Musculoskeletal Flashcards
components affecting gender and bone mass
–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)
osteoporosis
bone mineral density 2.5 standard deviations below peak bone mass
how is osteoporosis measured?
DEXA scan (results in a T-score)
T-score for normal bone density
-1 or greater
T-score for osteopenia
between -1 and -2.5
T-score for osteoporosis
less than or equal to -2.5
T-score for severe osteoporosis
less than -2.5
osteopenia
low bone mass
–thinning of the trabecular matrix of the bone before osteoporosis
osteoporosis
“pourous bone”
–characterized by low bone density and structural deterioration of the bone
–when actual breaks in the trabecular matrix have occurred
severe osteoporosis
osteoporosis with a history of a fragility fracture
bones susceptible to osteoporosis
hips, vertebrae, and wrists
osteoporosis characteristics
–low bone mass
–micro-architectural deterioration
–increase in bone fragility
–susceptibility to fracture = high
major risk factors for osteoporosis
–increased age
–female
–caucasian
–history of fractures as adult
–family history
–body weight < 127 pounds
–smoking
–alcohol use
–steroid and immunosuppressant use
minor risk factors for osteoporosis
–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
patho of osteoporosis
–increased bone resorption (increased osteoclast activity)
–decreased bone formation (decreased osteoblast activity)
–problems making new bone
–problems with too much bone resorption
early clinical manifestations of osteoporosis
none
late clinical manifestations of osteoporosis
–fractures
–pain
–loss of height
–stooped posture (kyphosis)
hip fractures
–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
clinical presentation of hip fractures
–sudden onset of hip pain before or after a fall
–inability to walk
–severe groin pain
–tenderness
–affected leg is externally rotated and shortened
goal of osteoporosis pharm
reduce fractures
primary prevention of osteoporosis fractures
–calcium
–vitamin D
treatment for osteoporosis
–promote bone formation
–decrease bone resorption
example of biphosphates
aldendronate (Fosamax)
MOA of aldendronate
binds permanently to surfaces of bones to inhibit osteoclast activity
adverse effects of aldendronate
–GI (N/V/D)
–esophageal ulcerations
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)
example of selective estrogen receptor modulators (SERMs)
Raloxifene (Evista)
MOA of raloxifene
–mimics estrogen by increasing bone density
–inhibits bone resorption
use of raloxifene
–used as prevention and treatment
–reduces risk of spinal fracture by 50%
adverse effects of raloxifene
–hot flashes
–leg cramping
black box warning for raloxifene
stroke risk
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
calcitonin-salmon (Miacalcin) MOA
inhibits bone marrow removal by osteoclasts
–slows down bone loss and increases spinal bone density
use of calcitonin-salmon
–treatment only
–not long-term
–reduces spinal fractures by 30%
–can reduce pain in someone with hip fractures
route for calcitonin-salmon
intranasal (nasal irritation)
fractures
any break in the continuity of bone that occurs when more stress is placed on the bone that it is able to absorb
causes of fractures
–traumatic fall
–fatigue (repeated, prolonged stress)
–pathologic (weakened bone, possibly spontaneous)
open (compound) fracture
fractured bone penetrates skin
closed (simple) fracture
does not break through the skin
transverse fracture
horizontal break across bone
spiral fracture
–fracture from twisting
–break at an angle
comminuted fracture
more than one fracture line and more than 2 bone fragments
impacted fracture
from heights
greenstick fracture
children; bone bending
clinical manifestations of fractures
Pain
Edema
Deformity
purpose of edema in fractures
natural splint
components of deformity
–loss of function
–abnormal mobility
complications of fractures
–delayed healing
–bone growth impairment
–compartment syndrome
–fat embolism syndrome
components of delayed healing
–delayed union
–malunion
–nonunion
delayed union
bone pain and tenderness increase
risk factors for delayed union
–tobacco
–increased age
–severe anemia
–uncontrolled DM
–decreased vitamin D
–hypothyroidism
–poor nutrition
malunion
improper alignment
nonunion
–no healing 4-6 months post-fracture
–causes: poor blood supply, repetitive stress, DM, infection
when do delayed healing complications occur?
3 months - 1 year after fracture
impaired bone growth
–pediatric consideration
–fracture through epiphyseal plate
–can delay future bone growth
what is compartment syndrome seen with?
–crush injuries
–cast
what does compartment syndrome result from?
increased pressure within limited anatomical space
tourniquet effect
–edema at fracture site puts intense pressure on soft tissue
–can lead to tissue hypoxia of muscles and nerves
manifestations of compartment syndrome
–edema
–loss or weakened pulses
–PAIN
treatment for compartment syndrome
fasciotomy
fat embolism syndrome
fat molecules in the lung following:
–long bone fracture
–major trauma
how do fat emboli get into the lungs?
–fat molecules from bone marrow or traumatized tissue
–released into blood stream –> lungs
symptoms of fat emboli
–hypoxemia
–altered LOC
–petechial rash (last symptom to occur)
treatment for fat emboli
supportive
osteomyelitis
an acute or chronic pyogenic infection of the bone
pyogenic
pus producing
cause of osteomyelitis
bacteria (staph aureus)
risk factors for osteomyelitis
–recent trauma
–diabetes
–hemodialysis
–IV drug use
–splenectomy
direct contamination (osteomyelitis)
open wound
–open fracture
–gunshot
–puncture
–surgery
surgery/insertion of meta plates or screws
indirect contamination (osteomyelitis)
from bloodstream
–most common
–bacteremia
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
local symptoms of osteomyelitis
–tenderness, warmth, redness
–wound drainage
–restricted movement
–spontaneous fracture
systemic symptoms of osteomyelitis
–fever
–positive blood culture
–leukocytosis
osteomyelitis pharm
–obtain culture
–empiric ABX therapy (nafcillin, cefazolin, vanc)
–bacteria-specific therapy
arthropathy
a joint disorder
–when the disorder involves inflammation of one or more joints –> arthritis
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
common joints affected by OA
–cervical spine
–lumbosacral spine
–hip
–knee
–hands
–first metatarsal phalangeal joint (big toe)
spared = wrist, elbow, ankle
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
etiology of OA
–stresses applied to joint
–degeneration of cartilage
–chronic disease
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
osteophytes
bone spurs caused by osteoblasts
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
physical exam findings in OA
–joint deformity
–joint tenderness
–decreased ROM
–Herbeden’s nodes
–Bouchard’s nodes
Herbeden’s nodes
distal interphalangeal joint
Bouchard’s nodes
proximal interphalangeal joint (closer to hand)
goals of treatment of OA
–manage pain
–maintain mobility
–minimize disability
goal of OA pharm
manage pain and reduce swelling
pharm for OA
–mild to moderate: NSAIDs, acetaminophen, topical capsaicin
–moderate to severe: NSAIDs (Rx strength), NSAIDs + colchicine, acetaminophen + tramadol, opioids, steroid injections
NSAIDs MOA
reduce production of prostaglandins
degenerative disc disease
–common cause of pain, motor weakness, and neuropathy
–most often occurs in lumbar or cervical spine
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
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
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
rheumatoid arthritis
–systemic, autoimmune
–type III hypersensitivity
–inflammatory disease of synovium
etiology of RA
–not well understood
–environmental and genetic factor (genetic link + trigger event)
risk factors for RA
–40-60s
–women
–tobacco use
–family history
RA patho
–immune cells attack synovial tissue
–immune cells: lymphocytes and macrophages
–produce rheumatoid factor (RF) –> antibody against the body’s own antibodies (IgG)
progression of RA
–cartilage destroyed by osteoclasts
–pannus develops
pannus
inflammation and exuberant proliferation of synovium
what does pannus lead to?
–bone erosion
–bone cysts
–fissure development
what is pannus?
scar tissue
early s/s of RA
–very little
–maybe joint discomfort
eventual joint manifestations in RA
–symmetrical
–pain, stiffness, motion limitation
–inflammation: heat, swelling, tenderness
advanced disease s/s of RA
–deformity and disability
–joint subluxation (misalignment)
systemic involvement in RA
–fatigue and malaise
–Sjorgren’s syndrome
–rheumatoid nodules
Sjorgren’s syndrome
destruction of moisture-producing gland (salivary and lacrimal)
–gritty, dry, itchy eyes
–fissured, dry tongue
rheumatoid nodules
–immune mediated granulomas
–develop around inflamed joints
–subcutaneous and firm, sometimes painful
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)
corticosteroids in RA
–usually prednisone
–rapid suppression of inflammation
–use only when symptoms not controlled with NSAIDs
–not best choice for long term therapy
classification of methotrexate
–antineoplastic
–anti-rheumatic
MOA of methotrexate
immunosuppressive
–interferes with metabolism of folate
route for methotrexate
PO or SQ/IV
adverse effects of methotrexate
–GI (nausea, anorexia, vomiting)
–bone marrow suppression
–shortened life expectancy
frequency for methotrexate
1x per week
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
hydroxychloroquine (Plaquenil) classification
–antimalarial
–anti-rheumatic
hydroxychloroquine (Plaquenil) MOA
unknown, anti-inflammatory processes
hydroxychloroquine (Plaquenil) effects
slow progression of RA when used in combo with other DMARDs
therapeutic uses of hydroxychloroquine (Plaquenil)
used alone or in combo with methotrexate for early/mild RA
adverse effects of hydroxychloroquine (Plaquenil)
retinopathy
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
gout
an inflammatory disease resulting from deposits of uric acid crystals in tissues and fluids within the body
patho of gout
–uric acid crystal deposits in tissues (HYPERURICEMIA)
–overproduction of uric acid
–under excretion of uric acid
what causes uric acid crystals to form?
from the breakdown of purines
where are purines found?
–made in body
–found in food: organ meats, shellfish, anchovies, herring, asparagus, mushrooms
where is uric acid normally excreted from?
the kidneys
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
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
phase 2 of gout
acute flares or attacks occur – hyperuricemia
phase 3 of gout
clinically inactive until the next flare
phase 4 of gout
chronic arthritis
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
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
gout complications
–tophi
–renal calculi
goal of gout pharm
–decrease symptoms of an acute attack and prevent recurrent attacks
–NSAIDs are usually first line therapy
allopurinol (Zyloprim) MOA
inhibits the xanthine oxidase enzyme, which prevents uric acid production
indications for allopurinol
patients whose gout is related to EXCESS uric acid production
prevention medication
adverse effects of allopurinol
–agranulocytosis
–aplastic anemia
–known to cause fatal skin reactions
–rash
when do you see effects of allopurinol?
2-6 weeks
drug interactions with allopurinol
anti-diabetes meds and warfarin
–hypoglycemia
–INR
labs to monitor with allopurinol
–WBCs (infection)
–serum uric acid
colchicine MOA
reduces inflammatory response to the deposits of urate crystals in joint tissues
uses of colchicine
gout flares and prophylaxis
colchicine specifics
–second line therapy
–powerful inhibitor of cell mitosis and can cause short-term leukopenia (bone marrow suppression)
adverse effects of colchicine
GI bleeding and urinary bleeding
contraindications of colchicine
any person with severe renal, GI, hepatic, or cardiac disorders, or bleeding disorders
route for colchicine
only PO
classification of probenecid (Benuryl)
uricosuric acid
MOA of probenecid
inhibits reabsorption of uric acid in kidney, promoting excretion
uses of probenecid
treats hyperuricemia with gout
recommendations for probenecid
used alone or in combo with allopurinol when not effective alone
adverse effects of probenecid
–GI upset
–dizziness or headache
–kidney/liver impairments
–lots of drug interactions
teaching points for probenecid
–take with food and drink
report:
–kidney and liver issues
–weight gain
–hematuria
–change in UOP
lupus patho
–B-lymphocytes are hyperactive and produce autoantibodies
–activated against DNA
–formation of immune complexes
–inflammatory response destroys tissue
what organ is lupus common in?
kidneys
ANA
antinuclear antibody
risk factors for lupus
–genetics
–female
–20-40 years old
–Black/AA
–environmental triggers
–allergy to antibiotics
–hormonal factors
–tobacco
s/s of lupus
–extreme fatigue
–photosensitivity
–butterfly rash
–fever
–weight changes
–unusual hair loss
–edema
CNS lupus symptoms
–HA
–dizziness
–seizures
–stroke
lupus symptoms in lungs
–pleuritis
–PEs
lupus symptoms with heart
–myocarditis
–endocarditis
lupus symptoms with kidneys
nephritis
lupus symptoms with blood vessels
vasculitis
lupus symptoms with blood
–anemia
–leukopenia
–thrombocytopenia
–blood clots
lupus symptoms with joints
arthritis
SLE flares
–acute exacerbation of symptoms
–warning signs:
fatigue
pain
headache
prevention of SLE flares
avoid triggers:
–sunlight exposure
–infection
–abruptly stopping a med
–stress
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)
similarities between RA and lupus
–autoimmune
–systemic inflammation
–multiple body system
–pharm
differences between RA and lupus
–RA = focus on joints
–SLE = multisystem
