physical disability conditions quiz #1

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Last updated 6:43 PM on 9/27/26
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185 Terms

1
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myocardial infarction (MI) is a result of...

- unstable angina

- reduced blood flow and O2 to the heart

- coronary artery blood vessel plaque rupture or thrombus

- reduced blood supply to the myocardium

- irreversible tissue damage and necrosis

- myocardium most prone to damage

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what is a STEMI MI?

the coronary artery is completely blocked by a blood clot

- more serious than NSTEMI

- requires immediate emergency correction

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what is a NSTEMI MI?

the coronary artery is only PARTIALLY blocked

- part of the heart isn't getting enough oxygen

- will need to be hospitalized until correction, but not usually emergency correction

4
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symptoms of myocardial infarction (MI)

- pain or no pain

- crushing sensation in chest, jaw, down left arm

- nausea and vomiting

- fatigue

- shortness of breath

- perspiration

- cool or clammy skin

- anxiety or restlessness

- women may have symptoms for a few weeks of general fatigue, sleep disturbance, shortness of breath, and anxiety. Women are also more prone to upset stomach

5
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diagnosis of myocardial infarction:

- blood tests that look for chemical makers

- EKG (ECG)

- angiogram

6
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treatment for myocardial infarction (MI)

Medications to dilate vessels and break up clots.

Followed by a procedure to improve blood flow. Atherectomy, Angioplasty, CABG

7
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what is Asthma?

a condition in which a person's airways become inflamed, narrow and swell, and produce extra mucus, which makes it difficult to breathe. (treatable)

8
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what are treatments for Asthma?

asthma can usually be managed with rescue inhalers to treat symptoms and controller inhalers that prevent symptoms.

severe cases may require longer-acting inhalers that keep the airways open, as well as oral steroids.

9
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Asthma symptoms...

wheezing and dyspnea

10
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what is peripheral vascular disease (PVD)?

- lack of blood supply to the LE resulting from stenosis or occlusion within arteries. Can also be caused by atherosclerosis.

11
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PVD symptoms:

- cold extremities

- numbness and tingling

- absence of hair

- ulcers

- aching extremities

- brown skin color

- itching

- ischemia

12
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PVD treatment:

- angioplasty

- atherectomy

- venous grafts

13
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what is a pulmonary embolism?

clot, air bubble, or fat particle travels through the venous system into the right side of the heart and out the pulmonary vasculature causing obstruction

14
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what is the cause of a pulmonary embolism?

an embolus breaks loose from a DVT and travels to lungs; blocks blood flow from the right side of the heart to the lungs

15
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pulmonary embolism symptoms:

- sudden dyspnea

- tachycardia

- tachypnea

- chest pain

- syncope

- cyanosis

- sweats

- low-grade fever

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pulmonary embolism treatment:

- anticogulants

- blood thinners

17
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what is chronic obstructive pulmonary disease (COPD)?

chronic airflow limitation; inflammatory; loss of elastic recoil; restricted airway; reduced expiratory airflow; decreased pulmonary function

18
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symptoms of COPD:

- fatigue

- constant dyspnea which worsens with exertion

- phlegm with couch

- wheezing

- edema in extremities

19
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what is congestive heart failure (CHF)?

- progressive weakened heart

- inefficient ability to pump blood to meet the body's metabolic needs; right or left side failure; can start on the left and progress to the right

- the heart chamber becomes enlarged causing inefficient pumping

- backup of blood into the venous system - overloads the tissue (congestion) causing distal edema in LE (primarily) however can in UE

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congestive heart failure (CHF) symptoms:

- dyspnea

- orthopnea

- rapid heartbeat

- fatigue

- exercise intolerance

- coughing

- weight gain

- LE edema

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congestive heart failure treatment:

- medications

- pacemaker

- cardiac rehab

- heart replacement

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what is Pneumonia?

inflammation of the air sac (Alveoli) in the lung causes by bacteria, viruses, fungi.

23
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what type of condition is osteogenesis imperfecta?

a hereditary condition with identifiable gene mutation.

24
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which gene is mutated in osteogenesis imperfecta?

COL 1A1 and COL 1A2 located in chromosome 17 and 7.

25
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what are the different types of osteogenesis imperfecta?

types I - IV

(types I and IV are the most prevalent in the USA and are the least severe; occur in the autosomal dominant pattern).

26
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what is osteogenesis imperfecta?

(brittle bone syndrome) brittle bones caused by an insufficient production of collagen and osteoblasts resulting in bone fragility.

27
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what are the implications of osteogenesis imperfecta?

- impaired quality, quantity, and geometry of bone material

- hyperextensible ligaments

- deafness in 35% of cases in the 3rd decade of life

28
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what are the risk factors (for fracture) associated with osteogenesis imperfecta?

accidents, overuse, participation in sports, falls, low physical function, decreased bone mineral density, poor nutrition (vitamin D), and other diseases or conditions (osteoporosis).

29
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what is osteoporosis?

a disease resulting in a decrease of mineral density or bone mass causing the bone to become brittle.

30
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what is lateral epicondylitis/tendonitis (tennis elbow)?

an overuse or force load injury due to the denigration of the tendon as the structure ages.

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which tendon is affected by lateral epicondylitis (tennis elbow)?

the common extensor tendon at its point of origin on the lateral epicondyle of the humerus.

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which muscle is most affected by lateral epicondylitis (tennis elbow)?

the extensor carpi radialis brevis (ECRB).

(sometimes with the extensor digitorium communis (ED))

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what type of symptoms are associated with lateral epicondylitis (tennis elbow)?

complaints of pain over the lateral portion of the elbow with decreased grip strength, in addition to tenderness to palpation over the lateral epicondyle.

34
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conservative treatment for lateral epicondylitis (tennis elbow) includes...

ice, rest, activity modifications, orthoses, corticosteroid injection, and strengthening.

35
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what are the two (2) phases of conservative treatment for lateral epicondylitis (tennis elbow)?

1) phase one focuses on reducing pain and restoration of tendon length (that has been reduced due to scarring of the tendon).

2) phase two introduces progressive (eccentric) strengthening.

36
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surgical intervention is suggested to treat lateral epicondylitis (tennis elbow) for a client that continues to experience decreased function due to debilitating pain despite....

6 to 12 months of conservative management.

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what is medial epicondylitis/tendonitis (golfer's elbow)?

pain, swelling, and tenderness to palpation over the medial aspect of the elbow.

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which tendon is affected by medial epicondylitis (golfer's elbow)?

the common flexor tendon at its point of origin on the medial epicondyle of the humerus.

39
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what muscle is most affected by medial epicondylitis (golfer's elbow)?

the pronator teres and flexor carpi radialis (FCR)

(and palmaris longus (PL)).

40
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treatment for medial epicondylitis (golfer's elbow) is the same as lateral epicondylitis (tennis elbow) except...

that stretches and strengthening are focused on wrist flexors.

41
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when is downs syndrome typically diagnosed?

during prenatal or infancy.

42
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what are the three types of downs syndrome?

trisomy 21 (955%), translocation (4%), and mosaicism (1%).

43
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what is the cause of downs syndrome?

sequencing of chromosome 21 (delayed myelination, fewer neurons, decreased synaptic density, decreased acetylcholine neurotransmitter receptor).

44
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what are the common deficits associated with downs syndrome?

- increased risk of abnormalities of almost every organ

- congenital heart defect

- sensory impairments (vision and hearing)

- endocrine abnormalities (hypothyroidism, poor development of the thyroid)

- obesity

- short stature

- decreased FMC

- decreased muscle tone

- orthopedic conditions (atlantoaxial subluxation, or a gap between C1 and C2)

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downs syndrome is the most common chromosomal cause of moderate to severe...

intellectual disability.

46
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when is prader-willi syndrome (PW) typically diagnosed?

before the age of 6.

47
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what is the cause of prader-willi (PW) syndrome?

multiple genes affected either paternally (paternal deletion) or maternally (maternal uniparental disomy).

48
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what is paternal deletion?

the result of missing genetic information from the copy of chromosome 15 inherited from the father (around 70%) of cases.

(results in mild to moderate mental retardation and significant behavioral problems, such as skin picking).

49
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what is maternal uniparental disomy?

when a person receives two copies of a chromosome or part of a chromosome, from one parents and no copy from the other parent.

(results in milder physical phenotype, better cognitive function, with higher verbal skills and fewer behavior problems, however they have decreased visual acuity and impaired stereoscopic vision compared with deletion subjects).

50
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prader-willi (PW) syndrome is the most common cause of...

obesity and intellectual disability.

51
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what are the characteristics of prader-willi (PW) syndrome?

hyperphagia and obesity.

52
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what is hyperphagia?

a lack of satiation after meals.

53
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what are the typical physical features associated with prader-willi (PW) syndrome?

- a round face

- narrow palpebral fissures

- short stature

- small genitalia

- short fingers and toes

- low muscle tone

54
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what are the typical behavioral and cognitive characteristics associated with prader-willi (PW) syndrome?

- mild intellectual disability

- poor attention

- obsessive behavior particularly around food (food hoarding and stealing are common)

- excessive skin picking

- remarkably good ability with puzzles

55
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when is fragile-x syndrome typically diagnosed?

in utero.

56
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fragile-x syndrome is the most common ___ cause of intellectual disability and autism spectrum disorder.

inherited.

57
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what causes fragile-x syndrome?

a full mutation of the FMRI resulting in deficiency of FMRI protein (FMRP).

(a fragile site on the long arm of an X chromosome is present, with breaks or gaps shown on the chromosomal analysis).

58
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what is FMRI protein (FMRP)?

an RNA binding protein that mainly regulates the translation of hundreds of genes.

59
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what are the typical characteristics associated with fragile-x syndrome?

- hyperactivity

- attentional problems

- poor eye contact

- hand-flapping

- anxiety

- hyperarousal

- lack of habituation to sensory stimuli

60
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what are the typical physical features associated with fragile-x syndrome?

- long face

- prominent ears

- hyperextensive finger joints and flat feet

61
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angleman syndrome is a severe ____ disorder with similar symptoms and characteristics of autism, cerebral palsy, and prader-willi (PW) syndrome?

neurogenic.

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what is the cause of angleman syndrome?

the maternal chromosome 15 has a deletion (one gene is affected).

63
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what is angleman syndrome typically diagnosed?

via an EEG.

64
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what are the typical characteristics of angleman syndrome?

- developmental delays

- seizures during childhood (but decrease by adolescence)

- sleep disorders

- a happy demeanor (frequently laughing, smiling, and excitability)

65
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what are the typical characteristics of angleman syndrome seen in infants (0-24 months)?

- lack of cooing or babbling

- inability to support one's head

- pull oneself up to stand

- delayed motor skills (ataxia (unstable), low tone)

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what are the typical characteristics of angleman syndrome seen in young children?

- lack of speech

- delayed ability to walk

- unstable gait or balance issues

- ataxia (tremor)

- increased anxiety

- intellectual disability

67
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what is impingement syndrome of the rotator cuff?

a problem of space (a closing of the space that creates inflammation and pain).

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what is neer's three stage classification of impingement?

1) < 25 years (reversible edema and hemorrhage from excessive overhead use)

2) 25 - 40 years (irreversible fibrotic changes to the rotator cuff following repeated episodes of mechanical inflammation)

3) > 40 years (bone spurs and tears, complete or incomplete, of the rotator cuff and long head of the bicep tendon).

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what are some non-impingement injuries that can lead to a rotator cuff tear?

- osteoarthritis

- adhesive capsulitis (frozen shoulder)

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what are the two (2) factors of non-impingement injuries?

1) intrinsic factors (degeneration)

2) extrinsic factors (trauma)

71
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what are some intrinsic factors associated with non-impingement injuries of the rotator cuff?

(underlying medical conditions or client factors we cannot control)

- age related degeneration of the joint

- hypo-vascularity

- calcification (changes in the joint space that contribute to injury, such as arthritis)

72
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what are some extrinsic factors associated with non-impingement injuries of the rotator cuff?

(occupational based or an event that happens that can be controlled/modified)

- repeated impingement of the rotator cuff tendons during upper extremity elevation (flexion, abduction) resulting in injury

- prolonged heavy lifting (especially without good shoulder stability)

- rotational injury

- trauma (falling on an outstretched arm)

73
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what are the typical treatments for a rotator cuff injury?

- anti-inflammatories

- immobilization (after repair)

- OT/PT

- surgery to attach the torn tendon back to the humeral head where it was torn (orthoscopic debridement, tendon repair)

74
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what are the symptoms of rheumatoid arthritis (RA)?

- autoimmune (can be sudden)

- systemic (affects every joint in the body)

- fever

- malaise (feeling of unwell)

- fatigue

- symmetrical pain and swelling (early AM stiffness)

- extra-articular organ involvement (can involve other organs in the body)

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what causes the joint changes associated with rheumatoid arthritis (RA)?

- synovitis

- pannus (inflammatory tissue) invades the bone and cartilage, eroding it

- rheumatoid nodules (cutaneous manifestation of RA)

- vasculitis (inflamed veins and arteries)

76
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what is rheumatoid arthritis (RA)?

continual swelling that weakens the ligaments and joint capsule, causing joint instability and joint deformity.

77
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how is rheumatoid arthritis (RA) typically diagnosed?

- history and physical exam

- laboratory tests (RA factor, an antibody found in about 85% of persons with RA)

- radiograph (x-rays) will not show changes initially; MRI is used for better imagining especially if surgery is indicated)

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what are the categories of rheumatoid arthritis (RA)?

1) reversible signs and symptoms (acute inflammation)

2) irreversible damage resulted from synovitis

79
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what are the stages of rheumatoid arthritis (RA)?

1) acute

2) subacute

3) chronic active

4) chronic inactive

80
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describe the condition of a patient presenting with acute rheumatoid arthritis (RA).

- limited motion

- pain

- tenderness at rest (increasing with activity)

- stiffness

- weakness

- tingling or numbness

- hot red joints

81
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describe the condition of a patient presenting with subacute rheumatoid arthritis (RA).

- limited motion and tingling

- stiffness only in the AM

- joints pink and warm

82
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describe the condition of a patient presenting with chronic active rheumatoid arthritis (RA).

- less pain, tingling, and tenderness

- increased activity level

83
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describe the condition of a patient presenting with chronic inactive rheumatoid arthritis (RA).

no signs of inflammation.

84
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what joints are commonly affected by rheumatoid arthritis (RA)?

- wrist (radial deviation)

- elbow

- MCP (ulnar deviation)

- PIP (swan neck or boutonnière deformity)

- ankle and MTP

- tempromandibular joints

- hip

- knee

- shoulders

- cervical spine

85
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what are the medical management strategies for rheumatoid arthritis (RA)?

- pharmacology (NSAIDS, COX2 inhibitors, salicylates, corticosteroids, analgesics, OPIODS)

- disease-modifying anti rheumatic drugs (DMARD, methotrexate)

- biologic response modifiers (super strength anti-inflammatory)

86
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what are the surgical management strategies for rheumatoid arthritis (RA)?

- synovectomy/tenosynovectomy (trigger finger)

- tendon repair

- CTR/CUTR

- arthroplasty (joint replacement of the knee, hip, MCP)

- arthrodesis (wrist, thumb, MCP, IP, cervical spine)

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what are the therapeutic management strategies (OT/PT) for rheumatoid arthritis (RA)?

- joint protection

- pain management

- splinting

- strengthening

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rheumatoid arthritis (RA) is a...

progressive, chronic disease.

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osteoarthritis (OA) is a...

progressive, local disease

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what is osteoarthritis (OA)?

the degenerative joint changes due to deterioration or loss of articular cartilage, causing reaction bone formation (osteophytes); inflammation is secondary as a result of the degeneration (not systemic inflammation).

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osteoarthritis (OA) is specific to the...

joint.

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which joints are most commonly affected by osteoarthritis (OA)?

- hand (CMC, PIP, and DIP)

- cervical and lumbar spine

- MTP of the feet

- knee and hip

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what are the stages of deterioration associated with osteoarthritis (OA)?

1) cartilage softens and loses elasticity

2) sections of cartilage wear away and decrease joint space

3) bone on bone articulation

4) bone ends thicken and form osteophytes (reaction bone formation)

5) joints loses its normal shape

6) cysts form

7) development of loose bones in the joint space

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how is osteoarthritis (OA) typically diagnosed?

same as rheumatoid arthritis (RA) without laboratory tests.

95
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what are the clinical signs and symptoms of osteoarthritis (OA)?

- joint pain, stiffness, tenderness

- crepitus (when the joint "catches")

- usually gradual onset

- increased discomfort with activity

- AM stiffness and stiffness after activity

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what is the medical management strategies for osteoarthritis (OA)?

- pharmacology (NSAIDS, COX2 inhibitors, salicylates, corticosteroids, analgesics, OPIODS)

- supplements

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what is the surgical management strategies for osteoarthritis (OA)?

joint replacement.

98
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what is the therapeutic management strategies (OT/PT) for osteoarthritis (OA)?

- joint protection

- pain management

- splinting

- strengthening

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what is a swan neck deformity?

PIP hyperextension with DIP hyperflexion.

<p>PIP hyperextension with DIP hyperflexion.</p>
100
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what is the cause of a swan neck deformity?

rupture of the lateral slips of the extensor digitorium (EDC) at the DIP or rupture of the flexor digitorium superficial (FDS) tendon.

(can result from trauma, but typically due to OA/RA)