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Flashcards in Muculoskeletal Deck (59)
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Tx of Gout

• Acute attacks: Pain and Inflm
o Colchicine (limits leukocyte migration to joint)
o Steroids

• DEC hyperuricemia
• INC Uric acid excretion
• Eliminate alcohol
• Dec protein in Diet


What is Muscular Dystrophy

• Skeletal Muscle degeneration (progressive) (later other muscle- Ex: heart)
o d/t atrophy, necrosis and pseudohypertrophy
• Not true muscle tissue, but instead adipose tissue


What are the types of muscular dystrophy based on?

What is the most common type?

• Types Based on
o muscle group, Age (0-60yrs)
o Rate of progression
o mode of inheritance

• Duchenne MD is most common
o 1 in 35000 (mainly males)


Et of Muscular Dystrophy

• Recessive, x linked trait
o (Male has only one X, only need one to cause disease, female other X will override disease...i.e. recessive)
o Mother is carrier to son

Note: Gene is on short arm of X chromosome


Where is the affected gene in Muscular dystrophy and what does it code for?

Gene is on short arm of X chromosome

Codes for DYSTROPHIN (Protein on membrane of muscle)
o Provides attachment of contractile filaments


Patho fo Muscular dystrophy

• Mutation-> altered protein -> poor contractile proteins attachment -> fiber necrosis with use -> poor repair and regeneration -> more necrosis -> Ca influx (into muscle) and E release (i.e. Creatine Kinase CK)
• Fibrofatty CT replaces muscle tissue
• More muscle use, increases Inflm damage


MNFTS of Muscular Dystrophy

• Asymptomatic until 2-3 yrs
• Progression of muscle weakness
• Respiratory and Cardiac muscle affected
• Usually death associated with resp or Cardiac complications


Dx of Muscular Dystrophy

• Hx
• Voluntary movement limited
• Serum CK (muscle damage marker)
• Biopsy (looking for dystophin)
• Carrier screening for gene


Tx for muscular dystrophy

• No cure
• Supportive and symptomatic care
• Provide for comfort and fx


What intake cause INC in Nitrogenous compounds?

Protein catabolism


Are secondary or primary bone cancers more common?

Secondary- large well vascularized


Describe some different kinds of Bone CA. How are they categorized? Which is the most common?

Osteosarcoma (most common)
• A Bone forming tumor (Bone cells)

Chondrosarcoma (cartilaginous cells)

Fibrosarcoma (fibrous cells)

(Osteoclastoma or Ewings)

Based on cell type (and aggression)


Where and in whom does Osteosarcoma generally present?

Is it Aggressive or slow progression?

• Usually in vicinity of knee
o Often in metaphysis of nearby long bone

• 75% before age of 20
o Older individuals with CA will general have other bone diseases

• Aggressive (metastasis to lung)


Describe Secondary Bone CA

(Incidence, Types of Lesions and common Primary sites)

• Bone is common secondary site
o ~50% of all CA spreads to bone
o > 85% from breast, lung and prostate

• lytic or blastic lesions
o Lytic- Malignant cells release enzyme/mediators that breakdown tissue

• Pain, swelling, fractures


Diagnosis of Bone CA

• X ray, CT, MRI
o Xray requires substantial bone change/damage to be visualized
• Biopsy
• Bone Scan (will only tell you density)


Tx of Bone CA

• Triad of Tx
• Block excision (tumor plus surrounding tissue) AND Restorative Grafting
• Amputations
• Deal with pain and prevent fractures


Describe the basic of how fractures are classified

• Most common bone lesion, break in continuity of bone
• Many classifications
o Cause, location, pattern, type
• Simple (closed)
• Compound (open) (pushes through skin)


Fraction descriptions by type

• Greenstick
o 1 broken and 1 bent surface
o In children (why?) -> Bone not fully matured, more flexible

• Pathologic
o d/t bone disorder (eg osteoporosis)

• Comminuted
o Multiple breaks at single site (fragments)


Fractures by pattern

• Oblique
o (break at around 45 degrees)
o d/t twisting force (e.g twisted ankle)
• Longitudinal
o Longitudinal break line


Fractures by appearance

• Burst fracture
o Bone breaks into multiple pieces
o Usually at end of bone

• Chip
o Often Small fragment near joint

• Displaced
o Bone separates at fracture line


Other common fracture names we discussed in class

Colees- wrist
Potts, distal fibula
Compression fracture on vertebrae


What causes a fracture (etiology)

Force overload on bone


MNFTS of Fracture

• PAIN (+swelling)
• Deformity
• l/o fx
• Hemorrhage (always bleed if not seen it’s in the bone, also first step of healing process
• Soft tissue injury


Fracture Tx

• Reduction (align bones)
• Immobilization and healing
• Preserve and restore Fx (physio)


State 4 stages of Fracture healing

(Descriptions later)

Hematoma formation

Soft Callus formation

Bony Callus Formation



Describe Hematoma Formation

AKA Blood clot
• 48 to 72hrs
• Gelatenous, provides some stability and begins alignment on bone ends
• Provide a framework/medium for cellular signaling through mediators
• Seals the fracture site
• Inflm cells appear (physiologic)
• Necrosis and removal of bone


Describe Soft Callus formation

• Characterized by appearance of fibrocartilage
• Granulation tissue (physiologic) to allow formation of new blood vessels Angiogenesis
• Appearance of Fibroblast and collagen
• Capillary buds give rise to new vessels


Bony Callus Formation

• Cartilage changes to spongy bone.
• Bone trabeculae
• Not yet weight bearing
• Osteoblasts appear in higher number



• Secondary remodeling builds bone back to original appearance (likely still some deformity)
• Extra material removed, spongy bone to compact bone