weight loss.
Diabetic ketoacidosis (DKA), also known as a diabetic emergency – above symptoms and deep rapid breathing.
High blood sugar.
“Fruity” breath odor.

162
Q

What are some symptoms of Hypoglycemia in Diabetes?

A

Low blood sugar, or hypoglycemia, is when an individual’s blood glucose drops below normal levels (70 mg/dL or less), signalling the need for immediate treatment.
Acute causes – not eating enough carbs; skipping meals; increase alcohol consumption; increase physical activity; illness.
Dizziness, nausea, shaking, weakness, blurred vision, seizures, unconsciousness.

163
Q

What is the average lifespan for people with Type I Diabetes? Type II?

A

Type I - ~12 years less than general population.
Type II - ~10 years less than general population.

164
Q

What is the focus of many OT assessments for Diabetes interventions?

A

Medical complications such as -
Vision screening and compensation for occupational participation.
Sensation assessments.
Wound care and amputation.
Cognitive interventions.

165
Q

What are some intervention options for Type I Diabetes?

A

Insulin replacement/glycemic control.
Pancreatic transplant.
Pancreatic islet cell transplant.
Physical activity.
Diet.

166
Q

What are some intervention options for Type II Diabetes?

A

Nutrition.
Exercise.
Metformin.

167
Q

What are some occupational participation concerns related to Diabetes?

A

Health management is  “developing, managing, and maintaining routines for health and wellness by engaging in self-care with the goal of improving, or maintaining health, including self-management, to allow for participation in occupations.”
A complete and thorough understanding of blood glucose monitoring, insulin dosage, dietary intake, device care and maintenance, the effects of activity and exercise, and signs and symptoms of hypo and hyperglycemia is essential.
Foot checks and health management (glucose monitoring) may have to be incorporated into ADLs like dressing and eating.

168
Q

What are some Macrovascular complications related to Diabetes?

A

Cardiovascular system (arthrosclerosis).
Hypertension and stroke.
Peripheral Artery Disease - decreased blood flow to periphery of body (pain/cramps with physical activity, muscle atrophy, hair loss, smooth/shiny skin, numb/blue toes, etc.)

169
Q

What are some Microvascular complications related to Diabetes?

A

Diabetic Retinopathy - microvascular changes to retina, blurred vision, impaired peripheral vision, “floaters” in visual field; can progress to complete blindness.
Diabetic Nephropathy - pathological/structural changes in kidney, leading cause of end stage renal disease.

170
Q

What are some Neurologic complications related to Diabetes?

A

Diabetic Peripheral Neuropathy and Foot Ulcers - peripheral neuropathy occurs in ~50% of cases; burning, tingling, pain, numbness, and/or loss of protective sensation; typically symmetrical and begins distally and progresses proximally; altered or loss of sensation can increase vulnerability to lesions/ulcers and infections.

171
Q

How are Infectious Diseases (HIV) commonly understood?

A

Using the epidemiologic triad - agent, host, and environment.

172
Q

How are Infectious Diseases classified?

A

Causative organism, means of transmission, and clinical grouping.

173
Q

List some individual and structural risk factors associated with HIV.

A

Individual - genetics, immunity (natural or through vaccine), age, preexisting health conditions, tobacco, and alcohol use.
Structural - poverty, homelessness, overcrowding, lack of clean water.

174
Q

Describe some symptoms found within each stage of HIV progression.

A

Stage 1 (acute clinical syndrome) - highly infectious, within 2-4 weeks of initial exposure; flulike symptoms = fever, headache, chills, rash, sore throat, fatigue, mouth ulcers, enlarged lymph nodes; can be asymptomatic).
Stage 2 (latent phase) - virus active and transmissible but reproducing at low levels; low symptoms; CD4 count decreases, can be prevented with current treatments.
Stage 3 (AIDS) - acquired immunodeficiency syndrome; measured by lowered CD4 count or development of opportunistic infection, weakness, weight loss, chills, fever, sweats, swollen lymph glands.

175
Q

When does an HIV diagnosis transition to become AIDS?

A

When a person’s CD4 cells fall below 200 cells per cubic millimeter of blood OR if the person develops one opportunistic infection.

176
Q

True or False - HIV mortality is primarily due to opportunistic infections.

A

True - Compromised immune system cannot fight it off.

177
Q

What are important factors to consider regarding occupational participation and Infectious Diseases?

A

The infectious agent.
Vulnerability of the person who becomes infected.
Availability of treatments for infections that do not resolve naturally.
Social, structural, and other contexts in which people live.
Isolation requirements (e.g., tuberculosis).
Role of stigma and barriers in - prevention, early detection, and treatment options.

178
Q

What are the three tumour cell types?

A

Benign (non-cancerous)
In situ (cancerous, but has not spread to other parts of the body)
Malignant (cancerous, metastasizes throughout body)

179
Q

How are Solid Tumours staged?

A

TNM -
T = size of tumour
N = nearby lymph node involvement
M = presence of metastasis
Also staged I through IV
I = cancer relatively small, contained within organ it started.
II = cancer has not spread to surrounding tissue but tumour is larger; cancer cells may spread into lymph nodes close to tumours.
III = cancer is large and may have spread into surrounding tissues and lymph nodes in area.
IV = cancer has spread throughout blood or lymphatic system from where it started to a distant site in the body.

180
Q

What is the possible etiology of Cancer?

A

Disease of the genes - potential errors in coding, production of faulty proteins, DNA damage (environmental).
Uncontrollable cell division.
Genetic inheritance.
Environmental carcinogens.
Lifestyle choices (excessive alcohol, tobacco).
Radiation (x-rays, UV waves).
Second hand tobacco smoke.
Obesity.
Aging.
Infections - HIV, Hep. B

181
Q

What are some common symptoms associated with Cancer?

A

Will vary depending on type and severity of cancer.
CAUTION -
C = change in bowel/bladder habits.
A = a sore that does not heal.
U = unusual bleeding/discharge.
T = thickening/lump.
I = indigestion/difficulty swallowing.
O = obvious change in a wart, mole, mouth sore.
N = nagging cough/hoarseness.

182
Q

What are some possible occupational participation impacts related to Cancer?

A

Cancer related pain - related to growth of tumour/side effect of treatment/tests; bone pain, tissue pain, organ pain, nerve pain, phantom pain; typically worsens with progression.
Cancer related fatigue - impact occupational performance in activities of daily living, sexual activity, leisure participation, social participation, rest and sleep, work engagement, and overall quality of life of those living with and beyond cancer; most common chronic effect of all cancers.

183
Q

True or False - Frailty is synonymous with aging.

A

False - there is a wide range of function, health, and ability of older adults.

184
Q

What is Frailty more predictive of compared to chronological age?

A

Quality of life, functional status, risk of adverse outcomes.

185
Q

True or False - Frail individuals are more likely to have disproportionate consequences from minor external stresses.

A

True - Likely to have worst consequences for things such as ground level falls, urinary tract infections.

186
Q

What are some ways in which Frailty may manifest as?

A

Decreased strength & energy
Increased help with ADLs
Feeling “slow”
More severe and longer response to minor stresses
Falls – changes in balance and gait
Frequent infections
Delirium
Fluctuating function – good and bad days

187
Q

What is the acronym used by healthcare providers to understand prevention and treatment of Frailty?

A

AVOID
A = Activity - physical activity at all stages and environment.
V = Vaccine.
O = Optimize medications.
I = Interact - opportunities for socialization, stimulation, and meaningful relationships.
D = Diet and nutrition.

188
Q

How can Frailty impact occupational participation?

A

The decline in muscle mass and strength caused by bed rest has been linked to falls, functional decline, increased frailty, and immobility.
Associated with increased hospitalization and institutionalization.
Can change where you complete your occupations and what meaningful occupations are available.
Use of a validated measure like the Clinical Frailty Scale or other outcome measures can help predict what kinds of occupations people need assistance with and provide appropriate support (e.g., homecare for help with dressing; family to take over lawn care).

189
Q

What are some common mechanisms of onset for Hand Injuries?

A

Crush injuries
Lacerations
Torsion (twisting, hyperextension, hyperflexion).
Repetitive/cumulative use
Burns

190
Q

What are some possible complicating factors in the healing of Hand Injuries?

A

Dirty wounds (infections)
Excessive scar formation
Complex Regional Pain Syndrome (CRPS)
Late intervention** will inform how much healing has already occurred
Severe tissue trauma
Poor oxygen supply
Poor blood supply
Extensive/diffuse edema

191
Q

Describe some general principles applied to the medical management of Hand Injuries.

A

Vascular supply - loss will result in necrosis (digit can fall off)
Bony stability
Nerve continuity - discontinuity results in loss of function
Tendon integrity
Ligament stability
Soft tissue intact/stable

192
Q

True or False - Scar strength is disproportional to scar volume.

A

False - scar strength is directly proportional to scar volume.

193
Q

True or False - Scar volume is inversely proportional to motion.

A

True.

194
Q

What are the three stages of healing as it relates to Hand Injuries? What is the rough duration of each?

A

Stage 1 - Hemostasis/Inflammation (0-14 days)
Stage 2 - Inflammatory/Tissue Repair (2-12 weeks)
Stage 3 - Scar Maturation/Remodeling (3-12 months)

195
Q

What is the difference between a contraction and a contracture in the skin healing process? Which is often a barrier to function?

A

Contraction - Normal healing process.
Contracture - Pathologic deformity caused by contraction of the scar; frequent barrier to function (limit movement).

196
Q

True or False - Sharp, clean nerve lacerations have better recovery rates than complex cut, crush, or stretch nerve injuries.

A

True.

197
Q

True or False - Older individuals recover better from nerve injuries.

A

False - The younger the better.

198
Q

True or False - A mixed nerve (e.g., sensory and motor) injury has better prognosis.

A

False - A pure sensory or motor nerve has better prognosis.

199
Q

What are some symptoms associated with Complex Regional Pain Syndrome?

A

Pain*, sympathetic changes (vascular, sudomotor, trophic), edema, stiffness.

200
Q

Describe some occupational impacts related to Hand Injuries.

A

Functional - can still “do”, but might “do” differently (occupational adaptation); restrictions may be “imposed”; immobilization interventions create barriers.
Psychological - coping mechanisms (initial avoidance)

201
Q

How are Spinal Cord Injuries named?

A

Based on which level the injury occurs.

202
Q

What are some of the most common causes of Spinal Cord injuries?

A

Motor vehicle collisions
Falls
Sports-related
Assault

203
Q

True or False - In an flexion injury (Spinal Cord), the force comes from below the head.

A

False - The force comes from behind (head jerks forward).

204
Q

Where does the impact come from in a hyperextension injury (Spinal Cord)?

A

From below the head/body.

205
Q

How are Spinal Cord Injuries most often classified? What are the levels?

A

Using the ASIA Impairment Scale.
Level A - Complete; no motor or sensory function preserved in the sacral segments S4 through S5.
Level B - Sensory incomplete; sensory but not motor function is preserved below the neurological level and extends through the sacral segments S4 through S5.
Level C - Motor incomplete; motor function preserved below the neurological level, majority of key muscles below the neurological level have a muscle grade <3.
Level D - Motor incomplete; motor function is preserved below the neurological level, majority of key muscles below the neurological level have a muscle grade of 3 or more.
Level E - Normal; motor and sensory function is normal.

206
Q

How is strength graded to determine the extent of a Spinal Cord Injury? What does each grade mean?

A

On a scale from 0-5.
0 - Total paralysis.
1 - Palpable or visible contraction.
2 - Active movement, full range of motion (ROM) with gravity eliminated.
3 - Active movement, full ROM against gravity.
4 - Active movement, full ROM against moderate resistance.
5 - Normal active movement, full ROM against full resistance.

207
Q

What level would a Spinal Injury need to occur at for the patient to lose the ability to breathe independently?

A

C4

208
Q

What level of Spinal Cord Injury would the abdominal muscles be affected?

A

T7-T12.

209
Q

What level of the Spinal Cord controls bladder and bowel control? What would an injury to this level cause?

A

S2-S5. Damage would result in urinary and fecal incontinence.

210
Q

What level of the Spinal Cord controls the triceps muscle?

A

C7.

211
Q

What levels of the Spinal Cord controls the intrinsic muscles of the hand?

A

C8-T1.

212
Q

What is Autonomic Dysreflexia? What are some common signs and symptoms?

A

An exaggerated ANS response. Occurs in people with spinal cord injuries above the T6 level.
Sudden, pounding headache, diaphoresis (excessive sweating), flushing, goosebumps, tachycardia followed by bradycardia.
Caused by an irritation of nerves below the level of injury.
Risk of stroke or death - blood pressure raises dramatically.

213
Q

What are some factors influenced by the depth of Burn Injury?

A

Survival rates, course and length of healing, medical and interdisciplinary treatment options, and scar formation.

214
Q

List two factors that may influence the severity of a Burn.

A

Temperature
Duration of exposure

215
Q

Describe the 3 zones of healing for Burn Injuries.

A

Coagulation - Most exposure; direct contact; irreversible tissue damage.
Statis - Decreased tissue perfusion, may recover with early intervention.
Hyperemia - Periphery of wound, likely to recover; goal is to reduce spread of necrotic tissue into this area.

216
Q

Describe key elements of a Superficial Burn.

A

Depth - Epidermis.
Appearance - Intact skin, blanchable erythema, and mild edema, brisk capillary refill, no blisters.
Causes - Scalds from low viscosity liquids, sunburn.
Sensation - Tactile and pain intact.
Healing Time - ~7 days; usually no scarring.

217
Q

Describe the key elements of a Superficial Partial Thickness Burn.

A

Depth - Epidermis with partial-thickness loss of dermis.
Appearance - Blanchable erythema, brisk capillary refill, blisters (serum filled, painful).
Causes - Scalds from low viscosity liquids, steam, brief exposure to flame or hot object, peeling sunburn.
Sensation - Tactile and pain intact.
Healing Time - 7-21 days; usually no scarring.

218
Q

Describe the key elements of a Deep Partial Thickness Burn.

A

Depth - Epidermis with deep partial-thickness loss of dermis; vascular system impacted.
Appearance - Non-blanchable erythema, sluggish capillary refill, thick, serum filled blisters (painful).
Causes - Scalds from low or high viscosity liquids or steam, exposure to flame, contact with hot object.
Sensation - Intact deep pressure, absent pinprick sensation, variable pain sensation.
Healing - ~3-5 weeks, scarring, may require grafts.

219
Q

Describe key elements of a Full Thickness Burn.

A

Depth - Full-thickness skin loss, can include skin, muscles, tendons, bones.
Appearance - non-blanchable, capillary refill absent, skin is white, waxy, leathery, dry, eschar may be present.
Causes - Liquid immersion, prolonged exposure to flame/hot objects, chemical, electricity, frostbite.
Sensation - Insensitive to pain.
Healing - Scarring, may require grafting.

220
Q

What is a typical progression of a burn survivor through healthcare system?

A

Hospital (ICU/critical care, acute care)
Inpatient (subacute rehabilitation)
Outpatient (clinics, home programs)

221
Q

What is the preferred type of graft to use for Burn interventions?

A

Autologus grafts - taken from a person’s own skin.
Allograft - temporary, taken from another person (body will reject).

222
Q

What are some benefits to using a Sheet Graft for Burn Injuries?

A

Thicker, more durable, cosmetically appealing.

223
Q

What are some benefits to using a Split Thickness (Mesh) Graft for Burn Injuries?

A

Decreased donor skin needed

224
Q

What is Debridement in reference to the treatment of Burn Injuries? Why is it done?

A

Cleansing and removal of non-adherent and nonviable tissue.
Necessary to decrease the potential for burn wound sepsis, to facilitate healing, and to prepare wound for grafting.
Painful procedure - medications used for pain management and to reduce anxiety.

225
Q

What are Hypertrophic scars?

A

Common in burn injuries (30-90%).
Delay in wound treatment increases risk of hypertrophic scarring (excess of collagen tissue).
Does not expand beyond injury site.
Can lead to wound contracture if scar crosses a joint.

226
Q

What are Keloid scars?

A

Excessive fibrosis, nodular proliferations that project beyond the margins of the original injury.

227
Q

What are Joint Contractures?

A

Shortening and tightening of the burn scar; permanent shortening producing deformity or distortion.

228
Q

What are some psychosocial impacts of Burn Injuries?

A

Substance use, depression, PTSD.
Chronic stress and psychosocial injury can impact wound closure and healing time.
Burns that are slow healing, disfiguring, painful and/or result in limb/joint dysfunction = higher psychosocial stress.

229
Q

What is a Traumatic Brain Injury?

A

Non-degenerative, non-congenital alteration in brain function caused by an external force.

230
Q

What are the three classifications of Traumatic Brain Injuries? How are they measured?

A

Mild - Loss of consciousness <30 minutes, post traumatic amnesia <24 hours, Glasgow Coma Scale score of 13 to 15.
Moderate - Loss of consciousness of 30 minutes to 24 hours, post traumatic amnesia of 24 hours to 7 days, GCS of 9 to 12.
Severe - Loss of consciousness >24 hours, post traumatic amnesia >7 days, GCS score of 3 to 8.

231
Q

What is meant by a “Primary Damage” regarding Traumatic Brain Injuries?

A

Caused by direct impact of the brain. Localized or diffuse damage.

232
Q

What is meant by “Secondary Damage” regarding Traumatic Brain Injuries?

A

Physiological response to injury - hours to days after the initial injury.
Inflammatory, immune responses.
Increased cranial pressure, decreased blood flow (ischemia).

233
Q

What is another term used for a Mild TBI? What are some common symptoms associated with a Mild TBI?

A

Concussion.
Symptoms - Headaches, dizziness, fatigue, visual disturbance, memory, and executive functioning difficulties.

234
Q

Can concussions be visualized on brain imaging (CT scans)?

A

No.

235
Q

What are 3 symptoms (related to a mild TBI) that indicate someone should seek emergency care?

A

Sudden or severe vomiting
Weakness or tingling/burning in arms/legs
Seizure or convulsion
Severe or worsening headache
Slurred speech

236
Q

Why is the Los Amigos Scale used in the classification of Traumatic Brain Injuries? Describe each level (Fig. 20.4).

A

Describes typical cognitive and behavioural patterns of recovery after a TBI.
Considers level of consciousness and reliance on assistance from others to carry out cognitive and physical function.
Level I - No response (appears asleep).
Level II - Generalized response.
Level III - Localized response.
Level IV - Confused, agitated response.
Level V - Confused, inappropriate, non-agitated response.
Level VI - Confused, appropriate response.
Level VII - Automatic, appropriate response.
Level VII - Purposeful, appropriate response.

237
Q

Why is the Glasgow Coma Scale used in the assessment of TBIs?

A

Assesses and communicates the level of consciousness of a person with an acute brain injury.
Assess response to stimuli across - eye opening, verbal response, motor response.

238
Q

True or False - Younger age at the time of a TBI improves survival rates and recovery.

A

True.

239
Q

What is Age-Related Macular Degeneration (AMD)? What are the two subtypes?

A

Low vision disorder that results in loss of central vision due to degeneration of the cells of the macular lutea, the center of the retina.
Dry AMD (atrophic)
Wet AMD (neovascular/exudative)

240
Q

What are common symptoms of wet and dry AMD?

A

Dry - slow, progressive loss of central vision (may take years to develop).
Wet - usually impacts one eye initially; primary symptom = acute loss of central vision that becomes permanent as the retina atrophies and is replaced by fibrous tissue; rapid loss of central vision that is described as wavy, blurry, or distorted.

241
Q

What is Glaucoma? What are the subtypes?

A

Damage to the optic nerve head, progressive loss of retina cell layer (tunnel vision). Increased intraocular pressure.
Open-angle
Angle-closure
Neovascular

242
Q

What are the signs and symptoms of Open-Angle Glaucoma?

A

Slow loss of peripheral vision.
Difficulty seeing in dim light.
Decreased contrast sensitivity.
Sensitivity to glare.
Blurred vision.
Decreased depth perception.

243
Q

What is the primary goal for treatments of Glaucoma? What is a common intervention for this disorder?

A

Reduce intraocular pressure.
Eye drops (topical ocular medication), laser therapy.

244
Q

What is a common OT intervention for individuals with Low Vision?

A

Compensatory adaptation to improve occupational participation.

245
Q

What is Cataracts?

A

Opacifications of the lens of the eye, which result from a buildup of opaque, broken proteins (crystallin’s) that stick together and form sheath like obstructions that decrease the amount of light reaching the retina.

246
Q

List some common signs and symptoms of Cataracts.

A

Foggy, blurry, cloudy vision.
Decreased visual acuity.
Decreased contrast sensitivity.
Glare disability- ability to see in presence of bright light.
Myopia – nearsightedness.
Described as looking through a “steamy glass”.
One eye usually affected earlier than other; both eyes most often involved.
Blindness possible if untreated.

247
Q

How can Vision Disorders impact Occupational Participation?

A

The extent of the impact on occupational performance depends on the type of low vision disorder, the stage of progression of that disorder, and the treatment that has been received.
May require early retirement from valued occupations like driving.
Can affect safety (i.e., community mobility, household navigation, stove/hot liquids, medication errors).
Role of stigma and lack of universal and accessible design (e.g., low lighting in restaurants).