Muculoskeletal Flashcards Preview

253-Green Patho > Muculoskeletal > Flashcards

Flashcards in Muculoskeletal Deck (59)
Loading flashcards...

Describe the layers of bone

Periosteum (soft covering with blood vessels)
Cortical, or Hard Bone (osteon)
Cancellous, or Spongy Bone (trabecular)
Bone Marrow (Blood cell producing)


Describe key cells of bone

What do the bone cells do?

Types of bone cell include osteoclasts, which break down bone tissue; osteoblasts, which build new bone tissue; osteocytes, which hold the bone together; and lining cells, which protect the bone.

The bone cells do many things for the skeletal system, such as the development of new bones and continual bone remodeling (the maintenance of bones and the homeostatic regulation of minerals in the body



• Low Bone Mass (loss of matrix/components)
• Porous bone
• Bone atrophy
• Bone becomes Fragile -> fractures common complication


Describe the Etiology of Osteoporosis

• Ageing
• Genetic Predisposition
• Endocrine changes (hormone levels and action change, Estrogen inhibits resorption)

• 2 major Risks
o Low peak bone mass (~30yrs= Max PBM)
o Post Menopause (INC in bone loss r/t E DEC that normally inhibits breakdown)


Describe the two types of bone remodelling

Bone remodeling (or bone metabolism) is a lifelong process where mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed (a process called ossification or new bone formation. (Pg 1442)


Describe Patho (i.e. progression) that lead to Osteoporosis

• Peak mass at ~30yrs
• Longitudinal bone growth stops at ~20 yrs
• Imbalance of formation and resorption
• INC loss post menopause
• Micro damage sets in from pressure/trauma


Describe MNFTS of Osteoporosis.

• Often silent until a fracture occurs (XR will show advanced osteo)
o Acute, severe pain

• Damage to vertebrae
o Change in Stature
o Distorted spine
o Breathing problems (r/t position)

Dentation problems


Dx of Osteoporosis

• Xray (shows later stages)
• Bone density Scan (using light to determine density in different skeletal areas- lumbar, radius and neck of femur key indicators)
o Result shown as a T value (1- 2.5) High = More porous


Tx Osteoporosis

• Prevent fractures
• Pain and disability
• Wt bearing activity (avoid injury/overexertion)
• Antiresorptive agents (osteoclasts)
• Anabolic agents (osteoblasts)
• Well balanced nutrition (Ca, Vit D and Calories)


What is Osteoarthritis

(Areas affected, progression)

• Degenerational joint disease (joint wear and tear, but other factors present)
o l/o cartilage and subchondral bone
• Weight bearing joints more affected
• Usually non inflammatory damage
• Slow progression


Etiology of Osteoarthritis

Differentiate primary and secondary

• Primary is idiopathic (but theories exist)
o Wear and tear with aging
• Genetic predisposition
o Suggests there may be genes that impact cartilage maintenance and minor repair proteins in cartilage.
o Easier cartilage dmage and poor repair

• Secondary
o Injury, obesity, repetitive motion, etc.
• NOTE: obesity increases wt bearing impact but also is considered a low grade inflm disease which impacts joint health


Describe physiologic joint Fx

 Chondrocytes maintain cartilage
 Articular cartilage (smooth cartilage + fluid reduces friction and had ability to withstand force [wt bearing])
• Dissipates force to bone


Pathology of Osteoarthritis

 Composition and properties of cartilage change -> cytokines (TNF and interleukins) -> proteases (excessively) -> destruction of cartilage

Chondrocyte damage -> impaired ability to heal cartilage

Cartilage deteriorates -> unprotected bone -> sclerosis (stiffening/hardening) of bone

Cysts (hollow/fluid) and fissures appear as fluid enters cracks in bone

Osteophytes form (projections/bone lesion) (worsen articulation) -> joint enlarges and deforms (see 59-6 for process)


MNTFS of Osteoarthritis

• Initial : non localized aching pain
• Later: activity related wt bearing pain (eventually constant)
• Crepitus
• Movement hurts, no movement joint stiffen
• Stiff Inflm joints


Dx of Osteoarthritis

• Hx and Px (no single test)
• X ray (not always useful)
• Labs (Inflm markers?, more simply eliminating other possibilities like septic arthritis, gout or other forms)


Tx of Osteoarthritis

Differentiate common vs severe

• Cartilage is not replaceable
• Monotherapy PRN (One at a time)
• Tylenol (1rst choice)
• Cox 2 inhibitors (inhibits enzyme cyclo-oxygenase)
( Cox 2 mediates/advances Inflm and leads to production of prostaglandins (pain)

• Severe: intra articular injection (often quick short term relief, but side effects means minimal long term use)
• Rehabilitation (physio)
• Sx- joint replacement


What is Rheumatoid arthritis

• Chronic autoimmune CT disease
o Inflm, deformed synovial joints


Etiology of Rheumatoid arthritis

• Multifactorial (complex trait)
• Genetic predisposition and Viral trigger? (Epstein Barr) (MHC/HLA + Trigger)


What is a type 3 Hypersensitivity

• Type3 H- IC are not destroyed by enzymes as normal-> into blood stream-> enter cap-> embed in Cap wall (throughout body)
• Impedes filtration + abnormal deposit (macrophage will destroy deposit) =Inflm
• Type 3 H is proceeded by infection


Patho of Rheumatoid arthritis

Do B cells or T cells cause Inflm? How?

• Altered T cell response -> targets synovial membrane (initially) -> inflammation and joint damage
• Altered B cells -> Abs production (rheumatoid factors RF) -> target tissues (connective in joints, later connective elsewhere in body)
• RF form IC’s -> deposit in synovial membrane -> Inflm

IGG (ab) - IGRF (Ag)


What does repeated inflm in joint bring about in Rheumatoid arthritis?

• Repeated Inflm -> deformity (granulation tissue – not normal in joint, more harm then good)

• Pannus (vascular, granulation tissue)
o Releases destructive enzymes
o Source if damaging Inflm cells
o Dec joint mobility (less space, more Inflm)


Examples of joints deformity cause by rheumatoid arthritis?

EX: Swan neck deformity, Ulnar drift/shift (Other MNFTS 59-2)


MNFTS of Rheumatoid arthritis

• Subtle onset
o Low grade fever malaise
• Increasing fatigue
• AM joint pain
• Stiffness after inactivity
• Non articular (as it progresses…could take decades)
o Heart, blood vessels, skin, lungs, eyes


Dx of rheumatoid arthritis

• Hx, Px (exclude other diseases)
• Xray and labs (like ANA... but limited use)
• Rheumatoid factor (only 75% of those with RA are positive in test)


Tx of rheumatoid arthritis

• Limit progression
• Pain (eg meloxicam or naproxen (NSAID)
• Start with plaquenil (eye exam q 6-12m- related to side effect) (its anti Inflm and immunomodulatory (anti malarial pill normally)
• Usually combination therapy e.g.
o Sulfasalazine( seen in IBD) and methotrexate (also used in IBD, CA Tx) (CBC, liver Es (liver damage) and Creatinine monthly)


What is Gout

crystal induced joint disease

R/t Uric Acid deposits in joints (by product of protein break down. Inflm occurs during removal by defense cells


Differentiate Primary and Secondary Gout

• Primary
o 90% of gout
o Metabolic (Purines-Adenine and Guanine)
o Mostly in Men
• Secondary
o Cell destruction (cell turnover… malignancies etc)
o Impaired Renal fx (poor excretion of by product)
o Others (beer and alcohol consumption, chemo)


Patho of Gout

• Altered purine metabolism -> Asymptomatic hyperuricemia

• Later: crystals deposit in synovial joints

• WBC influx and complement activation

• WBC phagocytize crystals -> WBC necrosis -> E release -> Inflm joint damage

• Recurrent acute attacks -> Tophi lesions (Tophus formed by accumulation of uric acid crystals, space occupying lesions)


Outline 5 Stages of Gout

1) Asymptomatic Hyperuricemia

2) acute Inflm and pain (overnight, 1 joint – usually large toe)
• uric acid crystalizes in synovial fluid not blood
• Toe also colder, plus inactivity overnight = crystallization
• Often following heavy meal or alcohol binge (high (purine content in beer) High intensity exercise (r/t protein breakdown)

3) Subsides in a week (with anti infm treatment)

4) Asymptomatic for months to years after)

5) Frequent recurrent attacks -> Permanent damage


Dx of Gout

• Serum and urine uric acid
• Uric acid in joints (Xray- more specific)