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NURS 350 > Exam 3 - alterations in musculoskeletal system > Flashcards

Exam 3 - alterations in musculoskeletal system Flashcards

1
Q

What kind of bone cells enable bone growth, repair, and change in shape?

A

bone cells

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2
Q

What is the act called where bone cells continually synthesize new bone tissue and dissolve old tissue?

A

remodeling

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3
Q

define osteoblasts; where do they come from?

A

bone-forming cells; from mesenchymal stem cells

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4
Q

define osteoclasts; what do they contain?

A

bone-reabsorbing; contain lysosomes with hydrolytic enzymes

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5
Q

define osteocytes; what osteocytes come from?

A

mature cells; once osteoblasts are finished with bone-forming, they become “imprisoned” in mineralized matrix and transform to osteocytes

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6
Q

What are 2 types of bone tissue?

A
  1. compact

2. spongy

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7
Q

What is compact bone tissue also called?

A

cortical

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8
Q

What is spongy bone tissue also called?

A

cancellous, trabecular

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9
Q

What is a break in the continuity of bone?

A

fracture

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10
Q

What is a complete fracture?

A

bone broken all the way through

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11
Q

What is an incomplete fracture?

A

damaged, but in 1 piece

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12
Q

what is an open or compound fracture?

A

skin broken

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13
Q

what is a closed fracture?

A

skin intact

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14
Q

What is a comminuted fracture?

A

when it is broken in 2 or more fragments

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15
Q

What is a linear fracture?

A

when the fracture is parallel to long axis of bones

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16
Q

What is oblique fracture?

A

when the fracture is at a 45 degree angle to bone shaft

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17
Q

What is a spiral fracture?

A

When the fracture encircles bone

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18
Q

What is a transverse fracture?

A

When the fracture is straight across bone

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19
Q

What kind of bones do children have?

A

flexible, growing bones

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20
Q

What are 3 types of incomplete fractures that occur in children?

A
  1. greenstick
  2. torus
  3. bowing
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21
Q

What is an incomplete fracture that perforates cortex and splinters spongy bone?

A

greenstick

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22
Q

What is an incomplete fracture that is characterized by the cortex buckling, but it does not break?

A

torus

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23
Q

What is an incomplete fracture that occurs from longitudinal force being applied to the bone? Hint: it involves paired radius-ulna or fibula-tibia with a complete fracture in one, while the other bends

A

bowing

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24
Q

What is a pathologic fracture?

A

break at a pre-existing abnormality by a force that would not normally cause the bone to break

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25
Q

What are pathologic fractures associated with?

A

tumors, osteoporosis, infections, and metabolic bone disorders

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26
Q

When do stress fractures occur?

A

occurs in bone that is repeatedly subjected to stress

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27
Q

When are stress fractures seen most? (2 things)

A
  1. seen in athletes

2. seen in bones without normal ability to deform and recover

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28
Q

What are fractures seen in athletes?

A

fatigue fracture

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29
Q

What are fractures seen in bones without normal ability to deform and recover?

A

insufficiency fracture

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30
Q

What is the healing process like after bone breakage?

A
  1. Bleeding occurs in the broken ends and a hematoma forms
  2. Hematoma organizes into a fibrous network
  3. Invasion by osteoblasts, lengthening of collagen strands, and calcium deposition
  4. A callus forms - new bone is built up as dead bone destroyed by osteoclasts
  5. Remodeling occurs - excess callus resorbed and trabecular bone laid down
  6. New bone tissue, not scar tissue, is formed during healing
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31
Q

What is rapid breakdown of muscle causing the release of intracellular components, including myoglobin into the extracellular space and bloodstream:

A

Rhabdomyolysis (Myoglobinuria)

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32
Q

What can rhabdomyolysis be a life-threatening complication of?

A

severe muscle trauma

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33
Q

What can rhabdomyolysis result in?

A
  1. hyperkalemia
  2. cardiac arrhythmia
  3. acute renal failure
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34
Q

what are the 3 manifestations of rhabdomyolysis?

A
  1. muscle pain
  2. weakness
  3. dark urine
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35
Q

what is excess myoglobin (an intracellular muscle protein) occurs in the urine due to muscle damage?

A

myoglobinuria

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36
Q

What is the most severe form of myoglobinuria?

A

crush syndrome

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37
Q

What is a less severe form of myoglobinuria?

A

compartment syndrome

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38
Q

What is a most recent problem involving myoglobinuria?

A

complication from cholesterol-lowering statins

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39
Q

what is myoglobinuria found after?

A

Found after viral infections, tetanus, heat stroke, strychnine poisoning, and fractures, excessive muscle activity in long distance runners, military recruits and after fraternity hazing

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40
Q

What is severe and fatal myoglibinuria associated with?

A

status epileptics and high-voltage shock

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41
Q

If myoglobinuria is caused by malignant hyperthermia, what can it lead to?

A

the severe muscle spasm and rhabdomyolysis can lead to RENAL FAILURE

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42
Q

What can myoglobinuria lead to?

A

Can lead to cerebral edema, pulmonary edema, DIC, and hypovolemic shock

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43
Q

What are 3 metabolic bone diseases?

A
  1. osteoporosis
  2. osteomalacia
  3. paget disease
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44
Q

What is 1 infectious bone disease

A

osteomyelitis

45
Q

What occurs in osteoporosis with old bone and new bone?

A
  1. old bone is resorbed faster than new bone is made

2. spongy bone exceeds loss of compact bone

46
Q

What is the most common metabolic disease and medical problem for older women?

A

osteoporosis

47
Q

What are potential causes of osteoporosis?

A
  1. Endocrine dysfunction (PTH, cortisol, TH, GH)
  2. Medications
  3. Vitamin D deficiency
  4. Underlying causes
  5. Low physical activity
  6. Abnormal BMI
48
Q

What is a major complication of osteoporosis?

A

fracture

49
Q

In pre-menopausal women, what is high? what does this inhibit?

A

estrogen; inhibits bone resorption

50
Q

Post-menopausal osteoporosis is most likely due to what?

A

estrogen deficiency and secondary causes

51
Q

What is RANKL?

A

cytokine receptor activator of nuclear factor kappa B ligand

52
Q

What is RANK?

A

receptor of RANKLY

53
Q

What is OPG?

A

decoy receptor of RANKL

54
Q

What is the patho of osteoporosis?

A
  1. RANKL, a member of TNF family, is expressed by osteoblasts and their precursors, and is needed for osteoclast development
  2. RANKL activates RANK, which is on osteoclasts and their precursors, to suppress apoptosis and increase survival/activation of osteoclasts
    - -> Increases bone resorption and bone loss
  3. OPG blocks RANKL by acting as a decoy
  4. Cytokines and hormones regulate RANKL and OPG balance
  5. Dysregulation leads to osteoporosis and other problems
55
Q

What increases RANKL expression?

A
  1. IL-1, 11, 17
  2. TNF alpha
  3. PTH
  4. glucorticoids
56
Q

What decreases RANKL expression?

A
  1. IL-4 and TGF beta

2. estradiol

57
Q

What increases OPG production?

A
  1. IL-1, -13, and –18
  2. TNF alpha and TGF beta
  3. Estradiol
  4. Leptin
  5. Mechanical strain
58
Q

What decreases OPG production?

A
  1. PTH and glucocorticoids

2. others

59
Q

What is inadequate or delayed mineralization of bone?

A

osteomalacia

60
Q

What proceeds normally in osteomalacia, and what does not occur?

A
  1. remodeling cycle occurs normally

2. calcification does not occur

61
Q

What is replaced bone like with osteomalacia?

A

soft instead of rigid

62
Q

What does osteomalacia result from?

A

lack of vitamin D

63
Q

True or false: osteomalacia is not like rickets

A

false; it is similar to rickets

64
Q

What is the major difference between osteomalacia?

A
  1. rickets occurs in growing bones of children

2. osteomalacia occurs in adults

65
Q

What is the patho of osteomalacia?

A
  1. Lack of vitamin D causes calcium ion concentration to fall
  2. Low calcium stimulates PTH to raise calcium, but phosphate is lost in urine
  3. When phosphate falls below a certain level, proper mineralization does not occur
66
Q

What is a state of increased metabolic activity of bone?

A

paget disease

67
Q

What does the excessive remodeling of bone in paget disease lead to?

A

leads to soft and enlarged bones

68
Q

What is paget disease a chronic acceleration of and deposition of?

A
  1. accelerated remodeling of spongy bone

2. deposition of disorganized bone

69
Q

Does paget disease have symptoms?

A

no, it is often symptomless

70
Q

What are 3 reasons why osteomyelitis is hard to treat?

A
  1. Bone has many small channels that are impermeable to cells and biochemicals of the defense system
  2. Capillaries of bone are sensitive to bacterial toxins–easily damaged; small clots lead to bone necrosis
  3. Bone cells have a limited capacity to replace bone destroyed by infections
71
Q

What are 3 inflammatory joint disorders?

A
  1. rheumatoid arthritis
  2. ankylosing spondylitis
  3. gout
72
Q

What is the most common joint disease?

A

osteoarthritis

73
Q

What is there loss and damage of with osteoarthritis?

A

articular cartilage in synovial joints

74
Q

What are 3 key features of osteoarthritis?

A
  1. inflammation
  2. mild synovitis
  3. thickening of joint capsule
75
Q

What is the secondary form of OA associated with?

A

associated with known risk factors

76
Q

What is the idiopathic form of OA associated with?

A

associated with age

77
Q

What are 4 risk factors for OA?

A
  1. increased age
  2. joint trauma
  3. long-term mechanical stress
  4. obesity
78
Q

What are the symptoms of OA?

A
  1. Pain (worsens with activity)
  2. Stiffness (diminishes with activity)
  3. Enlargement of the joint
  4. Tenderness, limited motion, muscle wasting
  5. Partial dislocation, deformity
79
Q

a. What loses its glistening appearance in OA?

b. What does bone become (hint: dense and hard)

A

a. cartilage

b. sclerotic

80
Q

What is the patho of OA?

A
  1. Cysts can develop in underlying bone and communicate with fissures in cartilage
  2. Pressure build-up in the cysts causes rupture
    - -> Cyst contents spill into synovial cavity
  3. Cartilage-coated bone cells grow outward and form spur-like projections
  4. Spurs break off and fall into synovial cavity
  5. Broken spurs irritate the synovial membrane
81
Q

What is an inflammatory autoimmune joint disease?

A

rheumatic arthritis

82
Q

What is RA systemic automminue damage to?

A

connective tissue, primarily in the joints (synovial membrane)

83
Q

What are the systemic symptoms of RA?

A
  1. Inflammation
  2. fever
  3. fatigue
  4. weakness
  5. anorexia
  6. weight loss
  7. generalized aching and stiffness
84
Q

What does RA result in? (hint: 3 things)

A
  1. joint pain
  2. deformity
  3. loss of function
85
Q

What is the cause of RA?

A

unknown

86
Q

What are 3 different patho processes involved in RA?

A
  1. Neutrophils and other cells in the synovial fluid become activated
  2. Inflammatory cytokines:
    - -> Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), interleukin-7 (IL-7), interleukin-21 (IL-21), induce enzymatic breakdown of cartilage and bone
  3. T cells also interact with synovial fibroblasts through TNF-α, converting synovium into a thick, abnormal layer of granulation tissue (pannus)
87
Q

What are physical symptoms of RA?

A

painful, tender, stiff joints

88
Q

What is a treatment option for RA?

A

DMARDS such as methotrexate

89
Q

What is a chronic inflammatory joint disease of the spine or sacroiliac joints causing stiffness and fusion of the joints?

A

ankylosing spondylitis

90
Q

What causes AS?

A

cause is unknown, but strong association with HLA-B27 antigen

91
Q

What is the PATHO of AS?

A
  1. Begins with the inflammation of fibrocartilage, mainly in vertebrae and sacroiliac joint
  2. Inflammatory cells infiltrate and erode fibrocartilage
  3. As repair begins, scar tissue ossifies and calcifies causing the joint to eventually fuse
92
Q

What are some manifestations of AS?

A
  1. low back pain in 20s; stiffness, pain, restricted motion
  2. loss of lumbar curvature (lordosis)
  3. increased concavity of upper spine (kyphosis)
93
Q

How does AS differ from RA?

A

RA - synovial membranes are involved at the site; AS - enthesis is the main site involved.

94
Q

How does the end result of AS differ from the end result of RA?

A

RA - end result is destruction and instability of synovial joints.
AS - end result is ossification and fusion of the joint

95
Q

What are 2 treatments for AS?

A
  1. physical therapy

2. NSAIDS

96
Q

What is a syndrome caused by either overproduction or under excretion of uric acid?

A

gout

97
Q

When uric acid crystals occur in synovial fluid, the inflammation is called what?

A

gouty arthritis

98
Q

What are risk factors of gout?

A
  1. male sex
  2. increasing age
  3. high intake of alcohol, red meat, and fructose
  4. drugs
99
Q

What are 5 manifestations of gout?

A
  1. Increase in serum urate concentration (hyperuricemia)
  2. Recurrent attacks of inflammation of a single joint
  3. Deposits of tophi in and around joints
  4. Renal disease
  5. Formation of renal stones
100
Q

What is gout linked to?

A

purine metabolism and renal function

101
Q

What is the breakdown product of purine nucleotides?

A

uric acid

102
Q

This with gout have sluggish what?

A

uric acid excretion

103
Q

What are manifestations of acute gouty arthritis?

A
  1. severe pain, especially at night

2. hot, red, tender joint pain

104
Q

What are signs of systemic inflammation with acute gouty arthritis?

A
  1. increased sedimentation rate
  2. fever
  3. leukocytosis
105
Q

What is chronic widespread diffuse join pain, fatigue, and tender joints?

A

fibromyalgia

106
Q

What are these symptoms characteristic of:
Increased sensitivity to touch
Absence of inflammation
Fatigue
Sleep disturbances/non-restorative sleep
Anxiety and depression
~80-90% of individuals affected are women (peak age 30-50)
Inflammation may play a role (autoimmune disorders often coexist)
Genetic factors
CNS dysfunction

A

fibromyalgia

107
Q

What is 1 neuroimmunoendocrine disease?

A

chronic fatigue syndrome

108
Q

What is chronic fatigue syndrome characterized by (4 things)?

A
  1. Cognitive impairment
  2. Severe postexertional fatigue
  3. Unrefreshing sleep
  4. Decreased physical activity that affects daily functioning
109
Q

What is involved with chronic fatigue syndrome?

A

psychologic and physiologic involvement

NURS 350 (6 decks)

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