▪ Review clinical manifestations of musculoskeletal diseases

▪ Explain the pathophysiology of bone fractures & osteoporosis

▪ Explain the pathophysiology osteomyelitis

▪ Explain the pathophysiology and types of osteoarthritis

▪ Explain the pathophysiology of impaired uric acid metabolism and gout

▪ Explain the pathophysiology of fibromyalgia

▪ Explain the pathophysiology of various skin lesions

▪ Explain the pathophysiology of pressure ulcers

▪ Explain the pathophysiology of scleroderma

▪ Explain the pathophysiology of burn

▪ Explain the pathophysiology of common inflammatory disorders of the skin and psoriasis

▪ Explain the pathophysiology of common skin cancers

▪ Bone tissue is a solid connective tissue (review anatomy and physiology of bone tissue)

– Cartilage is avascular while bone is very vascular

o This is why intraosseous access can be effectively used for emergency vascular access in emergency and trauma situations where vascular access is not possible

– The osteocyte is the “Mother Cell” for bone tissue

▪ Review of anatomy and physiology of the Integumentary System

Bone Fractures

▪ A fracture is a break in the continuity of a bone

Classifications:

▪ Complete or incomplete

▪ Closed or open

▪ Comminuted

▪ Linear

▪ Oblique

▪ Spiral

▪ Transverse

▪ Greenstick – children (just a bend)

▪ Pathologic

Pathophysiology:

▪ Broken bone causes damage to surrounding tissue, periosteum, and blood vessels with hematoma formation

– Inflammation process begins

▪ Bone tissue destruction triggers an inflammatory response and repair (callus formation)

Clinical manifestations:

▪ Numbness up to 20 minutes following injury

▪ Swelling, tenderness, pain, impaired sensation, muscle spasms, malalignment

Osteoporosis

▪ Porous poorly mineralized bone

Etiology:

▪ Decreased levels of estrogen and testosterone. Common in postmenopausal women (estrogen is an anabolic hormone)

▪ Inadequate levels of vitamin D (osteomalacia)

▪ Decreased physical activity level (age-related)

▪ Excess intake of caffeine, phosphorus, alcohol, nicotine

▪ Drug-induced eg glucocorticoids

Clinical manifestations:

▪ Bone aches, weakness & deformities, fractures

Pathophysiology:

▪ Reduced bone mass/density and an imbalance of bone resorption and formation

– Normal bone density = >833mg/cm2

– Osteopenic bone = 833-648 mg/cm2

– *Bone density <648 mg/cm2 = osteoporosis

Diagnostic Evaluation and Testing

▪ Bone histology:

– Usually normal but lacks structural integrity

– Thinning and perforations ▪ Bone densitometry (dual-energy x-ray absorptiometry [DXA, DEXA]) – Simple imaging test for determining bone density – Common in the diagnosis of osteoporosis

Osteomyelitis

▪ Bone infection with progressive inflammatory destruction, usually from bacteria

▪ Very serious

Etiology:

▪ Staphylococcal infection:

– Open wound (exogenous)

– Blood-borne (endogenous)

Risk factors:

▪ Trauma/surgery

▪ Immunocompromised patients

▪ Diabetes mellitus

▪ Poor vascular supply

▪ Peripheral neuropathy

Pathophysiology and clinical manifestations

▪ Acute or chronic inflammation

▪ Necrotic bone

▪ Pain, erythema, tenderness, swelling± abscess

▪ Fever

– Can be a cause for fever of unknown origin (FUO)

Osteoarthritis

▪ Inflammatory/degenerative joint disease

Etiology:

▪ Primary disease is idiopathic

▪ Genetic, biochemical, and biomechanical factors

Risk factors:

▪ Joint trauma, long-term mechanical stress

▪ Endocrine disorders (hyperparathyroidism)

▪ Obesity, aging

Pathophysiology:

▪ Local areas of degeneration and loss of articular cartilage

▪ Increased production of pro-inflammatory cytokines

▪ Tissue catabolism exceeds repair

▪ Thickening of the joint capsule

▪ Formation of bone spurs (osteophytes)

▪ Variable degrees of synovitis (inflammation of the synovial membrane)

Clinical manifestations:

▪ Pain (worsens with activity)

▪ Stiffness (diminishes with activity)

▪ Swelling of the joint

▪ Tenderness

▪ Limited mobility

▪ Deformity

Rheumatoid Arthritis

▪ Systemic inflammatory/autoimmune disease primarily affecting joints

Etiology:

▪ Multifactorial with strong genetic predisposition

▪ Association with HLA-DR4

– HLA (Human Leukocyte antigen) OR MHC (major histocompatibility complex):

o Group of proteins coded for by genes on chromosome 6 that makes for our tissue identity.

– There are 6 sets of genes in HLA forming two classes HLA I and II the pattern of which make us each unique.

o Class 1 = A, B, C.

o Class 2 = DR, DQ and DP.

– HLA typing/matching is required in organ transplantation to avoid/ reduce graft rejection

Pathophysiology:

▪ Primary site is synovial membrane

▪ Antibodies formed against joint tissue

▪ Type IV hypersensitivity (T cell mediated)

▪ Inflammatory cells, exudate & cytokines (TNF-α) leading to destruction of cartilage/bone

▪ Abnormal layer of granulation tissue (pannus)

– Pannus = granulation tissue that replaces the gaps on destroyed tissue.

Clinical manifestations:

▪ Insidious onset

▪ Affected joints: initially Wrists, MCPs, MTPs

▪ Symmetric joint involvement

▪ Morning stiffness

▪ Constitutional symptoms

▪ Joint deformities

▪ Subcutaneous nodules

▪ Presence of RF (rheumatoid factor) and ANA (antinuclear antibody) in serum

▪ *Specific criteria for diagnosis, published in the Journal of Arthritis and Rheumatology (“2010 Rheumatoid arthritis classification criteria” can be found at https://onlinelibrary.wiley.com/doi/full/10.1002/art.27584

Ankylosing Spondylitis

▪ Inflammatory joint disease of the spine or sacroiliac joints causing stiffening and fusion of joints (LOSE CURVATURE IN SPINE)

Etiology:

▪ Unknown

▪ Strong association with HLA-B27 antigen

Pathophysiology:

▪ Inflammation of fibrocartilage

▪ Inflammatory cells and fibrocartilage erosion

▪ Repair and scar tissue

▪ Calcification leading to joint fusion

Clinical manifestations:

▪ Early symptoms:

– Low back pain that begins in early 20s and progresses over time

– Stiffness

– Pain

– Restricted motion

▪ Loss of normal lumbar curvature (lordosis)

▪ Increased concavity of upper spine (kyphosis)

Gout

▪ Metabolic disorder that disrupts the body’s control of uric acid production or excretion

Etiology and Pathophysiology:

▪ Accelerated purine breakdown OR poor uric acid secretion in the kidneys

– Purines (nitrogenous bases) are required in DNA synthesis which is needed for cell division.

– With cell damage/death, there is breakdown of purines → increase in uric acid production

– Uric acid buildup is also caused by cancer chemotherapy

– Uric acid transforms into urea in order to be excreted via the kidney

– Uric acid buildup → hyperuricemia → deposition in various tissue

MTP (Metatarsophalangeal) joint of big toe (50% of initial attacks)

▪ Heel, ankle, instep of the foot, knee, wrist, or elbow

Risk factors:

▪ Male gender

▪ Increasing age

▪ High intake of alcohol, red meat, and fructose

▪ Drugs

Clinical manifestations:

▪ Recurrent attacks of monoarticular arthritis

▪ Tophi: deposits of urate crystals in and around joints

▪ Renal disease: glomerular, tubular, interstitial, vascular

▪ Renal stones

▪ Acute gouty attack:

– Severe pain, especially at night, with hot, red, tender joint & signs of systemic acute inflammation

Fibromyalgia

▪ Chronic widespread diffuse non-articular pain associated with fatigue and characteristic tender points. No joint pain.

Pathophysiology/clinical features:

▪ 80% to 90% are women, ages 25-45 yr, some adolescents

▪ Genetic predisposition: defective serotonin, catecholamines, and dopamine genes

▪ CNS sensitization

▪ Autoimmune disorders often coexist

▪ Overlaps with chronic fatigue syndrome and myofascial pain syndrome

Clinical manifestations:

▪ Diffuse, chronic (>3 mo) pain (burning/gnawing)

▪ Pain often begins in one location, especially neck and shoulders, then becomes more generalized

▪ Profound fatigue

▪ Increased sensitivity to touch

▪ Absence of inflammation

▪ Sleep disturbances / non-restorative sleep

Diagnosis

▪ Tenderness in eleven pairs of tender points along with a history of diffuse pain

▪ Diagnostic criteria*

Bone Tumors

▪ Can have different origins:

– Osteogenic: from bone cells

– Chondrogenic: from cartilage (chondroblast)

– Collagenic: from fibrous tissue (fibroblast)

– Myelogenic: from vascular tissue/marrow

Osteosarcoma

▪ Adolescents and young adults

▪ 38% of bone tumors

▪ Seniors with a history of radiation therapy

▪ Metaphysis of long bones

▪ Masses of osteoid

Chondrosarcoma

▪ Middle-aged and older adults

▪ Infiltrates trabeculae in spongy bone

▪ Metaphysis or diaphysis of long bones

▪ Lobules of hyaline cartilage

Fibrosarcoma

▪ Firm, fibrous mass of collagen, fibroblasts, and osteoclast-like cells

▪ Metaphysis of femur or tibia

▪ Lung metastasis is common

Myelogenic tumors

▪ Giant cell tumor

– Extensive bone resorption because of the osteoclastic origin of the giant cells

– Epiphyses of the femur, tibia, radius, or humerus

– Slow growth rate

Multiple Myeloma*

Muscle Tumors

Rhabdomyosarcoma

▪ Malignant tumor of striated muscle

▪ Usually muscles and CT in the eye, tongue, neck, larynx, nasal cavity, axilla, vulva, and heart

▪ Highly malignant with rapid metastasis

Disorders of the Integument

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