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Advance Pathophysiology > Lecture 7 Musculoskeletal & Rheumatological > Flashcards

Lecture 7 Musculoskeletal & Rheumatological Flashcards

1
Q

What does a ligament connect?

A

Connects bone to bone

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2
Q

explain the mechanism of injury to ligaments

A

1) injury = sprain
2) suddden overstretching, ROM, trauma
3) microfailing injury occurs before total failure

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3
Q

Grade 1 of ligament injury

A

Grade 1 = mild injury, stretching without instability
Tx: Rest, ice, compression, elevation, limit activities

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4
Q

Grade 2 of ligament injury

A

moderate, severe injury with a partial tear and instability
Tx: RICE, immobilize, pain management, promote recover/PT

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5
Q

Grade 3 of ligament injury

A

complete tear of ligament, significant swelling, bruising, pain, joint instability
Tx: surgical intervention, immobilization, pain management

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6
Q

What does a tendon connect

A

Bone to muscle

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7
Q

what type of injury is associated with tendon

A

Injury = Strain (think T for tendon)

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8
Q

Explain the pathophysiology of a strain

A

Injury occurs when stress surpasses the capability of the fibrous cords
Minor strain -> leads to complete tear/rupture

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9
Q

What is tendinitis

A

Inflammation of the tendon within sheath d/t injury/infection
S/Sx (all localized)
Aching at point of tendon attachment
Restricted joint motion
Pain with active ROM
Tx:
RICE, PT, corticosteroid injection

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10
Q

What is a joint capsule

A

Sac-like structure surrounding the synovial joint
Outer fibrous layer for structural support
Inner membrane for producing lubricating synovial fluid
Stabilizes the joint

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11
Q

Pathophysiology of a joint capsule injury

A

Fibrinous tissue builds up
Effusion can occur
ROM decreases (reduced capsular redundancy)
Prolonged immobilization -> capsule contraction (ex. Frozen shoulder)
Tx:
Injected corticosteroids to reduce the inflammation

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12
Q

Bone fractures (draw them out)

A

Displaced, non displaced, complete, incomplete, opne/compound

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13
Q

Types of fractures (draw them out)

A

transverse, spiral, longitudinal, oblique, conmminuted, impacted, stress, avulsion

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14
Q

Steps in the process of bone healing

A

1) hematoma formation
2) Fibrocartilaginous Callus Formation
3) Bony Callus Formation
4) Bone Remodeling

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15
Q

explain hematoma formation

A

Immune cells are stimulated to remove damaged tissue
Inflammatory response occurs over the course of 1-7 days
Vascular Endothelial Growth Factor (VEGF) released
Stimulates new blood vessel growth

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16
Q

Explain Fibrocartilaginous Callus Formation

A

Soft Callus Formation (Week 1-3)
Primarily composed of cartilage -> bridges any fracture gaps to stabilize bone
New blood vessels begin to grow into the area from VEGF
Mesenchymal stem cells differentiate to:
Fibroblasts
Chondroblasts (cartilage)
Osteoblast

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17
Q

explain Bony Callus Formation

A

Cartilage calcifies and is replaced by woven bone to create hard callus and stabilize the bone/restore strength
RANK-L
Protein that stimulates functionality of:
Chondroblasts
Chondroclasts
Osteoblasts
Osteoclasts
Cartilaginous callus reabsorbed, bone laid down
Proliferation of blood vessels
Calcification of callus and immature bone

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18
Q

Explain bone remodeling

A

Migration of osteoclasts/blasts
Balances resorption and formation
Replaces the callus with bone

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19
Q

what are the different types of complication in healing

A

delayed, fat emboli, DVT, osteomyelitis, compartment syndrome, osteonecrosis

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20
Q

What is delayed healing for 400

A

Dependent on amount of local damage done, secondary infection, systemic circulatory issues, nutritional issues
Medications (glucocorticoids suppress inflammation and healing)
Malunion
Bone fusion, improper alignment
Nonunion
Greater than 6 month delay in fusion

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21
Q

what is fat emboli for 600

A

Fat particles released from bone marrow
Especially pelvis and long bone fractures
24-72 hr after injury
S/Sx: similar to that of a pulmonary embolism/ other emboli
+ petechial rash (Check torso, axilla, conjunctiva), altered mental status
Dx:
CT PE, V/Q scan, CXR

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22
Q

what is DVT for 200

A

Formation 5+ days after injury (clot breaking off)
Increased risk d/t:
Multiple fractures, pelvic and long bone fractures, immobility, obesity, hx of clots, hypercoagulable disorders
Prevention
Early mobilization
VTE prophylaxis measures

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23
Q

what is osteomyelitis for 200

A

Infection of bone and local tissue through bacteremia or trauma/open wound in surrounding area
Indirect or direct introduction of foreign organism into bone
Usually from staph aureus
S/Sx:
Children
High fever, pain at site of bone involvement
Adults
More subclinical features
Fever, malaise, anorexia, night sweats, weight loss

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24
Q

what is compartment syndrome for 500

A

Accumulation of pressure in the soft tissue compartment
Decreases perfusion (by 30-40 mmHg) -> ischemic -> hypoxia and necrosis
Intrinsic or extrinsic causes (ex. Cast around limb)
S/Sx: 6 P’s
Pain (out of proportion to injury)
Paralysis
Paresthesia
Pallor
Poikilothermia (cool to touch)
Pulselessness
Tx:
Medical emergency!
Fasciotomy
Relief of pressure

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25
Q

what is osteonecrosis for 125

A

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

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26
Q

Types of metabolic bone disease

A

osteoporosis, hyperparathyroidism, renal osteodystrophy, Paget’s disease

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27
Q

Osteoporosis pathophysiology

A

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)

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28
Q

Osteoporosis Dx

A

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)

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29
Q

Osteoporosis s/s

A

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

30
Q

Osteoporosis Tx

A

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

31
Q

Hyperparathyroidism

A

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.

32
Q

Renal Osteodystrophy
pathophysiology

A

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!

33
Q

Renal Osteodystrophy. s/s

A

Bone pain and deformities + fractures
Muscle weakness
Impaired growth

34
Q

Renal Osteodystrophy Tx

A

Phosphate binders
Vitamin D analogs
Dialysis or parathyroidectomy

35
Q

Paget’ DIsease

A

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)

36
Q

Bone tumor prefixes

A

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

37
Q

Bone tumors s/s

A

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

38
Q

Osteosarcoma

A

Malignant
Bone forming
Pelvis and long bones of arm and legs

39
Q

Chondrosarcoma

A

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

40
Q

Ewing’s Sarcoma

A

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

41
Q

Osteochondroma

A

Benign
Cartilage forming
Occur in any bone formed by cartilage

42
Q

Giant Cell Tumor

A

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

43
Q

Rheumatoid Arthritis (RA) pathophysiology

A

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

44
Q

Rheumatoid Arthritis (RA) s/s

A

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

45
Q

Rheumatoid Arthritis (RA) Tx

A

DMARDs (antirheum)
NSAIDs
Corticosteroids

46
Q

Rheumatoid Arthritis (RA) Foss

A

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.

47
Q

Osteoarthritis (OA) Pathophysiology

A

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

48
Q

Osteoarthritis (OA) S/S

A

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

49
Q

Osteoarthritis (OA) Tx

A

NSAIDs to decrease pain and swelling
Joint injections
surgery

50
Q

Osteoarthritis (OA) Foss

A

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.

51
Q

Ankylosing Spondylitis pathophysiology

A

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

52
Q

Ankylosing Spondylitis s/s

A

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

53
Q

Ankylosing Spondylitis tx

A

NSAIDs
Topical corticosteroids
Avoid sun exposure (trigger)
Immunosuppressive agents

54
Q

Infectious arthritis pathophysiology

A

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

55
Q

Infectious arthritis s/s

A

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

56
Q

Infectious arthritis tx

A

Antibiotic therapy
Joint drainage

57
Q

Gout pathophysiology

A

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

58
Q

Gout attack

A

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

59
Q

Gout phase 1 asymptomic hyperuricemia

A

Asymptomatic hyperuricemia
Avoid purine rich foods and alcohol

60
Q

Gout phase 2 Acute gouty arthritis

A

Confirm with synovial aspirate of urate crystals

61
Q

gout phase 3 Intercritical gout

A

Ongoing process (crystals still found in synovial fluid)

62
Q

gout phase 4 Chronic tophaceous gout

A

Urate crystal deposit (tophi); chronic inflammation

63
Q

gout Tx

A

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

64
Q

Idiopathic Inflammatory Myopathies

A

Chronic muscle inflammation and weakness
Acquired, incurable
Systemic autoimmune disease

65
Q

Polymyositis

A

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

66
Q

Dermatomyositis

A

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

67
Q

Duchenne (dystrophies) pathophysiology

A

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

68
Q

Duchenne (dystrophies) S/S

A

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

69
Q

Duchenne (dystrophies) Tx

A

Slow progression through supportive therapy and glucocorticoids

70
Q

Diseases of Metabolism -general effects

A

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

71
Q

Mitochondrial Diseases-general effects

A

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

72
Q

Calcium Channel Disorders- general effects

A

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

Advance Pathophysiology (7 decks)

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