Musculoskeletal 1 Flashcards
Osteoporosis
more in women, loss of ovarian function
2 million fractures occur
characteristics
decreased bone strength
postmenopausal women
functional age
progress loss of bone tissue
osteoporosis manifestations and complications
vertebral and hip fractures
fractures occur at any skeletal site
> DVT and PE
increase mortality
Osteoporosis risk factors
chronic disease with inflammatory components
a chronic disease that increase the risk of falling
lack of calcium in the nutrition
lack of vit D deficiency esp with black people
estrogen deficiency
inactivity
chronic and various genetic and acquired diseases
medication
smoking
osteoporosis diagnosis
DXA scan: highly accurate X-ray
: standard of care
Guidelines for Bone Mass measurement:
all women by age 65
males at the age of 70 with absence of risk factors or related fractures
Vitamin D Level: < 12 ng/ml associated with vit D deficiency, leads to rickets in infants and children and osteomalacia in adults
12-20: inadequate for bone and overall health in healthy
21-50: Adequate
> 50 potential adverse effects to such high levels
treatment of osteoporosis
Vitamin D 3 50K U X 8 weeks then 2000U daily
calcium supplement
postmenopausal women with osteo
NEED: Bisophanate : increase bone turnover
Alendronate 70 mg PO weekly
Fosamax ( alendronate and Vitamin D
Osteoarthritis overview
most common type:
OA on rise
High prevalence in elderly
more common < 40
Prevalent > 60
more common with women
Negative impact on physical function
leading cause of disability
genetics:
50% inherited
genetic mutations
osteoarthritis clinical findings
Joint pain :
activity-related
synovitis
hip, knee 1st metatarsal phalange joint, cervical and lumbosacral spine
- most common chronic knee pain > 45 yrs
- spared wrist, elbow, and ankle
Stiffness:
-prominent in affected joint
-brief morning stiffness < 30 min
Bursitis
-knees and hips ( most common area)
heberden and buchard nodes
-structural abnormalities
osteoarthritis diagnosis
structural abnormalitits
symptoms
joint effusion
snovial fluid WBC > 1000
-septic arthritits or gout
non pharmacologic treatment:
-maintstay aletering loading and improving functionality
-avoid painful activities
-improve strenght and condtioning
- unloading the joint etither by redistribution or spliinting
pharmacolgic:
tylenol
oral and topical NSAIDs
glucorticoid injections
surgical
-refer to orthropedics
-hip and knee replacement
Acute Gouty arthritis
metabolic disease
- affects middle-aged to elderly men
-post-menopausal women
-OA, HTN, CKD - usually receiving diuretics
Purines
found in animal and plant products
converted to uric acid
leads to gout if not flushed out
gout characterization
acute or chronic arthritis
deposits of crystals in the joints and connective tissue
Complications:
deposition into the kidney interstitium
uric acid nephronlithiasis
clinical findings gout arthritis
first episode:
-evening hours
-joint pain and swelling
warm , red, and tender joints
early attacks subside 3-7 days
Precipitation factors:
-dietary access - organ meats
-trauma
-surgery
-excessive ethanol injestion
-hypouricemic therapy
serous medical illnessis
common early clinical manifestation:
-acute arthritis
-affects one joint
-polyarticular in subsiquent episodes
metarsophangela joint of 1st toe
-elderly advanced disease
-finger joints involved
- inflammed heberden’s or Buchard’s nodes
diagnosis of gout arthritis
Confirmed by arthrocentesis:
Needle-shaped monosodium urate (MSU) crystals- intracellular and extracellular
WBC 2000 - 60,000
Cloudy or chalky appearance
bacterial infections can co-exist
- culture fluid
Lab:
- serum uric acid levels
- UA
- CBC
-LFTs
-CMP
24-hour urine
> 800 mg of uric acid
excess purine
gouty arthritis treatment
- Mainstay treatment for acute attack
- NSAIDs
-naproxen, ibuprofen, tordol
Colchicine
-1.2 mg followed by 0.6 mg in 1 hour
glucocorticoids
po or IV
30-50mg day
Hypuricemic therapy for maintenance therapy:
not initiated during the acute attack
allopurinol 100-800mg day
-caution with thiazide use or PCN allergy
- life-threatening reactions
-systemic vasculitis
bone marrow suppression
-hepatitis
renal failure
Combine colchicine 0.6mg one or twice daily until hypouricemic x 6 months
Rheumatoid arthritis
chronic disease of unknown etiology
-most common chronic inflammatory arthritis
non-cure or preveintion
characterizations:
-symmetric polyarthritis
-articular cartilage and bone destruction
-functional disability
chances increase with age
- acquired between 25-55
plateaus at 75
Rheumatoid arthritis clinical findings
presenting symptoms;
inflammation of joints, tendons and bursa
early morning stiffness
eases with physcial activity
earliest joints involved
hands and feet
pattern of involvement
monoarticular or polyarticular
extra-articular manifestations
fatigue
subcutaneous nodules
lung involvement
pericarditis
peripheral neuropathy
vasculitis
hematologic abnormalities
rheumatoid arthritis work up and diagnosis
Inflammatory and biomarkers:
-ESR and CRP
anti-CCP s - 90% specificity
Rheumatoid factor - 50% specificity
Complete blood count:
-anemia
-leukocytosis mild
-thrombocytosis
joint aspiration:
confirms inflammatory nature
synovial WBC 75k -1000 mcl
negative culture
translucent to opagque yellow
arthritis treatment plan
primary :
-reduce inflammation and pain
-preservation of function
prevention of deformity
early pharmacologic intervention
non steroidal anti-inflammatory
provide relief however
do not prevent erosion
Do not alter disease progression
corticosteroids
anti-inflammatory effect
slow articular erosion rate
bridge before DMARDs
prednisone 5-10 mg a day
disease-modifying anti rheumatic drugs (DMARDs)
methotrexate
synthetic DMARDs
Methotrexate:
- 1st choice and well tolerated
-beneficial effect in 2-3 weeks
does have complications
-gastric irritation, stomatitis, cytopenias, hepatoxicity
Sulfasalazine:
-second line agent
-does have complications
hemolysis with G6PD deficiency
check G6DP level before initiation
hydroxychoroquine sulfate
-monotherapy with only mild dx
-combo therapy with conventional DMARDs
effecive combination
methrotrexate + Sulfasalazine + hydorxychoroquine
Rheumatoid arthritis treatment plan - biologics
Biologic DMRDs
tumor necrosis factor inhibitors (TNF-inhibitor)
-Etanercept, infliximab, Adalimumab and Goimumab
Most common therapy:
-methotrexate and TNF inhibitor
—- methotrexate should be on low dose folic acid can lead to folic deficiency
Supplement with folic acid
reduce side effects of MXT
fibromylagia
affects 3-10% of population
more common in women
age 20-50
similar across socioeconomic classes
cultural factors play a role in treatment
Unknown cause:
Theories of etiology exist non-proven
peripheral pain generator :
arthritis bursitis or tendonitis
neuropathies
inflammatory degenerative conditions
common characteristics
diffuse musculoskeletal pain and tenderness
absence of objective findings
clinical findings fibromyalgia
typical presentaion:
pain all over
pain above and below waist
pain involving the axial skeleton ( neck back and chest)
characteristics of pain
poorly localized
difficult to ignore
severe in intensity
associated with reduced functional capacity
increased pain sensitivity
examples: blood pressure cuff or skin roll tenderness
beyond the pain :
fatigue
unrefreshing sleep
cognitive dysfunction
anxiety and depression
fibromyalgia treatment
multidisciplinary approach
non-pharmacologic
CBT
meditation
exercise programs
pharmacologic
-amitriptyline
cymbalta or Celexa
Flexeril
Lyrica or gabapentin
septic arthritis overview
Most common cause:
-staphylococcus aureus and Neisseria gonorrhea
- mycobacteria, spirochetes, fungi and viruses
Young adults and adolescents
-Neisseria gonorrhea
adults of all ages;
50% staphylococcus aureus
Older adults:
33 % gram-negative bacilli, pneumococci, and beta-hemolytic streptococcal
Gram-negative infection:
accounts for 10%
common in injection drug users and immunocompromised
escherichia choli and pseudomonas aeruginosa
Risk factors:
rheumatoid arthritis - highest incisence
diabetes
hemodialysis
malignancy
immunosuppression
cirrhosis
IVDA
septic arthritis route of infections
Most common route :
hematogenous
-bacteria enter joint via blood steam
involves single join or few joints
> 1 joint 15% of cases
- the knee is most frequent
- ## rapid destruction of articular cartilagenearly all bacteria can cause septic arthritis
surface-associated adhesins
permit adherence to cartilage
endotoxins promote chondrocyte mediated breakdown of cartilage