Musculoskeletal 1 Flashcards

1
Q

Osteoporosis

A

more in women, loss of ovarian function
2 million fractures occur

characteristics
decreased bone strength
postmenopausal women
functional age
progress loss of bone tissue

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2
Q

osteoporosis manifestations and complications

A

vertebral and hip fractures
fractures occur at any skeletal site
> DVT and PE
increase mortality

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3
Q

Osteoporosis risk factors

A

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

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4
Q

osteoporosis diagnosis

A

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

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5
Q

treatment of osteoporosis

A

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

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6
Q

Osteoarthritis overview

A

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

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7
Q

osteoarthritis clinical findings

A

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

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8
Q

osteoarthritis diagnosis

A

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

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9
Q

Acute Gouty arthritis

A

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

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10
Q

gout characterization

A

acute or chronic arthritis
deposits of crystals in the joints and connective tissue

Complications:
deposition into the kidney interstitium
uric acid nephronlithiasis

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11
Q

clinical findings gout arthritis

A

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
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12
Q

diagnosis of gout arthritis

A

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

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13
Q

gouty arthritis treatment

A
  • 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

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14
Q

Rheumatoid arthritis

A

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

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15
Q

Rheumatoid arthritis clinical findings

A

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

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16
Q

rheumatoid arthritis work up and diagnosis

A

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

17
Q

arthritis treatment plan

A

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

18
Q

synthetic DMARDs

A

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

19
Q

Rheumatoid arthritis treatment plan - biologics

A

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

20
Q

fibromylagia

A

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

21
Q

clinical findings fibromyalgia

A

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

22
Q

fibromyalgia treatment

A

multidisciplinary approach

non-pharmacologic
CBT
meditation
exercise programs

pharmacologic
-amitriptyline
cymbalta or Celexa
Flexeril
Lyrica or gabapentin

23
Q

septic arthritis overview

A

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

24
Q

septic arthritis route of infections

A

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
25
Q

septic arthritis pathogenesis and organisms

A

surgery or penetrating injuries
staphylococcus aureus
other gran positive / negative

prostheric joints or artrosocpy
-coagulase negative staphylocci

human bites , decubitis ulcers or intra abdominal abcess
-anaerobic organisms

tramatic injuries
polymicrobial infections

foot penetrations
pseudomonas aeruginosa

sub acute chronic monoarthritis , oligoarthritis
mycobacterial or fungal infection

26
Q

clinical findings of septic arthritis

A

acute onset:
pain swelling , and heat

chills and fever
common
absent up to 20%

imagining:
plain radiographys
joint effusion and soft tissue swelling
joint space narrowing and bony erosions
indicates advanced infection

ultrasound
detect hip effusions
CT or MRI
demonstrate infection of the sacroiliac joint, sternoclavicular joint, and spine
use for IVDA patients will seed in these joints

laboratory work up
CBC
blood cultures
ESR and CRP

27
Q

septic arthritis diagnosis

A

synovial fluid analysis
critical for diagnosis

synovial leukocyte count
50,000 -100,000

gram stain and culture
positive in 75% of staphylococcus infections
positive in 50% of gram negative infections

synovial fluid color
turbid , serosanguinous or purulent

synovial total protien , LDH , glucose
total protien and LDH increased
glucose decreases

check for crystals
rule out gout

blood cultures
postive 50%

28
Q

septic arthritis treatment

A

recommend hospitilazation:
- iv antibiotic and pain control
-imaging
-consultation

broad spectrum abx
cover for staphylococci, streptococci and gram negative
vancomycin 1 g IV q12 and ceftriaxone 1-2 gram IV QD

Joint drainage:
consult orthopedics or IR
arthrocentesis
severe effusion:
-arthroscopic lavage and dibridement with drain placement

open surgical drainage
-conservative treatments failed

prosthetic joint infections
dependant on timing of infection
remvoval of prostetic

29
Q

Acute Osteomyelitis

A

Infection of the bone:
-various microorganisms with different routes
-spontaneous hematogenous osteomyelitis
-healthy individuals
-local microbial spread
-chronic conditions, compromised skin or tissue barrier
-require orthopedic repair

Cierry-mader staging system
-hematogenous spread
-vertebral column
-
Spread from contiguous site following surgery
-long bones
secondary infection dt vascular insufficiency
-long bones

etiology
- uti
skin or soft tissue compromise
intra vascular catheterization sites
endocardium

Most common underlying condition
diabeties

30
Q

Acute Osteomyelitis vertebral infection

A

higher occurrence in males and age-dependent
other names: disk space infection, septic discitis, spondylodiscitis, spinal osteomyelitis

Bacterial invasion:
microorganisms invade via the segmental arterial circulation and adjacent end plates
- infection spread into the disc

Alternative routes:
-retrograde seeding
-direct inoculation
-epidural infiltration
-trauma

micoorganism spectrum:
-the majority are monomicrobial
- staphylococcus aureus 40-50%
-streptococci 12 %
-gram-negative bacilli 20%

31
Q

Acute Osteomyelitis long bones

A

leading pathogenic source:
-exogenous infection
-post surgical or post traumatic

Microoganism spectrum
hematogenous
-S aureus

implant associated
- S aureus
- coagulase-negative staphylococci

Open fracture
-gram negative bacilli
-polymicrobial

infected implanted devices classification
-acute < 3 weeks
delayed 3-10 weeks
late , beyone 10 weeks

32
Q

clinical manifestations of acute osteomyelitis

A

presents in 2 week after bone infection:
inflammatory bone changes

chronic osteomyelitis:
presents -6 or more weeks after bone infection
bone destruction and sequestrum

verterbral colum infection S and S
fever and back pain
back pain leading symptoms 85%
-location of pain corresponds with infection

Neurologic deficits consider abscess
-radiculopathy
-weakness
-sensory loss
-bowel and bladder dysfunction
- paralysis

long bone infection
- pain and low-grade fever
manifest as clinical sepsis
local signs of inflammation

33
Q

acute osteomyelitis diagnosis

A

Imaging :
plane radiography
MRI w/wo contrast
CT W contrast

Laboratory work up
CBC, ESR, CRP, Blood cultures
-leukocytosis, and neutrophilia, low sensitivity
- elevated ESR and CRP high sensitivity
positive BC x dependent on ABX pre-treatment

High suspicion with negative blood cultures
-CT-guided open biopsy
-Culture bone
- aerobic, anaerobic, and fungal agents
histopathology

high suspicion with negative blood and tissue culture
Broad-range PCR analysis

34
Q

treatment of Osteomyelitis

A

acute osteomyelitis :
antibiotic alone

Chronic osteomyelitis:
-Antibiotics and debridement surgery

internal fixation infection therapeutic aim
-consolidation of the fracture
-prevention of chronic osteomyelitis
-stable implants can be maintained

vertebral infection therapeutic aim
-elimination of the pathogens
-protection from further bone loss
-relief of back pain
-prevention of complications
-stabilization if needed

35
Q

acute osteomyelitis treatment plan

A

Consultation:
ID
neuro/spine surgery
orthopedics

IV vs PO antibiotic regimine:
Optimal spectrum
bioavailability
Efficacy
normal intestinal function
no vomiting

Duration of antibiotic therapy:
4-6 weeks
regimen dependent on culture results
empirical coverage
vancomycin and cefepime