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NUR 326 Exam 4 > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

1
Q

components affecting gender and bone mass

A

–women have greater bone loss in early postmenopausal years
–women have lower peak density (reach fracture threshold earlier than men)
–men lose about a third less bone mass compared to women over a life time
–bone reabsorbed by osteoclasts > bone formed by osteoblasts (by age 30)

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2
Q

osteoporosis

A

bone mineral density 2.5 standard deviations below peak bone mass

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3
Q

how is osteoporosis measured?

A

DEXA scan (results in a T-score)

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4
Q

T-score for normal bone density

A

-1 or greater

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5
Q

T-score for osteopenia

A

between -1 and -2.5

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6
Q

T-score for osteoporosis

A

less than or equal to -2.5

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7
Q

T-score for severe osteoporosis

A

less than -2.5

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8
Q

osteopenia

A

low bone mass
–thinning of the trabecular matrix of the bone before osteoporosis

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9
Q

osteoporosis

A

“pourous bone”
–characterized by low bone density and structural deterioration of the bone
–when actual breaks in the trabecular matrix have occurred

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10
Q

severe osteoporosis

A

osteoporosis with a history of a fragility fracture

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11
Q

bones susceptible to osteoporosis

A

hips, vertebrae, and wrists

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12
Q

osteoporosis characteristics

A

–low bone mass
–micro-architectural deterioration
–increase in bone fragility
–susceptibility to fracture = high

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13
Q

major risk factors for osteoporosis

A

–increased age
–female
–caucasian
–history of fractures as adult
–family history
–body weight < 127 pounds
–smoking
–alcohol use
–steroid and immunosuppressant use

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14
Q

minor risk factors for osteoporosis

A

–thin, small frame
–lack of weight bearing exercises
–lack of calcium and/or vitamin D
–eating disorders
–gastric bypass
–lack of estrogen/testosterone
–excessive caffeine consumption

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15
Q

patho of osteoporosis

A

–increased bone resorption (increased osteoclast activity)
–decreased bone formation (decreased osteoblast activity)
–problems making new bone
–problems with too much bone resorption

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16
Q

early clinical manifestations of osteoporosis

A

none

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17
Q

late clinical manifestations of osteoporosis

A

–fractures
–pain
–loss of height
–stooped posture (kyphosis)

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18
Q

hip fractures

A

–linked to increased risk of mortality
–more common in those greater than 65
–more common in women
–most common location: proximal third of the femur

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19
Q

clinical presentation of hip fractures

A

–sudden onset of hip pain before or after a fall
–inability to walk
–severe groin pain
–tenderness
–affected leg is externally rotated and shortened

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20
Q

goal of osteoporosis pharm

A

reduce fractures

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21
Q

primary prevention of osteoporosis fractures

A

–calcium
–vitamin D

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22
Q

treatment for osteoporosis

A

–promote bone formation
–decrease bone resorption

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23
Q

example of biphosphates

A

aldendronate (Fosamax)

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24
Q

MOA of aldendronate

A

binds permanently to surfaces of bones to inhibit osteoclast activity

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25
Q

adverse effects of aldendronate

A

–GI (N/V/D)
–esophageal ulcerations

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26
Q

teaching points for aldendronate

A

–take with small amount of water
–don’t lie down for 30 minutes after taking
–do not take with food, other drinks, calcium, or vitamins for 2 hours (very low bioavailability)

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27
Q

example of selective estrogen receptor modulators (SERMs)

A

Raloxifene (Evista)

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28
Q

MOA of raloxifene

A

–mimics estrogen by increasing bone density
–inhibits bone resorption

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29
Q

use of raloxifene

A

–used as prevention and treatment
–reduces risk of spinal fracture by 50%

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30
Q

adverse effects of raloxifene

A

–hot flashes
–leg cramping

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31
Q

black box warning for raloxifene

A

stroke risk

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32
Q

teaching points for SERMs

A

–must take adequate calcium and vitamin D replacement to work
–d/c at least 72 hours before planned procedures, any prolonged immobilization periods (high risk of clots)
–do not smoke or drink alcohol
–do not use if pregnant

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33
Q

calcitonin-salmon (Miacalcin) MOA

A

inhibits bone marrow removal by osteoclasts
–slows down bone loss and increases spinal bone density

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34
Q

use of calcitonin-salmon

A

–treatment only
–not long-term
–reduces spinal fractures by 30%
–can reduce pain in someone with hip fractures

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35
Q

route for calcitonin-salmon

A

intranasal (nasal irritation)

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36
Q

fractures

A

any break in the continuity of bone that occurs when more stress is placed on the bone that it is able to absorb

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37
Q

causes of fractures

A

–traumatic fall
–fatigue (repeated, prolonged stress)
–pathologic (weakened bone, possibly spontaneous)

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38
Q

open (compound) fracture

A

fractured bone penetrates skin

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39
Q

closed (simple) fracture

A

does not break through the skin

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40
Q

transverse fracture

A

horizontal break across bone

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41
Q

spiral fracture

A

–fracture from twisting
–break at an angle

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42
Q

comminuted fracture

A

more than one fracture line and more than 2 bone fragments

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43
Q

impacted fracture

A

from heights

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44
Q

greenstick fracture

A

children; bone bending

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45
Q

clinical manifestations of fractures

A

Pain
Edema
Deformity

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46
Q

purpose of edema in fractures

A

natural splint

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47
Q

components of deformity

A

–loss of function
–abnormal mobility

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48
Q

complications of fractures

A

–delayed healing
–bone growth impairment
–compartment syndrome
–fat embolism syndrome

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49
Q

components of delayed healing

A

–delayed union
–malunion
–nonunion

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50
Q

delayed union

A

bone pain and tenderness increase

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51
Q

risk factors for delayed union

A

–tobacco
–increased age
–severe anemia
–uncontrolled DM
–decreased vitamin D
–hypothyroidism
–poor nutrition

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52
Q

malunion

A

improper alignment

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53
Q

nonunion

A

–no healing 4-6 months post-fracture
–causes: poor blood supply, repetitive stress, DM, infection

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54
Q

when do delayed healing complications occur?

A

3 months - 1 year after fracture

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55
Q

impaired bone growth

A

–pediatric consideration
–fracture through epiphyseal plate
–can delay future bone growth

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56
Q

what is compartment syndrome seen with?

A

–crush injuries
–cast

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57
Q

what does compartment syndrome result from?

A

increased pressure within limited anatomical space

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58
Q

tourniquet effect

A

–edema at fracture site puts intense pressure on soft tissue
–can lead to tissue hypoxia of muscles and nerves

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59
Q

manifestations of compartment syndrome

A

–edema
–loss or weakened pulses
–PAIN

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60
Q

treatment for compartment syndrome

A

fasciotomy

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61
Q

fat embolism syndrome

A

fat molecules in the lung following:
–long bone fracture
–major trauma

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62
Q

how do fat emboli get into the lungs?

A

–fat molecules from bone marrow or traumatized tissue
–released into blood stream –> lungs

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63
Q

symptoms of fat emboli

A

–hypoxemia
–altered LOC
–petechial rash (last symptom to occur)

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64
Q

treatment for fat emboli

A

supportive

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65
Q

osteomyelitis

A

an acute or chronic pyogenic infection of the bone

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66
Q

pyogenic

A

pus producing

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67
Q

cause of osteomyelitis

A

bacteria (staph aureus)

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68
Q

risk factors for osteomyelitis

A

–recent trauma
–diabetes
–hemodialysis
–IV drug use
–splenectomy

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69
Q

direct contamination (osteomyelitis)

A

open wound
–open fracture
–gunshot
–puncture
–surgery

surgery/insertion of meta plates or screws

70
Q

indirect contamination (osteomyelitis)

A

from bloodstream
–most common
–bacteremia

71
Q

patho of osteomyelitis

A

–pressure increases within bone
–causes local arteries to collapse
–decreases or eliminates supply of oxygen, nutrition, immune cells, and antibiotics
–leads to impaired healing

72
Q

local symptoms of osteomyelitis

A

–tenderness, warmth, redness
–wound drainage
–restricted movement
–spontaneous fracture

73
Q

systemic symptoms of osteomyelitis

A

–fever
–positive blood culture
–leukocytosis

74
Q

osteomyelitis pharm

A

–obtain culture
–empiric ABX therapy (nafcillin, cefazolin, vanc)
–bacteria-specific therapy

75
Q

arthropathy

A

a joint disorder
–when the disorder involves inflammation of one or more joints –> arthritis

76
Q

osteoarthritis (OA)

A

–degeneration of joints caused by aging and stress
–most common cause of disability in US
–obesity and longer life expectancy –> increase in OA

77
Q

common joints affected by OA

A

–cervical spine
–lumbosacral spine
–hip
–knee
–hands
–first metatarsal phalangeal joint (big toe)

spared = wrist, elbow, ankle

78
Q

risk factors of OA

A

–aging
–obesity
–history of participation in team sports
–history of trauma or overuse of joint
–heavy occupational work
–misalignment of pelvis, hip, knee, ankle, or foot

79
Q

etiology of OA

A

–stresses applied to joint
–degeneration of cartilage
–chronic disease

80
Q

OA patho

A

–prolonged excess pressure on joint wears away cartilage and subchondral bone exposed –> cyst development
–cysts move through remaining cartilage and destroys rest
–localized inflammation leads to more degradation
–chrondrocytes synthesize fluid called proteoglycans to try and repair –> swelling
–osteoblasts activation leads to bone spurs and synovial fluid thickening
–loss of cartilage narrows the joint space

81
Q

osteophytes

A

bone spurs caused by osteoblasts

82
Q

symptoms of OA

A

–deep, aching joint pain, esp. with exertion (relieved with rest)
–joint pain with cold weather
–stiffness in morning
–crepitus of joint during motion
–joint swelling
–altered gait
–limited ROM

83
Q

physical exam findings in OA

A

–joint deformity
–joint tenderness
–decreased ROM
–Herbeden’s nodes
–Bouchard’s nodes

84
Q

Herbeden’s nodes

A

distal interphalangeal joint

85
Q

Bouchard’s nodes

A

proximal interphalangeal joint (closer to hand)

86
Q

goals of treatment of OA

A

–manage pain
–maintain mobility
–minimize disability

87
Q

goal of OA pharm

A

manage pain and reduce swelling

88
Q

pharm for OA

A

–mild to moderate: NSAIDs, acetaminophen, topical capsaicin
–moderate to severe: NSAIDs (Rx strength), NSAIDs + colchicine, acetaminophen + tramadol, opioids, steroid injections

89
Q

NSAIDs MOA

A

reduce production of prostaglandins

90
Q

degenerative disc disease

A

–common cause of pain, motor weakness, and neuropathy
–most often occurs in lumbar or cervical spine

91
Q

patho of degenerative discs

A

–motor and sensory spinal nerves enter and exit from the spinal cord and travel through narrow openings of the vertebral bone
–intervertebral discs dehydrate and vertebral bone become compressed –> impinge on the entering and exiting nerves
–dysfunction of motor and sensory spinal nerves impedes movement and sensation in the extremities
–may see weakness and paresthesia

92
Q

lumbar s/s of DDD

A

–pain in lower back that radiates down the back of the leg (sciatica)
–pain in the buttocks or thighs
–pain that worsens when sitting, bending, lifting, or twisting
–pain that is minimized when walking, changing positions, or lying down
–numbness, tingling, or weakness in the leg
–foot drop

93
Q

cervical s/s of DDD

A

–chronic neck pain that can radiate to the shoulders and down the arms
–numbness or tingling in the arm or hand
–weakness of the arm or hand

94
Q

rheumatoid arthritis

A

–systemic, autoimmune
–type III hypersensitivity
–inflammatory disease of synovium

95
Q

etiology of RA

A

–not well understood
–environmental and genetic factor (genetic link + trigger event)

96
Q

risk factors for RA

A

–40-60s
–women
–tobacco use
–family history

97
Q

RA patho

A

–immune cells attack synovial tissue
–immune cells: lymphocytes and macrophages
–produce rheumatoid factor (RF) –> antibody against the body’s own antibodies (IgG)

98
Q

progression of RA

A

–cartilage destroyed by osteoclasts
–pannus develops

99
Q

pannus

A

inflammation and exuberant proliferation of synovium

100
Q

what does pannus lead to?

A

–bone erosion
–bone cysts
–fissure development

101
Q

what is pannus?

A

scar tissue

102
Q

early s/s of RA

A

–very little
–maybe joint discomfort

103
Q

eventual joint manifestations in RA

A

–symmetrical
–pain, stiffness, motion limitation
–inflammation: heat, swelling, tenderness

104
Q

advanced disease s/s of RA

A

–deformity and disability
–joint subluxation (misalignment)

105
Q

systemic involvement in RA

A

–fatigue and malaise
–Sjorgren’s syndrome
–rheumatoid nodules

106
Q

Sjorgren’s syndrome

A

destruction of moisture-producing gland (salivary and lacrimal)
–gritty, dry, itchy eyes
–fissured, dry tongue

107
Q

rheumatoid nodules

A

–immune mediated granulomas
–develop around inflamed joints
–subcutaneous and firm, sometimes painful

108
Q

goals of pharm for RA

A

–relieve pain and swelling
–slow or stop progression of disease
–long term drug therapy requires patient adherence (NSAIDs, glucocorticoids, DMARDs)

109
Q

corticosteroids in RA

A

–usually prednisone
–rapid suppression of inflammation
–use only when symptoms not controlled with NSAIDs
–not best choice for long term therapy

110
Q

classification of methotrexate

A

–antineoplastic
–anti-rheumatic

111
Q

MOA of methotrexate

A

immunosuppressive
–interferes with metabolism of folate

112
Q

route for methotrexate

A

PO or SQ/IV

113
Q

adverse effects of methotrexate

A

–GI (nausea, anorexia, vomiting)
–bone marrow suppression
–shortened life expectancy

114
Q

frequency for methotrexate

A

1x per week

115
Q

methotrexate teaching points

A

–pt needs folic acid supplementation
–no alcohol
–teratogenic
–higher risk of infection
–caution with liver and kidney disease
–aplastic anemia risk when using with NSAIDs
–monitor liver enzymes

116
Q

hydroxychloroquine (Plaquenil) classification

A

–antimalarial
–anti-rheumatic

117
Q

hydroxychloroquine (Plaquenil) MOA

A

unknown, anti-inflammatory processes

118
Q

hydroxychloroquine (Plaquenil) effects

A

slow progression of RA when used in combo with other DMARDs

119
Q

therapeutic uses of hydroxychloroquine (Plaquenil)

A

used alone or in combo with methotrexate for early/mild RA

120
Q

adverse effects of hydroxychloroquine (Plaquenil)

A

retinopathy

121
Q

biologic agents (DMARDs)

A

–target parts of the immune system that trigger inflammation that cause joint and tissue damage
–usually given in combo therapy with methotrexate
–can increase risk of severe skin or lung infections, skin cancers, serious allergic reactions
–very expensive

122
Q

gout

A

an inflammatory disease resulting from deposits of uric acid crystals in tissues and fluids within the body

123
Q

patho of gout

A

–uric acid crystal deposits in tissues (HYPERURICEMIA)
–overproduction of uric acid
–under excretion of uric acid

124
Q

what causes uric acid crystals to form?

A

from the breakdown of purines

125
Q

where are purines found?

A

–made in body
–found in food: organ meats, shellfish, anchovies, herring, asparagus, mushrooms

126
Q

where is uric acid normally excreted from?

A

the kidneys

127
Q

gout risk factors

A

–obesity
–HTN, DM, renal disease, sickle cell
–ETOH
–diet rich in meat and seafood
–use of diuretics
–most common in males
–African Americans

128
Q

phase 1 of gout

A

asymptomatic, but with elevated uric acid levels and deposits in tissues
–crystals accumulate and tissue is damaged
–tissue damage triggers acute inflammation

129
Q

phase 2 of gout

A

acute flares or attacks occur – hyperuricemia

130
Q

phase 3 of gout

A

clinically inactive until the next flare

131
Q

phase 4 of gout

A

chronic arthritis

132
Q

s/s of gout

A

–pain
–burning
–redness
–swelling and warmth
–fever
–symptoms present for days to weeks
–big toe is presenting joint for 50% of people with gout

133
Q

tophi

A

large hard nodules composed of uric acid crystals deposited in soft tissues
–may form below the skin around the joints
–can cause a local inflammatory response
–may drain chalky material

134
Q

gout complications

A

–tophi
–renal calculi

135
Q

goal of gout pharm

A

–decrease symptoms of an acute attack and prevent recurrent attacks
–NSAIDs are usually first line therapy

136
Q

allopurinol (Zyloprim) MOA

A

inhibits the xanthine oxidase enzyme, which prevents uric acid production

137
Q

indications for allopurinol

A

patients whose gout is related to EXCESS uric acid production
prevention medication

138
Q

adverse effects of allopurinol

A

–agranulocytosis
–aplastic anemia
–known to cause fatal skin reactions
–rash

139
Q

when do you see effects of allopurinol?

A

2-6 weeks

140
Q

drug interactions with allopurinol

A

anti-diabetes meds and warfarin
–hypoglycemia
–INR

141
Q

labs to monitor with allopurinol

A

–WBCs (infection)
–serum uric acid

142
Q

colchicine MOA

A

reduces inflammatory response to the deposits of urate crystals in joint tissues

143
Q

uses of colchicine

A

gout flares and prophylaxis

144
Q

colchicine specifics

A

–second line therapy
–powerful inhibitor of cell mitosis and can cause short-term leukopenia (bone marrow suppression)

145
Q

adverse effects of colchicine

A

GI bleeding and urinary bleeding

146
Q

contraindications of colchicine

A

any person with severe renal, GI, hepatic, or cardiac disorders, or bleeding disorders

147
Q

route for colchicine

A

only PO

148
Q

classification of probenecid (Benuryl)

A

uricosuric acid

149
Q

MOA of probenecid

A

inhibits reabsorption of uric acid in kidney, promoting excretion

150
Q

uses of probenecid

A

treats hyperuricemia with gout

151
Q

recommendations for probenecid

A

used alone or in combo with allopurinol when not effective alone

152
Q

adverse effects of probenecid

A

–GI upset
–dizziness or headache
–kidney/liver impairments
–lots of drug interactions

153
Q

teaching points for probenecid

A

–take with food and drink
report:
–kidney and liver issues
–weight gain
–hematuria
–change in UOP

154
Q

lupus patho

A

–B-lymphocytes are hyperactive and produce autoantibodies
–activated against DNA
–formation of immune complexes
–inflammatory response destroys tissue

155
Q

what organ is lupus common in?

A

kidneys

156
Q

ANA

A

antinuclear antibody

157
Q

risk factors for lupus

A

–genetics
–female
–20-40 years old
–Black/AA
–environmental triggers
–allergy to antibiotics
–hormonal factors
–tobacco

158
Q

s/s of lupus

A

–extreme fatigue
–photosensitivity
–butterfly rash
–fever
–weight changes
–unusual hair loss
–edema

159
Q

CNS lupus symptoms

A

–HA
–dizziness
–seizures
–stroke

160
Q

lupus symptoms in lungs

A

–pleuritis
–PEs

161
Q

lupus symptoms with heart

A

–myocarditis
–endocarditis

162
Q

lupus symptoms with kidneys

A

nephritis

163
Q

lupus symptoms with blood vessels

A

vasculitis

164
Q

lupus symptoms with blood

A

–anemia
–leukopenia
–thrombocytopenia
–blood clots

165
Q

lupus symptoms with joints

A

arthritis

166
Q

SLE flares

A

–acute exacerbation of symptoms
–warning signs:
fatigue
pain
headache

167
Q

prevention of SLE flares

A

avoid triggers:
–sunlight exposure
–infection
–abruptly stopping a med
–stress

168
Q

SLE pharm

A

–control symptoms
–NSAIDs (HA, musculo., pleuritis, pericarditis)
–high dose steroids (severe kidney dz, CNS)
–low dose steroids (arthritis)
–antimalarials (skin, musculo., prevention of kidney/CNS organ damage)
–immunosuppressives (severe organ involvement)

169
Q

similarities between RA and lupus

A

–autoimmune
–systemic inflammation
–multiple body system
–pharm

170
Q

differences between RA and lupus

A

–RA = focus on joints
–SLE = multisystem

NUR 326 Exam 4 (5 decks)

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