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NUR 326 > musculoskeletal > Flashcards

musculoskeletal Flashcards

1
Q

normal synovial (diarthrodial) joints

A

a synovial or diarthrodial joint is any joint that allows movement.

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2
Q

name the 4 major parts that the joint is made out of?

think A&P.

A

subchondral bone plate.
articular cartilage.
synovium.
joint capsule.

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3
Q

subchondral bone plate.

A

sub = under
chondral = cartilage
bone just underneath cartilage

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4
Q

articular cartilage.

A

covers bone of the joint. it provides a smooth slippery surface that allows free movement of joint.

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5
Q

synovium.

A

the space (synovial cavity) between 2 articulating bones.
there is a synovial membrane that is the inner lining of this cavity.
the synovial membrane secretes synovial fluid that lubricates joint surface and removes debris.

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6
Q

joint (articular) capsule.

A

surrounds joint.
unites articulating bones

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7
Q

3 phases of bone healing

A
  1. inflammatory
  2. reparative
  3. remodeling
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8
Q

what happens during the inflammatory phase

A

(1) hematoma forms at the fracture site (provides stability & aseptic inflammation occurs).
Duration: 1-3 days for hematoma; 3 days- 2 weeks for early repair

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9
Q

what happens during the reparative phase

A

fibrous cartilage (2)- formation of granular tissue containing blood vessels, fibroblasts, osteoblasts.
callous (3)- formation of callous. when granular tissue has matured.
ossification (4)- space in bone is bridged & fracture ends unite. callus replaced by trabecular bone.

duration: 6 weeks

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10
Q

what happens during the remodeling phase

A

remodeling (5): bone consolidation with final remodeling. Healing is complete.

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11
Q

when do women experience greater bone loss and at what rate does it continue?

A

women experience greater bone loss in early menopausal years & it continues at a gradual rate.

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12
Q

who has lower peak density, men or women?

A

women

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13
Q

who reaches “fracture threshold” earlier, men or women?

A

women

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14
Q

at around age 30: bone reabsorbed by osteoclast (< or >) bone formed by osteoblasts.

pick > or <.

A

>

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15
Q

factors that affect bone mass

A

age
gender
race
genetics
reproductive status
calcium levels
exercise

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16
Q

osteopenia

A

thinning of the trabecular matrix of the bone before osteoporosis.
t-score of -1 to -2.5

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17
Q

osteoporosis

A

bone mineral density 2.5 standard deviations below peak bone mass.
“porous bone”, common serious disease.
used when ACTUAL BREAKS in the trabecular matrix have occurred.

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18
Q

how is osteoporosis measured and how are results reported?

A

measured with DEXA scan.
reported in T-Score

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19
Q

osteoporosis is characterized by….

A

low density & structural deterioration of the bone

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20
Q

what bones do osteoporosis usually occur in?

A

the hips, vertebrae, & wrist (trabecular bones)

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21
Q

osteoporosis characteristics

A

low bone mass.
micro-architectural deterioration.
increase in bone fragility.
susceptibility to fracture is high.

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22
Q

MAJOR risk factors for osteoporosis

A

aging
female
Caucasian
hx of fracture as an adult
family hx/genetics
body wgt <127 lbs.
smoking
alcohol use
corticosteroid therapy & immunosuppressive drugs.

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23
Q

MINOR risk factors for osteoporosis

A

thin, small frame.
lack of wgt bearing exercise.
lack of calcium &/or vitamin D.
eating disorders
gastric bypass surgery.
lack of estrogen/testosterone
excessive caffeine consumption.

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24
Q

osteoporosis pathogenesis

A

increased bone resorption: osteoclast activity increased.
decreased bone formation: osteoblast activity decreased.

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25
Q

problems for osteoporosis can be….

A

failure to make new bone (osteoblasts).
too much bone resorption (osteoclasts).
both.

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26
Q

early clinical manifestations for osteoporosis

A

NONE

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27
Q

late clinical manifestations for osteoporosis

A

fractures
pain
loss of height
stooped posture (kyphosis)

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28
Q

complication of osteoporosis

A

hip fracture

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29
Q

True or false: osteoporotic hip fractures are linked to increased risk of morality

A

TRUE. death does not happen because of the fracture, death happens d/t complications & r/t immobility.

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30
Q

complications of a hip fracture

A

pneumonia, blood clots, sepsis, skin breakdown, immobility.

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31
Q

what age are hip fractures more common?

A

> 65

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32
Q

are hip fractures more common in men or women?

A

women

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33
Q

most common location of a hip fracture?

A

proximal third of the femur

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34
Q

hip fracture: clinical presentation

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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35
Q

goal of osteoporosis pharm

A

reduce fractures

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36
Q

primary prevention of osteoporosis

A

calcium - diet+supplement (elemental calcium) = 1200 to 2000mg daily
vitamin D- diet+ supplement= 800 to 1,000 IU daily.

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37
Q

treatment of osteoporosis help ……. & ………..

A

promote bone formation (increase osteoblast) & decrease bone resorption (decrease osteoclasts)

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38
Q

aldendronate

A

class: biphosphates
MOA: binds permanently to surfaces of bones to INHIBIT OSTEOCLAST ACTIVITY
Indication: osteoporosis, reduces fractures by 50%
SE: GI (N/V/D), esophageal ulcerations
teaching: take with water, DO NOT lie down for 30 minutes after taking, DO NOT take with food, other drinks, calcium, or vitamins for 2hrs (very low bioavailability)

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39
Q

raloxifene

A

class: selective estrogen receptor modulators (SERMs)
MOA: mimics estrogen by increasing bone density; INHIBITS BONE RESORPTION
INDICATION: prevention & treatment of osteoporosis; reduces risk of spinal fractures by 50%
SE: hot flashes, leg cramping
Black box warning: stroke risk
NC: must take adequate calcium and vitamin D; DC @ least 72hrs before planned procedures (any prolonged immobilization period, high risk of blood clotting); DO NOT smoke, drink alcohol, or use if pregnant.

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40
Q

calcitonin- salmon

A

class: hormone therapy
MOA: inhibits bone removal by osteoclasts. slows down bone loss & increases spinal bone density.
INDICATION: treatment only
SE: nasal irritation d/t intranasal route.
NC: reduces spinal fractures by 30%, must take for @ least 5yrs to see long term benefits.

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41
Q

define 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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42
Q

causes of fractures

A

traumatic- fall
fatigue- repeated, prolonged stress
pathologic- weakened bone, possibly spontaneous (high risk in elderly)

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43
Q

open (compound) fracture

A

fractured bone penetrates skin

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44
Q

closed (simple) fracture

A

does not break through the skin

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45
Q

transverse fractures

A

straight line.
90 degree angle to the length of the bone.
most common in traumatic falls

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46
Q

spiral fracture

A

twisting fracture

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47
Q

comminuted fracture

A

more than one fracture line & more than 2 fragments

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48
Q

impacted fracture

A

bone moves into each other
(ex. people who fall and land on their feet)

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49
Q

greenstick fracture

A

common in children
incomplete break
(think of a bone getting sliced but piece does not detach)

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50
Q

stress fracture

A

from repeated use or fatigue

51
Q

Clinical manifestations of fractures

A

the P.E.D
P = pain
E = edema (acts as natural splint)
D = deformity (loss of FUNCTION, abnormal MOBILITY).

52
Q

why are the 3 phases of bone healing important?

A

because a lot of the complications r/t fractures are r/t the healing process.

53
Q

name the 4 complications of fractures

A

delayed healing.
bone growth impairment
compartment syndrome
fat embolism syndrome

54
Q

complication Delayed healing

A

3 month to 1yr after fracture.
1. delayed union = bone pain & tenderness increase; RF: tobacco use, old age, severe anemia, uncontrolled DM, decreased vitamin D, hypothyroid, poor nutrition, infection, complicated breaks.
2. malunion = improper alignment
3. nonunion = no healing 4-6 months post-fracture; causes: poor blood supply, repetitive stress

55
Q

complication: impaired bone growth

A

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

56
Q

complication: compartment syndrome

A

seen with: crush injuries, cast
results from increased pressure within limited anatomic space.
“tourniquet effect”
manifestations: edema, loss/weakened pulse, PAIN

57
Q

what is the “tourniquet effect” in relation to compartment syndrome?

A

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

58
Q

complication: fat embolism syndrome: what is it?

A

fat molecules in lung following LONG BONE FRACTURE or major trauma

59
Q

complication: fat embolism syndrome: how do they get there?

A

fat molecules from bone marrow or traumatized tissue release into the blood stream and go into the lungs.

60
Q

complication: fat embolism syndrome
MANIFESTATIONS

A

hypoxemia, altered LOC or completely decreased LOC, petechial rash.

61
Q

osteomyelitis: definition

A

an acute or chronic pyogenic infection of bone

62
Q

osteomyelitis: cause

A

bacteria (staph aureus)

63
Q

osteomyelitis: risk factors

A

recent trauma
DM
HD
IVDU
splenectomy

64
Q

osteomyelitis: pathogenesis

A

pressure increases within the bone and causes local arteries to collapse.
decreases or eliminates supply of: oxygen, nutrition, immune cells, ANTIBIOTICS.
leads to impaired healing therefore difficult to treat.

65
Q

osteomyelitis: clinical manifestations (local & systemic)

A

local: tender, warm, red, wound drainage, restricted movement, spontaneous fracture
systemic: fever, positive blood culture, leukocytosis.

66
Q

osteomyelitis: pharm

A

obtain culture.
empiric abx therapy: nafcillin, cefazolin, vancomycin
bacteria specific therapy

67
Q

which joint do most disorder affect?

A

synovial joints

68
Q

Arthropathy

A

a joint disorder.

69
Q

Arthritis

A

inflammation of one or more joints

70
Q

route of contamination: direct

A

open wound: open fracture, gunshot, puncture (stabbing), surgery (sternotomy)
surgery/insertion of metal plates or screws

71
Q

route of contamination: indirects

A

from bloodstream (most common)
bacteremia

72
Q

osteoarthritis (OA): definition

A

degeneration of joints caused by aging & stress

73
Q

osteoarthritis (OA): common joint affected

A

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

74
Q

osteoarthritis (OA): spared joints

A

wrists, elbow, ankles

75
Q

osteoarthritis (OA): risk factors

A

aging >40
obesity
hx of participation in team sports (prolonged)
hx of trauma or overuse of joint
heavy occupational work
misalignment of pelvis, hip, knee, ankle, or foot

76
Q

osteoarthritis (OA): etiology

A

stresses applied to joint (wgt bearing)
degeneration of cartilage (excessive loading of healthy joint, normal loading of previously injured joint)
chronic disease.

77
Q

osteoarthritis (OA): pathophysiology

A

prolonged excess pressure on joint wears away cartilage & subchondral bone exposed that leads to cyst development.
cysts move through remaining cartilage & destroys the rest.
localized inflammation leads to more degradation.
chondrocytes synthesize fluid called proteoglycans to try & repair causing swelling.
osteoblast activation leads to bone spurs & synovial fluid thickening = less movement.
loss of cartilage narrows joints space.

78
Q

osteoarthritis (OA): clinical manifestations

A

Deep, aching joint pain, especially with exertion & Relieved with rest.
Joint pain with cold weather
Stiffness in morning
Crepitus of joint during motion
Joint swelling
Altered gait
Limited ROM

79
Q

osteoarthritis (OA): physical exam

A

joint tenderness
joint deformity
decreased ROM
fingers often involved: Herbeden’s nodes, Bouchard’s nodes

80
Q

Herbeden’s nodes

A

distal interphalangeal joint

81
Q

Bouchard’s nodes

A

proximal interphalangeal joint

82
Q

treatment goals for OA

A

Manage pain
Maintain mobility
Minimize disability

83
Q

goal of pharmacotherapy

A

manage pain and reduce swelling

84
Q

mild to moderate treatment for OA

A

acetaminophen, topical capsaicin, NSAIDS (OTC)

85
Q

moderate to severe treatment of OA

A

NSAIDS (Rx strength), NSAIDS + colchicine, acetaminophen + tramadol, opioids, steroid injections (into joint)

86
Q

NSAIDS

A

Use lowest effective dose possible
Can affect kidney function
Risk for GI bleed: risk increases dramatically with aging, Contraindicated for patients with PUD, Use with caution in those with history of GI bleeds or on anticoagulation therapy

87
Q

other treatments for OA

A

Dietary supplements: Chondroitin sulfate and glucosamine
Artificial joint fluid– contains hyaluronic acid
Joint replacement, arthroplasty

88
Q

Degenerative Disc Disease (DDD)

A

common cause of pain, motor weakness, & neuropathy.
most often occurs in the lumbar or cervical spine.
specific to spinal cord
effects men & women equally
2nd most common reason people visit the drs.

89
Q

Degenerative Disc

A

Intervertebral disc compression occurs with age.
Motor & sensory spinal nerves enter & exit from the spinal cord & travel through narrow openings of the vertebral bone.
With age, intervertebral discs dehydrate & vertebral bone become compressed & impinge on the entering & exiting nerves.
Dysfunction of motor & sensory spinal nerves impedes movement & sensation in the extremities.
May see weakness & paresthesia’s

90
Q

S/S of DDD: lumbar & cervical

A

lumbar: pain- lower back that radiates down the back of the leg (sciatica), in the buttocks or thighs, worsens when sitting, bending, lifting, or twisting, minimized when walking, changing positions, or lying down. Numbness, tingling, or weakness in the legs, Foot drop.
Cervical: Chronic neck pain can radiate to the shoulders & down the arms; Numbness or tingling in the arm or hand; Weakness of the arm or hand

91
Q

Rheumatoid arthritis (RA): definition

A

Systemic, autoimmune disease
Type III hypersensitivity
Inflammatory disease of synovium

92
Q

Rheumatoid arthritis (RA): etiology/ risk factors

A

Not well understood
Environmental and genetic factor: Genetic link + triggering event; Inappropriate immune response to joint injury.
Age: 40’s-60’s
Women
Tobacco use
Family history (genetic link)

93
Q

Rheumatoid arthritis (RA): pathogenesis

A

Immune cells attack synovial tissue
Immune cells: lymphocytes and macrophages
Produce rheumatoid factor (RF): Antibody against the body’s own antibodies (IgG), Formation of immune complex.

94
Q

Rheumatoid arthritis (RA): a progressive disease

A

Intensifying inflammatory response
Cartilage destroyed by osteoclasts
Pannus develops: inflammation and exuberant proliferation of synovium (hypertrophied synovium)
Pannus leads to: Bone erosion, Bone cysts, Fissure development.

95
Q

Rheumatoid arthritis (RA): clinical manifestations

A

EARLY: very little, maybe joint pain/discomfort, siffness.
EVENTUAL joint manifestations: Symmetrical, Pain, stiffness, motion limitation; Inflammation: heat, swelling tenderness; swelling in soft spongey and warm.
ADVANCED disease: deformity and disability, joint subluxation.

96
Q

Rheumatoid arthritis (RA): systemic involvement

A

Fatigue and malaise.
Potentially affects any and all body systems (Depending on severity).
IMPORTANT TO ASSESS THE HEART: can develop pericarditis, myocarditis.
Most common: Sjorgren’s Syndrome, Rheumatoid nodule

97
Q

Sjorgren’s Syndrome

A

destruction of moisture-producing gland (salivary and lacrimal)

98
Q

Rheumatoid nodules

A

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

99
Q

Goals of Pharm for RA

A

Relieve pain and swelling
Slow or stop progression of disease
Long term drug therapy requires patient adherence

100
Q

long term drug therapy for RA

A

NSAIDS
Glucocorticoids (short-term)
Disease-modifying anti-rheumatic drugs (DMARDS): slow/stop progression.

101
Q

Corticosteroids in RA

A

Rapid suppression of inflammation
Use only when symptoms NOT controlled with NSAIDS
Not best choice for long term therapy
Usually small doses <10mg/day (seen as small as 2.5mg)

102
Q

Methotrexate

A

CLASS: antineoplastic, anti-rheumatic, DMARD
MOA: : immunosuppressive
INDICATION: first line therapy
SE: GI, Bone marrow suppression, Shortened life expectancy.
NC: 11 black box warnings, need folic acid supplementation, NO alcohol (liver involvement), Teratogenic– NEVER for pregnant female, Higher risk of infection: contact HCP if there are signs of infection-Pneumocystis carinii, Caution with liver and kidney disease, Aplastic anemia risk when using with NSAIDs. MONITOR LIVER ENZYMES.

103
Q

hydroxychloroquine

A

CLASS: antimalarial, anti-rheumatic, DMARD
MOA: Unknown, anti-inflammatory processes; Slow progression of RA when used in combination with other DMARDs
INDICATION: Used alone or in combination with methotrexate for early/mild RA.
SE: retinopathy (rare)
NC: Very expensive, Can increase risk of severe skin or lung infections, skin cancers, serious allergic reactions, Biologic response modifiers, Target parts of the immune system that trigger inflammation that cause joint and tissue damage.

104
Q

Gout: definition

A

INFLAMMATORY disease resulting form deposits of uric acid crystals in tissues and fluids within the body.

105
Q

Gout: pathogenesis

A

Key Concept: URIC ACID CRYSTAL deposits in tissues

106
Q

Gout: etiology

A

HYPERURICEMIA
Overproduction & Under excretion of uric acid

107
Q

Gout: risk factors

A

Obesity
Preexisting diseases: HTN, DM, Renal disease, sickle cell anemia
Consuming ETOH (beer and spirits)
Diet rich in meat and seafood
Use of diuretics
Most common in males
African Americans

108
Q

phases of gout

A

Phase 1: ASYMPTOMATIC but with elevated serum uric acid levels & deposits in tissues, Crystals accumulate & tissue is damaged, Tissue damage triggers ACUTE INFLAMMATION
Phase 2: ACUTE FLARES or attacks occur- hyperuricemia.
Phase 3: CLINICALLY INACTIVE until the next flare – continued hyperuricemia. May be months or years before the next flare. Later, reoccurring attacks get closer and closer together
Phase 4: CHRONIC ARTHRITIS – joint pain and other sx present most of the time

109
Q

What causes uric acid crystals to form?

A

From the breakdown of PURINES
Body makes purine
Found in food: organ meats, shellfish, anchovies, herring, asparagus, mushrooms
Normally, uric acid dissolves in the blood and excreted by the kidneys.

110
Q

Gout: Clinical Manifestations

A

PAIN: may be mild or excruciating, usually the lower extremities.
Burning
Redness
Swelling and warmth
Fever
Symptoms present for days to weeks
Metatarsophalangeal joint of the big toe is the presenting joint for 50% of people with gout.

111
Q

Gout complications

A

Tophi.
renal calculi.

112
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

113
Q

Goal of Gout Pharm

A

Decrease symptoms of an acute attack AND prevent recurrent attacks

114
Q

what is usually the first line therapy for gout?

A

NSAIDS

115
Q

allopurinol

A

CLASS: Xanthine oxidase enzyme inhibitors
MOA: inhibits the xanthine oxidase enzyme, which PREVENTS uric acid production
INDICATION: pts whose gout is r/t EXCESS uric acid production (as seen by hyperuricemia); PREVENTION MEDICATION.
SE: : agranulocytosis, aplastic anemia, known to cause fatal skin reactions (SJS/TENS)
NC: interactions: anti-diabetic meds & warfarin. monitor WBC/RBC

116
Q

colchicine

A

CLASS
MOA: reduces inflammatory response to the deposits or urate crystals in joint tissues.
INDICATION: gout flares and prophylaxis
SE:GI & urinary bleeding.
contraindicated: : any person with severe renal, GI, hepatic or cardiac disorders, or bleeding disorders
NC: second line therapy, PO only. Powerful inhibitor of cell mitosis and can cause short-term leukopenia: Bone marrow suppression.

117
Q

Probenecid

A

CLASS: Uricosuric Agent
MOA: Inhibits reabsorption of uric acid in kidney, promoting excretion.
INDICATION: Treats hyperuricemia with gout
SE: GI upset, Dizziness or headache, Kidney/Liver impairment, Lots of drug interactions
NC: Used alone or in combination with allopurinol when not effective alone

118
Q

Lupus: Pathogenesis

A

B-lymphocytes are hyperactive and produce autoantibodies
MAJOR antibody produced: ANA: antinuclear antibody.
Activated against DNA
Formation of: Immune complexes
Can impact all major organ systems!
Inflammatory response destroys tissue

119
Q

Lupus: Predisposing Factors

A

Genetic factors
Gender: females
Age: 20-40
Race: Black/African Americans Higher likelihood
Environmental Triggers (EX. sun exposure)
Allergy to antibiotics
Hormonal factors (EX. birth control that contains estrogen, or women who start menstruation before 10)
Tobacco use

120
Q

Lupus: Manifestations

A

Extreme fatigue
Photosensitivity
Butterfly rash*
Fever
Weight changes
Unusual hair loss
Edema
Raynaud’s Phenomena*

121
Q

Lupus: Manifestations (think organs)

A

CNS: HA, dizziness, seizures, stroke
Lungs - Pleuritis, pleural effusions
Heart - Myocarditis & endocarditis
Kidneys - Nephritis**
Blood vessels - Vasculitis
Blood - Anemia, leukopenia, thrombocytopenia, blood clots
Joints - Arthritis

122
Q

SLE: Flares

A

Clinical course: exacerbations & remissions
A flare is: acute exacerbation of symptoms
Warning signs of a flare: Fatigue, Pain, Headache.
Prevention: recognize warning signs and avoid triggers- Sunlight exposure, Infection, Abruptly stopping a medication, Stress

123
Q

SLE: Pharmacotherapy

A

GOAL: to control symptoms
NSAIDS
high dose corticosteroids
low dose corticosteroids
antimalarials (hydroxychloroquine)
immunosuppressives (methotrexate)

NUR 326 (13 decks)

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