Gold Level Clinical Application Templates Flashcards

1
Q

What is Alzheimer’s Disease?

What causes it?

A

a progressive neurological disorders that results in deterioration and irreversible damage within the cerebral cortex and subcortical areas of the brain resulting in the breakdown of several processes that normally sustain brain cells

Exact etiology is not known but there are amyloid plaques, cerebral atrophy and neurofibrillary tangles within the cytoplasm that result in an inflammatory process that causes damage to the nervous system and damage to the smooth muscle and arteries in the brain

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2
Q

How do patients with Alzheimer’s Disease typically present?

A

patients in early stages will usually have a noted change in higher cortical functions such as subtle changes in memory, impaired concentration, and difficulty learning new things, word finding issues, depression, and poor judgement

In middle stages patient will have behavioral and motor issues such as aphasia, apraxia, perseveration, agitation and violent or socially unacceptable behavior

End stage Alzheimer’s Disease sees the patient have no ability to learn new tasks and severe loss of long term memory and vegetative symptoms such as incontinence, functional dependence, and inability to speak

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3
Q

How is Alzheimer’s Disease managed with PT?

A

focus on maximizing remaining functional ability and family/caregiver education

PT can be useful to increase independence but it cannot alter or cease the progression of Alzheimer’s Disease

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4
Q

What is the typical outcome for patients with Alzheimer’s Disease?

A

this is a chronic and progressive disorder and the typical course of the disease averages between 7 and 11 years, the leading cause of death for patients with Alzheimer’s Disease is dehydration or infection

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5
Q

What is Amyotrophic Lateral Sclerosis (ALS)?

A

a chronic degenerative disease that produces both upper and lower motor neuron impairment due to demyelination, swelling in the axons, and atrophy within the cerebral cortex, premotor areas, sensory cortex and temporal cortex

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6
Q

What causes Amyotrophic Lateral Sclerosis (ALS)?

Which populations are at higher risk?

A

exact etiology is not know but leading theories are genetics, a slow acting virus, metabolic disturbances, or lead/aluminum toxicity

men are at higher risk and typical age of onset is between 40 and 70

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7
Q

How do patients with Amyotrophic Lateral Sclerosis (ALS) typically present?

A

Early ALS signs can include both upper and lower neurons symptoms.

Upper motor neuron symptoms can include loss of motor inhibition, clonus, positive Babinski sign and spasticity

Lower motor neuron symptoms usually present distally to proximally and includes asymmetric weakness, cramping and atrophy

Eventually patients with ALS will exhibit fatigue, oral motor impairments, motor paralysis, and respiratory paralysis

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8
Q

What are some primary indicators for diagnosis a patient with Amyotrophic Lateral Sclerosis (ALS) based on symptoms?

A

If a patient has motor impairments without any sensory impairments and if they have upper and lower motor neuron symptoms

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9
Q

What medication is typically used for patients with Amyotrophic Lateral Sclerosis (ALS)?

A

Riluzole (Rilutek)

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10
Q

What is the typical plan of care for patients with Amyotrophic Lateral Sclerosis (ALS) in PT?

What is the typical outcome for patients with ALS?

A

Maximize function and educate family/caregivers

this is a fast acting disease that usually kills the patient within 2-5 years after diagnosis, PT cannot alter or cease the progression of this disease

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11
Q

What is Carpal Tunnel Syndrome?

A

compression of the median nerve in the carpal tunnel due to increased pressure via inflammation or entrapment which can lead to ischemia, numbness, and motor disturbances in the median nerve distribution

usually effects women more than men and typical age of onset is 35-50 years old

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12
Q

How do patients with Carpal Tunnel Syndrome clinically present?

A

patients will typically present with sensory changes and paresthesia along the median nerve distribution which may radiate up the arm

Other common signs and symptoms are night pain, hand weakness, muscle atrophy, decreased grip strength, and decreased wrist mobility

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13
Q

What tests can help confirm a diagnosis of Carpal Tunnel Syndrome?

A

Tinel’s Test

Phalen’s Test

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14
Q

What is Central Cord Syndrome?

A

an incomplete spinal cord lesion that most often results from cervical hyperextension

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15
Q

How do patients who sustain an injury which results in Central Cord Syndrome typically present clinically?

A

motor loss that is greater in the upper extremities than lower extremities and is most severe distally in the UEs

sensory loss below the level of the lesion is usually limited but can be variable

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16
Q

Which ligament is typically injured in patients with Central Cord Syndrome?

A

Ligamentum Flavum

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17
Q

What is Cerebral Palsy?

A

an umbrella term used to describe a group of non-progressive movement disorders that result from brain damage and is the most common cause of permanent disability in children

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18
Q

How do patients with Cerebral Palsy typically present?

A

Depends on the extent of damage and what which limbs are involved, there are mild, moderate, and severe cases

general characteristics include abnormal muscle tone, poor postural control, high risk for hip dislocations, balance impairments, intellect, vision, hearing, and perceptual skills can also be affected

Intellectual disability and epilepsy are present in 50-60% of children diagnosed with Cerebral Palsy

All characteristics are classification dependent.

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19
Q

What is the difference between spastic Cerebral Palsy and athetoid Cerebral Palsy?

A

Spastic: involves upper motor neuron damage

Athetoid: damage to the basal ganglia

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20
Q

What is Duchenne Muscular Dystrophy?

A

a progressive neuromuscular degenerative disorder that manifests symptoms once fat and connective tissue begin to replace muscle that has been destroyed by the disease process

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21
Q

What causes Duchenne Muscular Dystrophy?

A

A mutation in the dystrophin gene Xp21 that normally codes for the muscle membrane protein dystrophin

this is a recessive gene so Duchenne Muscular Dystrophy only affects males and females are carriers

22
Q

How do patients with Duchenne Muscular Dystrophy usually present clinically?

A

usually diagnosed between ages 2 and 5

first symptoms are a waddling gait, proximal muscle weakness, clumsiness, toe walking, excessive lordosis, large calves, and difficulty climbing stairs

Gower’s sign is typical and issues with upper extremity, thoracic, and shoulder girdle musculature weakness

usually some cognitive disability as well

Rapid progression with patient being unable to ambulate by age 10-12 typically and death typically occurring in teenage years

23
Q

What is Erb’s Palsy?

A

an upper brachial plexus injury or palsy that usually results from a difficult birth, C5 and C6 are typically the nerve roots which are most affected leading to loss of function of the rotator cuff, deltoid, brachialis, coracobrachialis, and biceps

most common palsy relating to the brachial plexus

24
Q

How do infants who have Erb’s Palsy typically present?

A

with a “waiter’s tip” deformity which is a loss of shoulder function, loss of elbow flexion, loss of forearm supination, and the hand being positioned in a pinch grip manner

25
Q

What is Guillain-Barre Syndrome (Acute Polyneuropathy)?

A

a temporary inflammation and demyelination of the peripheral nerve’s myelin sheaths, potentially resulting in weakness with a distal to proximal progression, sensory impairment, and possible respiratory paralysis

26
Q

How do patients with Guillain-Barre Syndrome (Acute Polyneuropathy) typically present clinically?

A

typically young adults or patients between 50 and 80, slightly more prevalent in Caucasian males

initially presents with distal symmetrical motor weakness and will likely experience mild distal sensory impairments and transient paresthesia

weakness will progress towards the UEs and head and disability usually peaks between 2-4 weeks after onset then is stagnant for 2-4 weeks and slowly gets better after a few months to a year

Can be life threatening if there is respiratory paralysis

27
Q

What is the common outcome for patients who suffer from Guillain-Barre Syndrome (Acute Polyneuropathy)?

A

Most patient achieve full recovery but 20% do have some neurological deficits, and 3-5% of patient will die from respiratory paralysis

28
Q

What causes Guillain-Barre Syndrome (Acute Polyneuropathy)?

A

Etiology is unknown but it is believed to be an auto-immune response to a previous respiratory infection, influenza, immunization, or surgery

29
Q

What is Huntington’s Disease (Huntington’s Chorea)?

A

a neurological disorder of the CNS and is characterized by degeneration and atrophy of the basal ganglia (specifically the striatum) and cerebral cortex within the brain

the atrophy leads to extensive loss of small and medium sized neurons and an overall decrease in the quantity and activity of GABA and acetylcholine neurons that are produced in these areas

30
Q

How do patients who have Huntington’s Disease (Huntington’s Chorea) typically present clinically?

A

average age is between 35-50

patients initially present with involuntary choreic movements and a mild alteration in personality

involuntary facial expression are common and as the disease progresses an ataxic gait will be present and speech disturbances are common

Late stage Huntington’s in characterized by a decrease in IQ, dementia, depression, dysphagia, inability to ambulate or transfer, and progressive choreic movements

31
Q

What is the common outcome for patients diagnosed with Huntington’s Disease (Huntington’s Chorea)?

A

Usually die within 15-20 years after diagnosis

32
Q

What causes Huntington’s Disease (Huntington’s Chorea)?

A

it is a genetically transmitted disease linked to chromosome four and to the gene identified as IT-15

33
Q

What is Multiple Sclerosis?

A

a condition that produces patches of demyelination within the brain and spinal cord that results in plaque development that decreases the efficiency of nerve impulse transmission and produces symptoms that vary based on location and extent of demyelination

34
Q

What causes Multiple Sclerosis?

What populations are most at risk for developing Multiple Sclerosis?

A

etiology is unknown but it is believed to have a genetic component or caused by a slow acting virus or possibly environmental

Highest incidence in patients between 20 and 35 and almost twice as common in females compared to males

also a high incidence in population in temperate climates

35
Q

How do patients who have Multiple Sclerosis typically present in the clinic?

A

initial symptoms include visual problems, paresthesia and sensory changes clumsiness, weakness, ataxia, balance dysfunction, and fatigue

36
Q

What are the different types of Multiple Sclerosis?

What are the differences between the types?

A

relapsing-remitting: has bouts of symptoms (relapses) followed by long durations of no symptoms (remitting)

secondary-progressive: Starts as relapsing-remitting MS but progressively loses bouts of remission and relapse and symptoms progress without going away

primary-progressive: Symptoms progress steadily with no bouts of remission like you normally see in secondary-progressive

progressive-relapsing: Least common form of MS where symptoms will relapse and remit but progressively get worse and worse with each new relapse

37
Q

What does PT intervention focus on for patients with Multiple Sclerosis?

A

regulation of activity level, relaxation and energy conservation techniques, normalization of tone, balance activities, gait training, and core stabilization

38
Q

What is Parkinson’s Disease?

A

a primary degenerative disorder characterized by a decrease in production of dopamine within the Substantia Nigra portion of the basal ganglia which creates an imbalance between dopamine and acetylcholine which produces the symptoms of Parkinson’s Disease

39
Q

How will patients with Parkinson’s Disease typically present clinically?

A

Symptoms usually begin with a resting tremor in the hands (sometime called pill-rolling tremors) or feet that increases with stress and disappears with movement or sleep

balance disturbances, difficulty rolling in bed, fine motor impairments are common and can progress to hypokinesia, sluggish movements, akinesia and a festinating/shuffling gait

Patient can also notice “freezing” of gait, speech, blinking, and movements of the arms and also have very little facial expressions

40
Q

What medications are typically used for treating patients with Parkinson’s Disease?

A

Dopamine replacement drugs such as Levodopa, sinemet, or madopar

these drugs are designed to minimize bradykinesia, rigidity, and tremors

41
Q

What is Myelomeningocele Spina Bifida?

A

a form of spina bifida in which there is an incomplete fusion of the posterior vertebral arch with both meninges and spinal cord protruding outside the neural arch which may or may not be covered by skin

Most commonly found in the lumbar or sacral region (75%)

42
Q

What impairments can be linked to Myelomeningocele Spina Bifida?

A

motor and sensory loss below the defect, hydrocephalus, Arnold-Chiara type 2 malformation, clubfoot, scoliosis, bowel and bladder dysfunction, and learning disabilities

Latex allergy is common

43
Q

What are the three types of Spina Bifida?

A

Occulta (incomplete fusion of the posterior vertebral arch with no neural tissue protruding)

Meningocele (incomplete fusion of the posterior vertebral arch neural tissue/meninges protruding outside the neural arch)

Myelomeningocele (incomplete fusion of the posterior vertebral arch with both meninges and spinal cord protruding)

44
Q

What is the prognosis for patients born with Myelomeningocele Spina Bifida?

A

a near normal life expectancy as long as the patient receives consistent and thorough health care

functional outcomes depend on the level of the injury, amount of support, and severity of impairments

45
Q

How can Myelomeningocele Spina Bifida be caught early on in pregnancy?

A

by testing of alpha-fetoprotein (AFP) in the blood at week 16 of gestation

46
Q

What is the likely functional outcome for patients with a complete C7 tetraplegia spinal cord injury?

A

outcomes include independence with feeding, grooming, dressing, self-range of motion, independent manual wheelchair mobility, independent transfers, and independent driving with adapted automobiles

47
Q

What are the lowest innervated muscle for patient with a complete C7 tetraplegia spinal cord injury?

A

triceps, extensor pollicis longus and brevis, extrinsic finger extensors, and flexor carpi radialis

48
Q

What is the highest level of function patients with a complete L3 paraplegia SCI will be able to achieve?

A

should be able to live completely independent with education regarding the management of their disability

49
Q

What are the major limitations patients with a complete L3 paraplegia SCI may experience?

A

sexual dysfunction, a nonreflexive bladder, need for a bowel program, UTIs, muscle contractures, and pressure sores

50
Q

What are the most distal muscles that should have at least partial innervation in patients who have a complete L3 paraplegia SCI?

A

gracilis, iliopsoas, quadratus lumborum, rectus femoris, and sartorious and full use of BUEs

51
Q

What is Thoracic Outlet Syndrome?

A

a group of disorders that present with symptoms secondary to neurovascular compression of the fibers of the brachial plexus usually between the points of the interscalene triangle and the inferior border of the axilla or over the first rib

52
Q

What tests can help confirm a diagnosis of Thoracic Outlet Syndrome?

A
Roos
Adson maneuver
Wright test
Halstead maneuver
Allen Test