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)
2
Q
osteoporosis
A
bone mineral density 2.5 standard deviations below peak bone mass
3
Q
how is osteoporosis measured?
A
DEXA scan (results in a T-score)
4
Q
T-score for normal bone density
A
-1 or greater
5
Q
T-score for osteopenia
A
between -1 and -2.5
6
Q
T-score for osteoporosis
A
less than or equal to -2.5
7
Q
T-score for severe osteoporosis
A
less than -2.5
8
Q
osteopenia
A
low bone mass
–thinning of the trabecular matrix of the bone before osteoporosis
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
10
Q
severe osteoporosis
A
osteoporosis with a history of a fragility fracture
11
Q
bones susceptible to osteoporosis
A
hips, vertebrae, and wrists
12
Q
osteoporosis characteristics
A
–low bone mass
–micro-architectural deterioration
–increase in bone fragility
–susceptibility to fracture = high
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
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
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
16
Q
early clinical manifestations of osteoporosis
A
none
17
Q
late clinical manifestations of osteoporosis
A
–fractures
–pain
–loss of height
–stooped posture (kyphosis)
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
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
20
Q
goal of osteoporosis pharm
A
reduce fractures
21
Q
primary prevention of osteoporosis fractures
A
–calcium
–vitamin D
22
Q
treatment for osteoporosis
A
–promote bone formation
–decrease bone resorption
23
Q
example of biphosphates
A
aldendronate (Fosamax)
24
Q
MOA of aldendronate
A
binds permanently to surfaces of bones to inhibit osteoclast activity
25
adverse effects of aldendronate
--GI (N/V/D)
--esophageal ulcerations
26
teaching points for aldendronate
--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)
27
example of selective estrogen receptor modulators (SERMs)
Raloxifene (Evista)
28
MOA of raloxifene
--mimics estrogen by increasing bone density
--inhibits bone resorption
29
use of raloxifene
--used as prevention and treatment
--reduces risk of spinal fracture by 50%
30
adverse effects of raloxifene
--hot flashes
--leg cramping
31
black box warning for raloxifene
stroke risk
32
teaching points for SERMs
--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
33
calcitonin-salmon (Miacalcin) MOA
inhibits bone marrow removal by osteoclasts
--slows down bone loss and increases spinal bone density
34
use of calcitonin-salmon
--treatment only
--not long-term
--reduces spinal fractures by 30%
--can reduce pain in someone with hip fractures
35
route for calcitonin-salmon
intranasal (nasal irritation)
36
fractures
any break in the continuity of bone that occurs when more stress is placed on the bone that it is able to absorb
37
causes of fractures
--traumatic fall
--fatigue (repeated, prolonged stress)
--pathologic (weakened bone, possibly spontaneous)
38
open (compound) fracture
fractured bone penetrates skin
39
closed (simple) fracture
does not break through the skin
40
transverse fracture
horizontal break across bone
41
spiral fracture
--fracture from twisting
--break at an angle
42
comminuted fracture
more than one fracture line and more than 2 bone fragments
43
impacted fracture
from heights
44
greenstick fracture
children; bone bending
45
clinical manifestations of fractures
Pain
Edema
Deformity
46
purpose of edema in fractures
natural splint
47
components of deformity
--loss of function
--abnormal mobility
48
complications of fractures
--delayed healing
--bone growth impairment
--compartment syndrome
--fat embolism syndrome
49
components of delayed healing
--delayed union
--malunion
--nonunion
50
delayed union
bone pain and tenderness increase
51
risk factors for delayed union
--tobacco
--increased age
--severe anemia
--uncontrolled DM
--decreased vitamin D
--hypothyroidism
--poor nutrition
52
malunion
improper alignment
53
nonunion
--no healing 4-6 months post-fracture
--causes: poor blood supply, repetitive stress, DM, infection
54
when do delayed healing complications occur?
3 months - 1 year after fracture
55
impaired bone growth
--pediatric consideration
--fracture through epiphyseal plate
--can delay future bone growth
56
what is compartment syndrome seen with?
--crush injuries
--cast
57
what does compartment syndrome result from?
increased pressure within limited anatomical space
58
tourniquet effect
--edema at fracture site puts intense pressure on soft tissue
--can lead to tissue hypoxia of muscles and nerves
59
manifestations of compartment syndrome
--edema
--loss or weakened pulses
--PAIN
60
treatment for compartment syndrome
fasciotomy
61
fat embolism syndrome
fat molecules in the lung following:
--long bone fracture
--major trauma
62
how do fat emboli get into the lungs?
--fat molecules from bone marrow or traumatized tissue
--released into blood stream --> lungs
63
symptoms of fat emboli
--hypoxemia
--altered LOC
--petechial rash (last symptom to occur)
64
treatment for fat emboli
supportive
65
osteomyelitis
an acute or chronic pyogenic infection of the bone
66
pyogenic
pus producing
67
cause of osteomyelitis
bacteria (staph aureus)
68
risk factors for osteomyelitis
--recent trauma
--diabetes
--hemodialysis
--IV drug use
--splenectomy
69
direct contamination (osteomyelitis)
open wound
--open fracture
--gunshot
--puncture
--surgery
surgery/insertion of meta plates or screws
70
indirect contamination (osteomyelitis)
from bloodstream
--most common
--bacteremia
71
patho of osteomyelitis
--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
local symptoms of osteomyelitis
--tenderness, warmth, redness
--wound drainage
--restricted movement
--spontaneous fracture
73
systemic symptoms of osteomyelitis
--fever
--positive blood culture
--leukocytosis
74
osteomyelitis pharm
--obtain culture
--empiric ABX therapy (nafcillin, cefazolin, vanc)
--bacteria-specific therapy
75
arthropathy
a joint disorder
--when the disorder involves inflammation of one or more joints --> arthritis
76
osteoarthritis (OA)
--degeneration of joints caused by aging and stress
--most common cause of disability in US
--obesity and longer life expectancy --> increase in OA
77
common joints affected by OA
--cervical spine
--lumbosacral spine
--hip
--knee
--hands
--first metatarsal phalangeal joint (big toe)
**spared = wrist, elbow, ankle**
78
risk factors of OA
--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
etiology of OA
--stresses applied to joint
--degeneration of cartilage
--chronic disease
80
OA patho
--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
osteophytes
bone spurs caused by osteoblasts
82
symptoms of OA
--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
physical exam findings in OA
--joint deformity
--joint tenderness
--decreased ROM
--Herbeden's nodes
--Bouchard's nodes
84
Herbeden's nodes
distal interphalangeal joint
85
Bouchard's nodes
proximal interphalangeal joint (closer to hand)
86
goals of treatment of OA
--manage pain
--maintain mobility
--minimize disability
87
goal of OA pharm
manage pain and reduce swelling
88
pharm for OA
--mild to moderate: NSAIDs, acetaminophen, topical capsaicin
--moderate to severe: NSAIDs (Rx strength), NSAIDs + colchicine, acetaminophen + tramadol, opioids, steroid injections
89
NSAIDs MOA
reduce production of prostaglandins
90
degenerative disc disease
--common cause of pain, motor weakness, and neuropathy
--most often occurs in lumbar or cervical spine
91
patho of degenerative discs
--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
lumbar s/s of DDD
--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
cervical s/s of DDD
--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
rheumatoid arthritis
--systemic, autoimmune
--type III hypersensitivity
--inflammatory disease of synovium
95
etiology of RA
--not well understood
--environmental and genetic factor (genetic link + trigger event)
96
risk factors for RA
--40-60s
--women
--tobacco use
--family history
97
RA patho
--immune cells attack synovial tissue
--immune cells: lymphocytes and macrophages
--produce rheumatoid factor (RF) --> antibody against the body's own antibodies (IgG)
98
progression of RA
--cartilage destroyed by osteoclasts
--pannus develops
99
pannus
inflammation and exuberant proliferation of synovium
100
what does pannus lead to?
--bone erosion
--bone cysts
--fissure development
101
what is pannus?
scar tissue
102
early s/s of RA
--very little
--maybe joint discomfort
103
eventual joint manifestations in RA
--symmetrical
--pain, stiffness, motion limitation
--inflammation: heat, swelling, tenderness
104
advanced disease s/s of RA
--deformity and disability
--joint subluxation (misalignment)
105
systemic involvement in RA
--fatigue and malaise
--Sjorgren's syndrome
--rheumatoid nodules
106
Sjorgren's syndrome
destruction of moisture-producing gland (salivary and lacrimal)
--gritty, dry, itchy eyes
--fissured, dry tongue
107
rheumatoid nodules
--immune mediated granulomas
--develop around inflamed joints
--subcutaneous and firm, sometimes painful
108
goals of pharm for RA
--relieve pain and swelling
--slow or stop progression of disease
--long term drug therapy requires patient adherence (NSAIDs, glucocorticoids, DMARDs)
109
corticosteroids in RA
--usually prednisone
--rapid suppression of inflammation
--use only when symptoms not controlled with NSAIDs
--not best choice for long term therapy
110
classification of methotrexate
--antineoplastic
--anti-rheumatic
111
MOA of methotrexate
immunosuppressive
--interferes with metabolism of folate
112
route for methotrexate
PO or SQ/IV
113
adverse effects of methotrexate
--GI (nausea, anorexia, vomiting)
--bone marrow suppression
--shortened life expectancy
114
frequency for methotrexate
1x per week
115
methotrexate teaching points
--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
hydroxychloroquine (Plaquenil) classification
--antimalarial
--anti-rheumatic
117
hydroxychloroquine (Plaquenil) MOA
unknown, anti-inflammatory processes
118
hydroxychloroquine (Plaquenil) effects
slow progression of RA when used in combo with other DMARDs
119
therapeutic uses of hydroxychloroquine (Plaquenil)
used alone or in combo with methotrexate for early/mild RA
120
adverse effects of hydroxychloroquine (Plaquenil)
retinopathy
121
biologic agents (DMARDs)
--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
gout
an inflammatory disease resulting from deposits of uric acid crystals in tissues and fluids within the body
123
patho of gout
--uric acid crystal deposits in tissues (HYPERURICEMIA)
--overproduction of uric acid
--under excretion of uric acid
124
what causes uric acid crystals to form?
from the breakdown of purines
125
where are purines found?
--made in body
--found in food: organ meats, shellfish, anchovies, herring, asparagus, mushrooms
126
where is uric acid normally excreted from?
the kidneys
127
gout risk factors
--obesity
--HTN, DM, renal disease, sickle cell
--ETOH
--diet rich in meat and seafood
--use of diuretics
--most common in males
--African Americans
128
phase 1 of gout
asymptomatic, but with elevated uric acid levels and deposits in tissues
--crystals accumulate and tissue is damaged
--tissue damage triggers acute inflammation
129
phase 2 of gout
acute flares or attacks occur -- hyperuricemia
130
phase 3 of gout
clinically inactive until the next flare
131
phase 4 of gout
chronic arthritis
132
s/s of gout
--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
tophi
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
gout complications
--tophi
--renal calculi
135
goal of gout pharm
--decrease symptoms of an acute attack and prevent recurrent attacks
--NSAIDs are usually first line therapy
136
allopurinol (Zyloprim) MOA
inhibits the xanthine oxidase enzyme, which prevents uric acid production
137
indications for allopurinol
patients whose gout is related to EXCESS uric acid production
**prevention medication**
138
adverse effects of allopurinol
--agranulocytosis
--aplastic anemia
--known to cause fatal skin reactions
--rash
139
when do you see effects of allopurinol?
2-6 weeks
140
drug interactions with allopurinol
anti-diabetes meds and warfarin
--hypoglycemia
--INR
141
labs to monitor with allopurinol
--WBCs (infection)
--serum uric acid
142
colchicine MOA
reduces inflammatory response to the deposits of urate crystals in joint tissues
143
uses of colchicine
gout flares and prophylaxis
144
colchicine specifics
--second line therapy
--powerful inhibitor of cell mitosis and can cause short-term leukopenia (bone marrow suppression)
145
adverse effects of colchicine
GI bleeding and urinary bleeding
146
contraindications of colchicine
any person with severe renal, GI, hepatic, or cardiac disorders, or bleeding disorders
147
route for colchicine
only PO
148
classification of probenecid (Benuryl)
uricosuric acid
149
MOA of probenecid
inhibits reabsorption of uric acid in kidney, promoting excretion
150
uses of probenecid
treats hyperuricemia with gout
151
recommendations for probenecid
used alone or in combo with allopurinol when not effective alone
152
adverse effects of probenecid
--GI upset
--dizziness or headache
--kidney/liver impairments
--lots of drug interactions
153
teaching points for probenecid
--take with food and drink
report:
--kidney and liver issues
--weight gain
--hematuria
--change in UOP
154
lupus patho
--B-lymphocytes are hyperactive and produce autoantibodies
--activated against DNA
--formation of immune complexes
--inflammatory response destroys tissue
155
what organ is lupus common in?
kidneys
156
ANA
antinuclear antibody
157
risk factors for lupus
--genetics
--female
--20-40 years old
--Black/AA
--environmental triggers
--allergy to antibiotics
--hormonal factors
--tobacco
158
s/s of lupus
--extreme fatigue
--photosensitivity
--butterfly rash
--fever
--weight changes
--unusual hair loss
--edema
159
CNS lupus symptoms
--HA
--dizziness
--seizures
--stroke
160
lupus symptoms in lungs
--pleuritis
--PEs
161
lupus symptoms with heart
--myocarditis
--endocarditis
162
lupus symptoms with kidneys
nephritis
163
lupus symptoms with blood vessels
vasculitis
164
lupus symptoms with blood
--anemia
--leukopenia
--thrombocytopenia
--blood clots
165
lupus symptoms with joints
arthritis
166
SLE flares
--acute exacerbation of symptoms
--warning signs:
fatigue
pain
headache
167
prevention of SLE flares
avoid triggers:
--sunlight exposure
--infection
--abruptly stopping a med
--stress
168
SLE pharm
--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
similarities between RA and lupus
--autoimmune
--systemic inflammation
--multiple body system
--pharm
170
differences between RA and lupus
--RA = focus on joints
--SLE = multisystem
