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PTA > Pathophysiology II > Flashcards

Pathophysiology II Flashcards

test 1

1
Q

T or F?
RA is a systemic autoimmune disorder (abnormal antibodies attack your own body) that affects the joints and connective tissues of the body

A

True

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2
Q

Who does RA mostly affect?

A

Young and middle-aged women, usually in the small joints of hands and feet

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3
Q

What does RA overall do?

A

Produces chronic inflammation and thickening of the synovial membrane of joints

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4
Q

T or F?
RA can often cause sx’s of chronic illness by affecting the blood vessels, heart, and lung

A

True

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5
Q

What are some other conditions that RA includes under its umbrella?

A

Juvenile arthritis, lupus, scleroderma, polymyositis, and dermamyositis

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6
Q

T or f?
The pathophysiology of RA is not fully understood

A

True

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7
Q

How does RA being?

A

Begins as a state of persistent cellular activation, leading to autoimmunity and immune complexes in joints and other organs

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8
Q

Where is the initial disease site of RA? What happens there?

A

Synovial membrane (synovitis) - swelling and congestion results in immune cells coming in, leading to pain, stiffness, and limited ROM. Synovitis leads to hypertrophy and excessive synovial fluid

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9
Q

What is the vascular granulation tissue called that dissolves collagen as it extends over the articular cartilage, destroying joint tissues?

A

Pannus - the dissolved cartilage can lead to adhesions, fibrosis, or bony anklyosis (stiffness/fixation of jt)

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10
Q

What are the three phases of progression of RA and what are they caused by?

A
  1. Initiation phase - caused by non-specific inflammation
  2. Amplication phase - caused by T cell activation
  3. Chronic inflammatory phase - tissue injury occurs from cytokines, interleukins 1 and 6, and tumor necrosis factor - alpha
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11
Q

Ra is highest in women at what percent?

A

69%

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12
Q

What is the mean age of diagnosis of RA?

A

56 yo

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13
Q

In affected pts, RF is present in what percent of them?

A

66%

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14
Q

What percent of affected patients show evidence of erosions in the first year?

A

20%

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15
Q

What is the rate of people being diagnosed with RA in the US?

A

41 per 100,000 people

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16
Q

How many people are estimated to have RA in the US?

A

1.5 million

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17
Q

What provokes our immune system into action, causing it to respond directly or by production of antibodies?

A

Antigens

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18
Q

What makes RA an autoimmune disease?

A

People who have RA produce antibodies to fight their own antibodies like RF or ACPA

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19
Q

T or F? RA is believed to be hereditary and can be triggered by viral infections

A

True

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20
Q

What greater risk are you at if a first degree family member is diagnosed with RA?

A

4x higher risk of developing RA

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21
Q

What are some environmental factors that can predispose you to RA?

A

Chemicals, pollution, secondhand smoke, and trauma

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22
Q

In women, can hormonal changes trigger RA?

A

Yes

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23
Q

What is the most strongly associated risk factor of RA and by what % does it increase your risk?

A

Smoking increases risk of RA by 2. 4%

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24
Q

T or F?
RA produces no noticeable deformities and destruction of the MCP joints

A

False - there is noticeable deforming and destruction of the MCP joints

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25
Q

Where can nodules appear in the body?

A

Hands, feet, and elbow

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26
Q

What are some other sx’s that can occur with RA?

A
  • Pleuritis: inflamed pleura layer of the lungs
  • Anemia: when blood does not have enough healthy RBC’s (this is why CBC is a test for RA)
  • Valvulitis: inflammation of valves of the heart
  • Lung fibrosis: scarring of lungs causing SOB
  • Kidney problems
  • Cardiovascular problems
  • Glaucoma: eye disease causing vision loss and blindness due to damage of optic nerve
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27
Q

What can happen with RA and the neck and spinal cord?

A

It can affect the neck and spinal cord causing damage, which can lead to paralysis or even death

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28
Q

Clinically, what are we going to see in an RA pt?

A

C/O fatigue and weight loss, symmetric joint swelling, pain, and stiffness (which is more prominent in the morning)

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29
Q

Between what ages of women is onset of disease highest?

A

20-40 yo

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30
Q

T or F? RA can produce spontaneous atlantoaxial subluxation due to laxity of ligaments and TMJ issues

A

TRUE - don’t have RA pt’s be jumping or intensely running, bobbing their head

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31
Q

Specifically in the hands, what can we see occur with RA?

A
  1. Ulnar drift of MCP’s
  2. Volar subluxation
  3. PiP swelling
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32
Q

Swan neck or Boutonniere deformity of fingers? PiP hyperextension and DiP flexion

A

Swan neck

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33
Q

Swan neck or Boutonniere deformity? DiP extension and PiP flexion

A

Boutonniere

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34
Q

How does mallet finger occur of the DiP joint occur?

A

The extensor digitorum tendon ruptures, pulling DiP into flexion

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35
Q

Rheumatoid nodules are present in what % of people with RA?

A

20-25%

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36
Q

What is the term for inflammation of lining of the sheath surrounding a tendon that can be found in a pt with RA?

A

Tenosynovitis

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37
Q

T or F?
Muscle atrophy doesn’t happen until later after diagnosis and is mostly in the knees and feet?

A

FALSE - muscle atrophy around affected joints can be present early and mostly in the intrinsic hand muscles and quads

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38
Q

Can pts with RA have a lot of de-conditioning that results in decreased cardiorespiratory status, muscle strength, and flexibility?

A

YES

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39
Q

When it comes to cardiopulmonary complications of pts with RA, what has greatest prevalence?

A

Ishemic heart disease (accelerated atherosclerosis)

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40
Q

What is first evaluated when trying to diagnose?

A

Causes of the arthritic sx’s. Rule out and test for things like lupus, cancer, scleroderma, hormone disorders, Sjorgen’s syndrome, etc

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41
Q

Can diagnosis of RA be based on family history, physical exam, and lab tests? What labs tests are done?

A

YES! RF is tested, CBC, ESR (which will be +), synovial fluid analysis, and serum protein electrophoresis

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42
Q

What is the prognosis of RA?

A

It is really poor because there is no way to reverse it. The damage cannot be undone, so the goal of treatment is to prevent further damage and manage the RA

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43
Q

What is our role in treating pt’s with RA?

A
  • Joint function and muscle strength is priority!!!
  • Low impact aerobic (conserve energy)
  • Aquatic therapy (takes off stress of gravity on joints)
  • Heat or ice packs and massage
  • Assisting pt with maintaining strength, tone, and fitness
  • Stretching, flexibility exercises, and strength training
  • Minimize stiffness and swelling
  • EDUCATE THEM!!
  • Manage flare-ups
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44
Q

What 2 things are used for pain management of RA?

A

Anti-inflammatory meds and analgesics (pain-killers)

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45
Q

What are used in the short term for acute attacks of RA?

A

Corticosteroid

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46
Q

Penicillimine is a drug in what class of treating RA?

A

Anti-rheumatic drugs

47
Q

When treating an RA pt, do you want to conserve their energy and protect their joints with things like splints if needed?

A

yes

48
Q

Do some RA pts get to a point where joint replacements surgically are needed to improve quality of life?

A

Yes

49
Q

Between Stage 1-4 of RA, which is characterized by maybe having radiographic evidence of osteoporosis and no destructive changes on an X-ray?

A

Stage 1, early

50
Q

Between Stage 1-4 of RA, which is characterized by having radiographic evidence of osteoporosis, with or without subchondral bone destruction and slight cartilage destruction, no joint deformities and possibly limited ROM, adjacent muscle atrophy, and extra-articular soft tissue lesions like nodules and tenosynovitis?

A

Stage 2, moderate

51
Q

Between Stage 1-4 of RA, which is characterized by having radiographic evidence of cartilage and bone destruction and osteoporosis, joint deformity, extensive muscle atrophy, and extra-articular soft tissue lesions, nodules, and tenosynovitis?

A

Stage 3, severe

52
Q

Between stage 1-4 of RA, which is characterized by having radiographic evidence of cartilage and bone destruction and osteoporosis, joint deformity, extensive muscle atrophy, extra-articular soft tissue lesions, nodules, and tenosynovitis, and fibrous or bony ankylosis?

A

Stage 4, terminal

53
Q

T or F? OA is also known as degenerative joint disease and is joints wearing out from use

A

True

54
Q

Is osteoarthritis the leading cause of disability in the US?

A

Yes

55
Q

Zooming in on joints wearing out, what specifically is degenerating make the surface more rough than normal?

A

The articular cartilage is the primary change - it is degenerating and is more rough than normal (with this, bone spurs can occur)

56
Q

What are some triggers of OA?

A
  • Tissue damage from injuries
  • Transmission of inflammatory mediators from the synovium into cartilage
  • Defects in cartilage metabolism
57
Q

T or F? Eventually with OA, there is subchondral sclerois with bone spurs on the edges of the joint, then synovial inflammation and thickening. Contractures and tendinitis can develop

A

True

58
Q

With OA, can the surrounding muscles of a joint and menisci of the knee be weakened and damaged?

A

Yes

59
Q

T or F? Articular cartilage has nerves and blood vessels and lymphatic vessels

A

False - in articular cartilage there are no nerves, blood vessels, or lymphatic vessels

60
Q

How does articular cartilage receive nutrition and eliminate waste?

A

Diffusion through synovial fluid and by facilitated imbibition (absorption of fluid by a solid body)

61
Q

What is the first osteoarthritic change to occur when OA starts?

A

Increase in water content

62
Q

T or F? As articular cartilage is being destroyed, the joint space narrows and can be seen on x-rays

A

True

63
Q

What is the first notable change in cartilage characterized by?

A

Mild fraying or “flaking” of superficial collagen fibers

64
Q

After the initial fraying and flaking of superficial collagen fibers of articular cartilage, what does it proceed to?

A

Deeper flaking or fibrillation occurs in greater areas of weight bearing

65
Q

T or F? The articular cartilage in a joint can degenerate to a point that the exposed subchondral bone can become necrotic

A

True

66
Q

T or F? Osteophytes may be fibrous, cartilaginous, or bony, and this process is very well understood

A

FALSE - the process is not well understood, but osteophytes CAN be fibrous, cartilaginous, or bony

67
Q

How many people in the US are believed to have OA?

A

20 million

68
Q

OA affects women __% of the time, and later in life than men

A

60% of the time

69
Q

_____ out of every _____ people have some form of OA

A

1 out of every 13 people have some form of OA

70
Q

By what age does 50% of the population have x-ray evidence of OA in at least 1 joint?

A

Buy age 65, 50% of the population has some x-ray evidence of OA in at least 1 joint

71
Q

T or F? OA is relatively common in adults in their 40s

A

True

72
Q

Can osteoarthritis affect younger people who have had bad joint injuries?

A

Yes

73
Q

Is OA the most common form of arthritis?

A

Yes

74
Q

What is the etiology of OA?

A

It has an unknown origin - it depends on the amount of wear and tear on joints and the severity

75
Q

What are some risk factors of OA?

A
  • Excessive wear or injury to joints
  • Family history
  • Female gender (higher onset)
  • Obesity
  • Increasing age
76
Q

T or F? Age it self causes OA and is considered normal with the aging process

A

FALSE - aging itself does not cause OA and should not be considered synonymous with “normal” aging processes

77
Q

T or F? Many OA related changes seen at the cellular and tissue level are opposite those seen with normal aging

A

True

78
Q

Genetic factors account for ___%-___% of radiographic OA at the hand, hip and knee and as much as ____% at the spine

A

Genetic factors account for 39% - 65% of radiographic OA at the hand, hip and knee and as much as 70% at the spine

79
Q

Repetitive microtrauma involved with kneeling and heavy lifting are relating to development of OA at the ____

A

Knees

80
Q

What 2 things are associated with greater prevalence of knee and hip OA with varus being the strongest predictor of disease progression

A

Malalignment (varus and valgus)and LLD (leg length descrepancy)

81
Q

T or F? There can be femoroacetabular impingement (FAI) at the hip if OA develops there

A

True

82
Q

What joints does OA usually affect?

A

Weight bearing joints like hands, hips, knees, and spine (one of the main difference between RA and OA)

83
Q

Does OA affect MCP joints?

A

No - just DIP and PiP, which will appear crooked

84
Q

In hips and knees, where does the articular cartilage degeneration occur and what forms there? What might a pt need at this point to improve quality of life?

A

In hips and knees, articular cartilage degeneration occurs at the end of long bones and bone spurs will form, limiting movement. A pt at this stage might need a THA or TKA

85
Q

What are the most common signs and symptoms that lead to diagnosis of OA?

A

Pain and swelling, loss of ROM, and bony deformity

86
Q

Does OA have a bilateral, symmetrical presentation?

A

NOOO! Only RA does

87
Q

Is OA a systemic disease with systemic complaints?

A

No, only RA is

88
Q

T or F? OA affects the CMC, DiP, PiP, neck, lumbar spine, hips, knees and MTP of big toe

A

True

89
Q

What is common clinical finding in OA that is another word for a pop?

A

Crepitus - can progress from a painless grating feeling to a really painful, high pitched sound as a result of bone on bone

90
Q

T or F? Cartilage degeneration is the cause of pain

A

FALSE - Cartilage degeneration is NOT the cause of pain since it is aneural.

91
Q

In the hands and fingers, what does OA look like?

A

Reduced ROM, poor grip strength, bony nodes. Usually tender in the early stages and restricts fine skills later in the disease

92
Q

OA can also affect the CMC joint of the thumb leading to decreased function, what does that lead to?

A

Decreased gripping and grabbing function

93
Q

In the hips, how does OA present?

A

Sx’s are usually insidious at onset and can include a limp and decreased ROM

94
Q

With hip OA, how is the leg have a tendency to be situated as?

A

Flexed, ER, and abducted, with IR really painful and hard

95
Q

If you have decreased hip ROM because OA, what does this affect?

A

Slower walking speed, decreased stride length, poor balance leading to falls, and you’re having to use a lot more energy to walk

96
Q

In knees with OA, how does it present as in the early stages?

A

There is pain with weight bearing activities
Ex. climbing stairs or squatting

97
Q

With knee OA, does prolonged sitting cause pain and stiffness?

A

Yes

98
Q

Does knee OA more commonly affect the medial or lateral joint?

A

Medial joint - there is a higher weight bearing load placed on this compartment (results in pseudolaxity of the MCL, strengthening of the LCL, and gene varus)

99
Q

If there is patellofemoral compartment OA, what is the hallmark for this?

A

Anterior knee pain

100
Q

T or F? With knee OA, joint locking and buckling due to damage of menisci and ligaments can lead to increase falls.

A

True

101
Q

What is the most common site of OA in the feet?

A

MTP joint of big toe

102
Q

Can OA affect our walking?

A

YES! - It can disrupt forefoot involvement, leading to poor push off while walking and gives poor balance

103
Q

Can hammer toes occur in OA and how?

A

YES! Extensors become shortened and pull toe up

104
Q

What parts of the spine are most susceptible to OA?

A

Lower cervical and mid to lower lumbar

105
Q

What is the only true synovial joint in the spine?

A

Facet joints

106
Q

What positions give relief to someone with OA?

A

Lying and spinal flexion

107
Q

Can the facet joints of the spine have bone spurs?

A

Yes - this contributes to lateral and central lumber stenosis and thus nerve impingement

108
Q

Pain is increased in what motions with a pt who has spine OA?

A

Extension, rotations, and when standing or sitting

109
Q

What ways is OA diagnosed

A

X-ray, physical exam, pt history

110
Q

What is typically shown on an x-ray of someone with OA

A

Narrowing of joint spaces, bone spurs, cyst formation, and subchondral sclerosis

111
Q

What two ways can OA be diagnosed?

A
  1. Primary - idiopathic/no known prior event
    A. localized - one or two joints affected
    B. generalized - 3+ joints affected
  2. Secondary - etiology can be identified
    A. Trauma
    B. Biomechanics factors
    C. Congenital malformation
    D. Other musculoskeletal disease
112
Q

What is treatment for OA?

A

-Non weight bearing exercise like biking or swimming
- Rest
- Heat (only when sx’s are not flared)
- Meds - analgesics and anti-inflammatories
- If severe: steroid injections into joint capsules
- Joint replacement: hips, knees, shoulders
- Arthroscopic procedure preceding these d/t bone spurs and torn cartilage

113
Q

What are some things the PTA can assist the pt with?

A

General fitness, low impact aerobics,
cardiovascular exercise, strengthening, and ROM exercise

114
Q

What is the prognosis of OA?

A

It varies: sx’s can start and go away randomly. Most pts can maintain daily functions unless hips or spine are severely involved

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