Module 11: MSK Abnormalities (b) Flashcards

1
Q

Complete Fractures

-6 types

A
  1. Comminuted — bone breaks into more than 2 fragments
  2. Linear — Bone splits in two — LONG WAYS
  3. Oblique —Slanted fracture to shaft of bone
  4. Spiral — Encircles the bone — Twisting motion Fx
  5. Transverse — Perpendicular to long bone
  6. Pathological — Secondary to preexisting abnormality
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2
Q

Complete Fractures

-Comminuted Fx

A
  1. Bone breaks into more than two fragments
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3
Q

Complete Fractures

-Linear Fx

A
  1. Fracture runs PARALLEL to the long axis of the bone — Spits the bone in two LONG WAYS
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4
Q

Complete Fractures

-Oblique Fx

A
  1. Fracture of the shaft of the bone is slanted
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5
Q

Complete Fractures

-Spiral Fx

A
  1. Encircles the bone where there is often a TWISTING MOTION to cause the Fx
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6
Q

Complete Fractures

-Transverse Fx

A
  1. Fracture line perpendicular to long axis of the bone
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7
Q

Complete Fractures

-Pathological Fx

A
  1. Break that occurs at the side of a PREEXISTING ABNORMALITY such as tumors, osteoporosis or osteomyelitis
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8
Q

Incomplete Fractures

-4 types

A

Incomplete fractures are mostly in PEDIATRIC PATIENTS — Bones are more elastic**

  1. Greenstick Fx — Radius, ulna or humerus S/P FOOSH
  2. Torus Fx — Distal Radius Fx s/p FOOSH
  3. Bowing Fx — Radius and ulna affected s/p FOOSH
    —Have all of the above on differential in clinic
  4. Stress Fx — Repetitive or strenuous activity — runners and soldiers who carry 90-100 lbs on their backs while marching
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9
Q

Rhabdomyolysis

-Info/Causes

A
  1. Life-threatening complication of severe muscle trauma w/ muscle cell loss caused by:
    - Trauma —Compartment syndrome & Crush injury
    - Immobilization & prolonged muscle compression — Ex: intoxication (passed out pt’s), Stroke, elderly fall
    - Illicit drug use
    - Muscle Overexertion — Weekend warrior and untrained athletes that Go Hard
    - Certain meds — Statins, erythromycin, colchicine, corticosteroids
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10
Q

Rhabdomyolysis

-Patho

A
  1. Striated muscle is damaged causing rapid release or breakdown of muscle — Myoglobin and Potassium are released into blood stream and extracellular space
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11
Q

Rhabdomyolysis

-Clinical Manifestation “Classic Triad”

A
  1. Muscle pain
  2. Weakness
  3. Dark Urine (from myoglobin)

Complications

  • Hyperkalemia — can cause V fib or V tach
  • Metabolic Acidosis — Results from release of intracelular PHOSPHORUS & SULFATE
  • Acute Renal Failure — Myoglobin becomes precipita the in tubule and obstructs flow through nephrons causing renal damage
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12
Q

Rhabdomyolysis

-Complications

A
  1. Hyperkalemia — can cause V fib or V tach
  2. Metabolic Acidosis — Results from release of intracelular PHOSPHORUS & SULFATE
  3. Acute Renal Failure — Myoglobin becomes precipita the in tubule and obstructs flow through nephrons causing renal damage
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13
Q

Osteoporosis

-Types

A

Peak bone mass is around age 30.

  1. Primary Osteoporosis — Found in post menopausal women
  2. Secondary Causes
    - Men w/ osteoporosis — 20%
    - Include hormonal imbalances such as — endocrine disorders, DM, hyperparathyroidism, hyperthyroidism
    - Substances such as — corticosteroids, tobacco, alcohol
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14
Q

Osteoporosis

-Patho

A

Osteoporosis — poorly mineralized bone — Thick vertical trabeculae w/ absence of horizontal trabeculae

  1. Post-menopausal Osteoporosis
    - Influenced heavily by estrogen levels — Significant changes seen in post-menopausal women
    - Up to 20% of bone loss occurs w/in 1st 5 years of menopause.
  2. Estrogen stimulates osteoprotegerin (OPG) secretion. OPG down regulates osteoclast production — Less OPG means increased bone resorption
  3. Insulin-Like growth factor: Less production with aging
  4. Posphorus intake —Phosphorus intake, Ex in carbonated drinks, will cause imbalance between CA and Phos, resulting in weakened bones.
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15
Q

Osteoporosis

-Clinical Manifestations

A
  1. Pain — resulting from fx’s
  2. Bone deformity — Kyphosis is most common clinical finding
  3. Fx’s — results from brittle bones — Most serious are hip fx’s
  4. Diminished height
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16
Q

Osteoporosis

-Tx

A
  1. PREVENTION — KEY to preventing osteoporosis is to start early
    - Regular moderate weight-bearing exercises
    - Calcium intake sufficient
    - Sufficient intake of magnesium
17
Q

Osteoporosis

-Risk Factors

A
  1. Slender, female, Caucasian, alcohol users, smokers, & steroid users are at highest risk

Common Fx’s

  • Crush fx’s especially at T8 and below
  • Hip & Cole’s fx’s are most common
18
Q

Osteomalacia

A
  1. Deficiency of Vitamin D lowers the absorption of calcium from the intestines
  2. Bone formation progresses to osteoid formation, but calcification does not occur — result is soft bones
  3. Clinical Manifestations — Pain, bone fx’s, vertebral collapse, bone malformation
19
Q

Paget’s Disease

-Info

A
  1. Increased metabolic activity that ENLARGES and softens the affected bones
  2. Genetic and viral component
  3. Patho — State of increased metabolic activity in bone — Usually localized. Accelerated rate of bone formation and resorption
    - Usually affects the SKULL and bones of the axial skeleton
20
Q

Paget’s Dz

-Clinical Manifestations

A
  1. In the SKULL — Thickened portions can cause altered mental status and even dementia
  2. If thickening is where cranial nerves exit the skull, Manifestations include
    - Impaired motor function, deafness, atrophy of optic nerve
21
Q

Osteomyelitis

-Info

A
  1. Pyogenic (pus forming) bone infection usually caused by staph aureus
  2. Bacteria can either enter through
    - Exogenous — open fx are most common, penetrating wounds (punching someone in the mouth), surgical procedures
    - Endogenous — Bloodborne
22
Q

Osteomyelitis

-Phases

A

Phase 1. Infection spreads through the periosteum along bone shaft & into bone marrow — In adults it affects the cortex
Phase 2. Periosteum has lifted off the rest of the bone
Phase 3. Lifting of periosteum disrupts the bone’s blood supply and can cause DEAD BONE
Phase 4. INVOLUCRUM — new PERIOSTEAL bone formation
—Involucrum is rare in adults as periosteum is attached and doesn’t want to move
—In adults, infection weakens the CORTEX and makes pathologic Fx more likely

23
Q

Osteomyelitis

-Clinical Manifestations

A
  1. Acute and chronic inflammation
  2. Fever
  3. Pain
  4. Necrotic bone
    —BONE DEATH results from blockage of small vessels

Small channels like Haversian and Volkmann’s channels make defense in the bone difficult to mount

24
Q

Bone Tumors

-Origination

A
  1. Osteogenic — bone cells — Osteosarcomas
  2. Chondrogenic — cartilage
  3. Collagenic — From connective tissue
  4. Myelogenic — From Bone marrow
25
Q

Bone Tumors

-Consistent Findings in ALL malignant Bone Tumors

A
  1. Increased nuclear-cytoplasmic ratio
  2. Irregular bone borders
  3. Excess chromatin in the nucleus
  4. Prominent nucleolus (where biogenesis of ribosomes occur)
  5. Increase in the mitotic rate
26
Q

Osteoarthritis

-Info

A
  1. Degeneration and loss of articular cartilage, sclerosis of bone underneath cartilage, and formation of bone spurs (osteophytes)
    - Primary Dz is idiopathic
  2. Erosion/thinning of cartilage — bone on bone contact that creates significant pain
  3. Joint pain r/t overuse that is typically relieved by rest
  4. Joint stiffness (worse in the morning) & improves w/in about 30 minutes of movement
  5. Heberden nodes — DIP
  6. Bouchard nodes — PIP
27
Q

Rheumatoid Arthritis

-Info

A
  1. Inflammatory joint Dz — Systemic autoimmune damage to connective tissue, primarily in joints (Synovial membrane)
  2. Activation of adaptive immune system and the T & B cells — Stimulation of fibroblasts
  3. PANNUS formation — T cells actually stimulate synovial fibroblasts, and they convert the synovium into thick layer of granulated tissue
  4. Joint fluid presents w/ inflammatory exudate in synovial joint
  5. SYMMETRIC joint swelling, joint deformities of synovial joints — smaller distal joints are affected first — ulcer deviation & subcutaneous nodules
28
Q

Rheumatoid Arthritis

-Clinical Manifestations

A
  1. Systemic effects — Fever, Fatigue, Weakness
  2. Nodules in organs — Caplan syndrome — intrapulmonar nodules in the lungs
  3. Autoantibodies (RF) — 50-90% specificity and sensitivity
  4. Anti-citrullinated protein antibody (ACPA) — 95% specific
29
Q

Ankylosis Spondylitis

-Info

A
  1. Autoimmune inflammatory Dz — Causes abnormal BONE PRODUCTION
  2. Chronic inflammatory joint dz of the spine or sacroiliac joints — causes stiffening and fusion of joints — Primary site = ENTHESIS
30
Q

Ankylosis Spondylitis

-Patho

A
  1. Begins w/ inflammation of the fibrocartilage — vertebrae & sacroiliac joint
    - As repair begins, scar tissue ossified and calcifies — Narrows the spine = SPINAL STENOSIS
  2. Causes
    - Low back pain, stiffness, pain, restricted motion, loss of normal lumbar curvature
    - Elderly manifestation = back pain & spinal stenosis
  3. Treat w/ Physical Therapy
31
Q

Gout

-Info

A
  1. Metabolic disorder that disrupts the body’s control of uric acid production or excretion
  2. R/T purine metabolism
  3. Manifests high levels of urid acid in the blood and other body fluids
  4. Occurs when the uric acid concentration increases high enough levels to crystallize
32
Q

Gout

-Types

A
  1. Primary — etiology is unknown

2. Secondary — Pt’s diet — high purine foods —Ex: Organ meats, game meats

33
Q

Gout

-Mechanisms for Crystal Deposition TEST

A
  1. Crystals deposit in connective tissues throughout the body — called TOPHI**
  2. Mechanisms for crystal deposition **TEST
    - Lower body temperature
    - Changes in ion concentration and pH — ACIDIC environment
    - Trauma
34
Q

Gout

-Stages (3)

A

Stage 1: Asymptomatic hyperuricemia — High irate levels w/ NO SYMPTOMS — irate levels seen on blood draw

Stage 2: Acute gouty arthritis — Attacks actually develop and its a milder form

Stage 3: Tophaceous Gout — TOPHI deposition — Assess helix of the ear - MOST COMMON place for TOPHI**TEST