Lecture 7 Musculoskeletal & Rheumatological Flashcards

Question

what is osteonecrosis for 125

Answer 1

Result of unmanaged/ineffectively treated osteomyelitis Necrotic bone can separate from healthy bone into dead segments called sequestra Tx: 4-6 weeks antibiotic therapy Debridement (abscesses) Amputation Involucrum formation blocks success of abx therapy Encapsulates sequestra

Answer 2

osteoporosis, hyperparathyroidism, renal osteodystrophy, Paget's disease

Answer 3

Rate of bone resorption exceeds bone formation Osteoclasts breaking down bone mineral and calcium to release into bloodstream Callus bone lost faster than cortical bone Etiology Hormonal/estrogen deficiency Poor calcium Disuse of bone (ex. Low amount of weight bearing exercise)

Answer 4

Bone Mineral Density (BMD) Scan DXA Scan T-Score < 2.5 Osteoporosis (increased likelihood of breakage) Btw -1.0 and -2.5 Osteopenia (decrease in bone mineral density)

Answer 5

Trabeculae (wavy matrix) decreased Width and bone mass decreased Fractures d/t fragility

Answer 6

Calcium and Vitamin D supplements Bisphosphonates Slow bone resorption PTH Weight bearing activity to strengthen bone

Answer 7

PTH -> stimulates Calcium release from bone States of elevated PTH activity Primary Secondary Ex. low blood calcium triggering release, dysregulation by pituitary, tumor secreting PTH, etc.

Answer 8

Bone Disorder resulting from impaired kidney function (CKD) Decreased renal function Hyperphosphatemia Decreased active Vitamin D Hypocalcemia d/t decreased intestinal calcium absorption Results in elevated PTH -> Bone breakdown!

Answer 9

Bone pain and deformities + fractures Muscle weakness Impaired growth

Answer 10

Phosphate binders Vitamin D analogs Dialysis or parathyroidectomy

Answer 11

Abnormal bone remodeling resulting in structurally disorganized bones Excessive remodeling (built too fast) Lowered structural integrity, hypertrophy Etiology unknown Viral or genetic components hypothesized S/Sx: Bone pain Skeletal deformities Fractures Fatigue and anemia (d/t elevated serum calcium)

Answer 12

Osteo = bone Chondro = cartilage Oma = tumor/swelling Sarcoma = cancer forming in body soft tissue

Answer 13

Localized Pathologic fracture Pain/swelling/mass Systemic Fatigue, weight loss, fever Lymphadenopathy

Answer 14

Malignant Bone forming Pelvis and long bones of arm and legs

Answer 15

Cartilage forming Occurring in cartilage of arm, leg, and pelvic bone Malignant transformation of benign bone tumors

Answer 16

Neither cartilage or bone forming Medullary cavity of pelvis and long bones (femur, humerus, tibia, clavicle)

Answer 17

Benign Cartilage forming Occur in any bone formed by cartilage

Answer 18

Tumors of Unknown Origin Neither cartilage or bone forming Derived from osteoclasts Can spread to lungs (unpredictable) S/Sx: Pain and pathologic fracture in cancellous ends of arm and leg bones

Answer 19

Autoimmune inflammatory disease Targets synovial joints Formation of pannus (inflamed granulation tissue) Erodes the cartilage and bone

Answer 20

Bilateral symmetric polyarthritis Red, warm, painful joints (smaller) Diffuse musculoskeletal pain Morning stiffness over 60 min Boutonniere and swan neck deformities d/t joint calcification and narrowing spaces

Answer 21

DMARDs (antirheum) NSAIDs Corticosteroids

Answer 22

For disease onset; in RA, pain typically develops quickly, over weeks or months. With RA, morning stiffness lasts longer than 30 minutes, often an hour or more. In RA, pain tends to be more constant and severe.

Answer 23

Breakdown of cartilage and underlying bone Joint pain and stiffness Mechanical etiologies

Answer 24

Morning stiffness ( about 30 min) Heberden/Bouchard nodes Bone spurs (osteophytes) Pain worsens with activity, relieved by rest

Answer 25

NSAIDs to decrease pain and swelling Joint injections surgery

Answer 26

In OA, pain develops gradually over years and is associated with chronic overuse of the joint (this is what the slide is referring to as “usage-related”) . Within the disease processes, there are variations in pain and stiffness patterns. In comparison with OA, morning stiffness typically improves within 30 minutes (with movement). Stiffness typically improves with use in OA, but once the activity is finished, it can reoccur and may be associated with an increase in pain. For OA physical activity can both increase and decrease pain. Some activity types can make acutely pain worse, while over time regular exercise/ can usually help improve overall symptoms. (Acutely, pain can worsen with activity and improve with rest)In OA, one of the things that can contribute to variations in symptoms and increased pain and stiffness with any movement is the development of bone spurs. As the cartilage breaks down and the bone edges wear and boney cysts form. Osteophyte activity is stimulated due to joint damage leading to excessive boney growth. Typically you see this along the joint edges and in weight bearing joints. Bone spurs alter the pain/stiffness presentation as they can alter the mechanics of movement within the joint space.

Answer 27

Multisystem inflammatory, autoimmune disease Progressive stiffness and fusion of axial skeleton Chronic inflammation leading to new bone formation -> resulting spinal fusion From B-lymphocyte overactivity

Answer 28

Arthralgias Synovitis Butterfly rash (from systemic consequence) Low back pain and stiffness, limited spinal mobility

Answer 29

NSAIDs Topical corticosteroids Avoid sun exposure (trigger) Immunosuppressive agents

Answer 30

Can mimic other arthritis and gout Etiology Can result from tick bite in area Usually from staph. aureus

Answer 31

Red, swollen, painful joint Synovium is edematous and forming exudate from infection Fever, chills Systemic infection

Answer 32

Antibiotic therapy Joint drainage

Answer 33

Inflammatory arthritis caused by urate crystals depositing in joints/joint spaces Hyperuricemia (necessary predisposing factor)

Answer 34

Acute attack Sudden onset of severe pain, redness, swelling, warmth of joint (usually great toe) Chronic gout Tophi formation (in soft tissue)

Answer 35

Asymptomatic hyperuricemia Avoid purine rich foods and alcohol

Answer 36

Confirm with synovial aspirate of urate crystals

Answer 37

Ongoing process (crystals still found in synovial fluid)

Answer 38

Urate crystal deposit (tophi); chronic inflammation

Answer 39

NSAIDs, steroids, colchicine (prophylactic or early tx) die modification low on purines Avoid rich meats, alcohol, and sugary drinks to lower your risk of gout flare-ups! Dammit Bobby

Answer 40

Chronic muscle inflammation and weakness Acquired, incurable Systemic autoimmune disease

Answer 41

Muscle weakness of neck (progress from proximal skeletal muscle) S/Sx: Dysphagia, dyspnea, dysphonia Tx: corticosteroids, immunosuppressives

Answer 42

Inflammatory myopathy characterized by muscle inflammation and skin rash From immune mediated muscle damage S/Sx: Gottron’s papules (raised red/violet lesions) Tx: IVIG, immunosuppressives, corticosteroids

Answer 43

Progressive muscle degeneration from impaired dystrophin production Lacking dystrophin leads to muscle fiber instability Progressive muscle weakness

Answer 44

Difficulty with motor tasks Gowers sign Children using hands to climb up from floor d/t weakness Progressive cardiomyopathy Respiratory failure Loss of ambulation by ~ age 12

Answer 45

Slow progression through supportive therapy and glucocorticoids

Answer 46

Abnormal metabolism of carbs, fats, proteins Enzyme deficiencies can lead to accumulation of toxic substrates or lack of essential biochemical products S/Sx: Neuro: developmental delay, seizure, neurodegeneration Muscle weakness Growth failure Manage with diet and enzyme replacement therapies

Answer 47

Defective energy production from mitochondrial gene mutation Oxidative stress and abnormal cell signaling Multisystemic Sx Neurological symptoms Cardiomyopathy (dilated or hypertrophic)

Answer 48

Abnormal channel activity resulting in disrupted muscle contraction/neurotransmission Muscle weakness and arrhythmia Hypotonia