MSK (Final) Flashcards
(77 cards)
1
Q
Fractures
A
• breaks in the rigid structure of bone
• most common traumatic MSK disorder
• classified based on direction of fracture line, number of fracture lines, etc.
2
Q
Primary causes of fractures
A
falls
motor vehicle accidents
sports related injuries
3
Q
Secondary causes of fractures
A
conditions that weaken the bone (osteoporosis, Paget’s disease, bone cancer)
4
Q
Simple fracture
A
a single break with bone ends maintaining their alignment and position
5
Q
Transverse fracture
A
straight across the bone shift
6
Q
Oblique fracture
A
at an angle to the bone shaft
7
Q
Spiral fracture
A
twists around the bone shift
8
Q
Comminuted fracture
A
multiple fracture lines and bone pieces
9
Q
Greenstick fracture
A
an incomplete break in which the bone is bent and only the outer curve of the bend is broken
commonly occurs in children because of minimal calcification, and often heals quickly
10
Q
Compression fracture
A
bone is crushed or collapses into small pieces
11
Q
Complete fracture
A
broken into 2+ separate pieces
12
Q
Open/Compound fracture
A
skin is broken, bone fragments/edges may be angled and protrude out of the skin
causes more damage to soft tissue and increases risk for infection
13
Q
Closed fracture
A
skin is intact
14
Q
Impacted fracture
A
one end of the bone is forced into adjacent bone
15
Q
Pathologic fracture
A
results from a weakness in the bone structure secondary to conditions such as tumors or osteoporosis
16
Q
Stress/fatigue fracture
A
occurs from repeated excessive stress
common in the tibia, femur, and metatarsals
17
Q
Depressed fracture
A
occurs in the skull when the broken piece is forced inward on the brain
18
Q
Fracture healing
A
- hematoma (blood clot) forms
- necrosis of broken bone ends occurs from blood vessel damage
- fibroblasts invade the clot within a few days
- fibroblasts secrete collagen fibers, which form a mass of cells and fibers called a callus
- callus bridges the broken bone ends together inside and outside over 2-6 weeks
- osteoblasts invade the callus and slowly convert it to bone from 3 weeks to several months (usually 4-6 weeks)
19
Q
Fracture complications
A
• delayed union, malunion, nonunion (may occur due to poor nutrition, inadequate blood supply, malalignment, premature weight bearing)
• compartment syndrome
20
Q
Compartment syndrome
A
a serious condition that results from increased pressure in a compartment, usually the muscle fascia in the case of fractures
pressure impinges on the nerves and blood vessels present within compartment, potentially compromising the distal extremity
requires prompt identification and treatment to prevent permanent tissue damage
21
Q
Compartment syndrome manifestations
A
• excruciating pain that is beyond what would be expected given the injury
• 6 P’s (pain, parasthesia, poikilothermia (inability to regulate temp), pallor, paralysis, pulselessness)
22
Q
Fatembolism (fracture complication)
A
fat enters the bloodstream, usually after a long bone fracture (outcome can be fatal if emboli travel to vital organs)
M: hypoxemia, neurological dysfunction, petechia on head or trunk
PREVENTION=EARLY IMMOBILIZATION OF FRACTURE
23
Q
Osteomyelitis (fracture complication)
A
infection of bone tissue
can take months to resolve and result in bone or tissue necrosis
24
Q
Osteonecrosis/Avascular necrosis (fracture complication)
A
death of bone tissue due to loss of blood supply
can result from displaced fractures or dislocations
25
Route of infection to joint (osteomyelitis)
1. hematogenous route
2. dissemination from osteomyelitis
3. spread from adjacent soft tissue damage
4. diagnostic or therapeutic measures
5. penetrating damage by puncture or cutting
26
Fracture manifestations
• deformity (*angulation, shortening, rotation*)
• swelling and tenderness at the site
• inability to move affected limb
• CREPITUS!!!
• pain
• parasthesia
• muscle flaccidity progressing to spasms
27
Dislocations
separation of two bones at a joint
may be complete or partial (*subluxation*)
most common in shoulder and clavicle joints
**causes deformity, immobility, and damage to nearby ligaments and nerves**
28
Causes of dislocations
• sudden impact to the joint
• congenital conditions
• pathologic states (*arthritis, ligament injuries, paralysis, neuromuscular disease*)
29
Dislocation manifestations
• visibly out of place, discolored or deformed joint
• limited movement
• swelling/bruising
• intense pain, especially with movement or weight bearing
• paresthesia near the injury
30
Sprains
injury to a ligament that often involve stretching/tearing
severity described using a grading scale
most common in the ankle and knee
**CAUSES:** forcing a joint into unnatural position (*twisting ones ankle*)
31
Sprain manifestions
• edema
• pain
• bleeding
• joint stiffness
• limited function
• disability
• discoloration (*usually bruising*)
32
Strains
injury to a muscle/tendon that often involves stretching/tearing
may occur suddenly or develop over time
lower back most common site
**results from awkward muscle movement or excess force that can be caused by an accident, improper use of muscle or overuse of muscle**
33
Risk factors for strains
• excessive physical activity
• improper stretching prior to activity
• poor flexibility
34
Manifestations of strains
• pain
• stiffness
• difficulty moving the affected muscle
• skin discoloration (*often bruising*)
• edema
**severity described using a grading scale**
35
Herniated Intervertebral Disk (HID)
**protrusion of the nucleus pulposus through the annulus fibrosus**
• may occur suddenly or gradually
• can exert pressure on the spinal cord
• sensory, motor or autonomic function may be impaired depending on location
• most frequently involves the lumbosacral region, sometimes cervical disks
• can result in permanent neurologic damage if pressure on nerve tissue and/or blood supply is prolonged
36
HID Causes
• improper body mechanics
• lifting heavy objects
• repetitive use
• trauma
• vertebral stress secondary to obesity
• degenerative changes (*aging, demineralization*)
37
HID Manifestations
**may be asymptomatic**
• sciatica
• pain, parasthesia, or weakness in lower back and one leg, or neck, shoulder, chest, or arm
• low back pain or leg pain that worsens by *sitting, coughing, sneezing, laughing, bending or walking*
• limited mobility
38
Osteoporosis
**progressive loss of bone calcium that leaves bones brittle**
• can occur due to multiple pathogenetic mechanisms that interact to cause either a *decrease in osteoblast activity* or an *increase in osteoblast activity*
SPONGY BONE BECOMES POROUS (vertebrae and wrist) AND COMPACT BONE BECOMES THIN
39
Osteoporosis Causes
• genetic predisposition
• dietary imbalances (*low Ca, protein, vitamin C, vitamin D; high P*)
• hormonal fluctuations (*menopause, **LOW ESTROGEN AND TESTOSTERONE***)
• physical inactivity
40
Risk factors of osteoporosis
• advancing age
• female
• underweight
• undergoing GI procedures (*gastrectomy, GI bypass*)
• being white
• asian descent
• smoking
• excessive alcohol or caffeine consumption
• certain meds (*corticosteroids, chemo, thyroid replacements, heparin, antacids*)
• **certain health conditions (CUSHINGS, THYROID DYSFUNCTION, BONE TUMORS, MALABSORPTION, ANOREXIA NERVOSA)**
41
Complications/Manifestations of osteoporosis
**C:** pathologic fractures (typically in wrist, hip, spine)
**often asymptomatic in early stages**
• osteopenia (*bone mass that is less than expected for age, ethnicity, gender*)
• bone pain or tenderness
• fractures with little or no trauma
• low back and neck pain
• kyphosis
• height reduction (*as much as 6 in.*) over time
42
Rickets
soft, weak bones in children, usually because of an extreme and prolonged vitamin D, Ca, or P deficiency
**Ca and P shift out of the bone if the blood levels become too low, leading to weak and soft bones**
43
Osteomalacia
adult form of rickets
**Ca and P shift out of the bone if the blood levels become too low, leading to weak and soft bones**
44
Risk factors of rickets/osteomalacia
• vitamin D deficiency (*being bedbound, institutionalized people, working indoors, darker skin tones, strong sunscreen use, celiac, cystic fibrosis, undergoing gastrectomy*)
• dietary imbalances
• genetic influences
• renal disease
• liver disease (*in children*)
45
Manifestations of rickets/osteomalacia
**develop slowly as bones weaken; become apparent in children as soft bones cannot support growing child**
• fractures
• difficulty with ambulation
• skeletal deformities (*bowed legs, asymmetrical skull, scoliosis, kyphosis, pelvic deformities, sternum projection*)
• delayed growth in height or limbs
• dental problems
• bone pain
• muscle cramps or weakness
46
Paget Disease
**progressive metabolic condition characterized by excessive bone destruction that occurs along with the replacement of bone by fibrous tissue and abnormal bone**
• new bone is bigger but weakened and filled with new vessels
• results in fragile, misshapen bones
• may occur in 1/2 areas of skeleton or throughout the body
47
Paget Disease Causes
exact cause unknown, but thought to be caused by a virus capable of increasing osteoclast activity or genetic defects that produce an increase in interferon-6
*more common in men, central european descent, people with family history*
48
Paget Disease manifestations
**vary depending on affected area; often insidious in onset and may be asymptomatic early**
• bone pain
• skeletal deformities (*bowing of the legs, asymmetrical skull, enlarged head*)
• fractures
• headache
• hearing and vision loss
• joint pain or stiffness
• neck pain
• reduced height
• warmth over the affected bone
• parasthesia or radiating pain in the affected region
• hypercalcemia
49
Osteoarthritis
**degenerative joint disease characterized by local deterioration of articulating cartilage and its underlying bone as well as bony overgrowth**
• cartilage surface becomes rough and worn, interfering with joint movement
• knees, hips, and joints in hand and spine are most commonly affected, more common in women
*not inflammatory in origin, but inflammation results from tissue irritation*
50
Osteoarthritis pathogenesis
1. tissue damage triggers enzyme release from local cells, accelerating cartilage disintegration
2. subchondral bone becomes exposed and damaged, cysts and osteophytes (*bone spurs*) develop as the bone attempts to remold itself
3. osteophytes and cartilage pieces break off into the synovial cavity, further increasing irritation
4. nearby muscles and ligaments may become weakened and loose
5. results in joint space narrowing, joint instability, stiffness and pain
51
Osteoarthritis causes
idiopathic or excessive mechanical stress on joint (*obesity, overuse, injury, congenital MSK condition*)
52
Osteoarthritis manifestations
**gradual onset, usually beginning after age 40; often develop slowly and worsen over time**
• joint pain that worsens during/after movement or weight bearing
• joint tenderness with light pressure
• joint stiffness, especially upon rising in the AM or after a period of inactivity
• enlarged, hard joints
• limited joint ROM
• crepitus
• hard nodules around affected joint (*bone spurs*)
53
Rheumatoid arthritis
systemic autoimmune condition involving multiple joints; primarily affects synovial membrane but can also affect other organs
• remissions and exacerbations, progressing with each exacerbation
• usually starts with an acute inflammatory episode after which the joint may appear to recover
**macrophages and helper Ts travel to synovium and produce pro-inflammatory cytokines=systemic and joint manifestations**
54
Rheumatoid arthritis pathogenesis
**synovitis, pannus formation, cartilage erosion, fibrosis, ankylosis**
1. synovium thickens because of the cumulative effect of the reoccurring inflammation
2. thickened synovium eventually invades and destroys the cartilage and bone within the joint
3. muscles, tendons and ligaments weaken and stretch
4. joints can lose their shape and alignment
55
Rheumatoid arthritis causes/risk factors
usually affects joints bilaterally, most common in wrists, fingers, knees, feet and ankles
*exact cause unknown, but thought to be a genetic vulnerability that permits a virus or bacterium to trigger the disease*
**RISK FACTORS:** female, family history, advancing age (*however there is a juvenile form*), smoking
56
Rheumatoid arthritis manifestations
**usually insidious onset, progressively worsens; initially seems to mimic acute viral syndrome**
• fatigue
• anorexia
• low grade fever
• lymphadenopathy
• malaise
• muscle spasms
• morning stiffness lasting more than an hour
• warmth, tenderness, and stiffness in joints when not used for as little as 1 hour
• bilateral joint pain
• swollen and boggy joints
• limited joint ROM
• contractures and joint deformity (*boutonniere deformity and swan neck deformity*)
• unsteady gait
• depression
• anemia
57
Gout
**inflammatory disease resulting from deposits of uric acid crystals in tissues and fluids**
*results from hyperuricemia caused by an overproduction or under excretion (most common) of uric acid*
58
Uric acid
by product of breaking down purines, a substance naturally found in the body and in certain foods (*organ meats, shellfish, anchovies, herring, asparagus, mushrooms*)
59
Causes/Risk factors of gout
**not all people with hyperuricemia have gout; MOST COMMON IN MEN AND AAs**
• inborn error in metabolism
• overweight or obese
• certain diseases (*HTN, diabetes mellitus, renal disease, sickle cell anemia*)
• consuming alcohol (*beer and spirits*)
• certain meds (*diuretics*)
• eating a diet rich in meat and seafood
60
Asymptomatic phase of gout
uric levels climb in the bloodstream and crystals deposit in tissue; crystals accumulate, damaging tissue
61
Acute flares or attack phase of gout
tissue damage triggers acute inflammation; most initial attacks in LE (*great toe*)
**PAIN, BURNING, REDNESS, SWELLING, WARMTH AT AFFECTED JOINT LASTING DAYS TO WEEKS**
62
Intercritical period; phases of gout
after attack subsides, the disease is clinically *”inactive” until next flare*; hyperuricemia and crystal accumulation continue
PERIODS BETWEEN ATTACKS BECOME SHORTER AS DISEASES PROGRESSES
**REOCCURRING ATTACKS OFTEN PRECIPITATED BY SUDDEN INCREASES IN SERUM URIC ACID**
63
Chronic gouty arthritis phase of gout
joint soreness and aching present most of the time
may also develop tophi that can drain or renal calculi
64
Gout manifestations
**vary depending on phase**
• intense pain at affected joint that frequently starts at night and is often described as throbbing, crushing, burning or excruciating
• joint warmth, redness, swelling and tenderness (even to light touch)
• fever
• joint deformities
• limited joint mobility
65
Ankylosing Spondylitis “bamboo spine”
**progressive inflammatory disorder affecting sacroiliac joints, intervertebral spaces and costovertebral joints**
• inflammation starts in vertebral joints of lower back at sacroiliac joints and progresses up the spine
• *NEW BONE FORMS IN AN ATTEMPT TO REMODEL THE INFLAMMATORY DAMAGE!!*
• results in joint fibrosis and calcification; **JOINTS BECOME ANKYLOSED**
• vertebrae appear square and the vertebral column goes rigid and loses curvature
66
Ankylosing Spondylitis Complications
**genetics seem to play a role in development (*HLA-B27 gene is present*)**
more common in *males, 20-40 yrs*
• kyphosis
• osteoporosis
• respiratory compromise
• endocarditis
may experience periods of remission and exacerbation
67
Ankylosing Spondylitis manifestations
• intermittent lower back pain (*early*)
• pain and stiffness that typically worsens with inactivity and improves after activity
• lower back pain that evolves to include entire back
• pain in other joints (*shoulders, hips, LE*)
• muscle spasms
• fatigue
• low grade fever
• weight loss
• kyphosis
68
Muscular Dystrophy
**group of inherited, no inflammatory disorders characterized by degeneration of skeletal muscle; 9 forms (*including Becker MD, Duchenne MD, myotonic MD, limb girdle MD*)**
• common across all types is the presence of muscle protein abnormality (*dystrophin*) that causes muscle dysfunction, weakness, muscle fiber loss, inflammation and may involve other tissue (*cardiac and smooth muscle*)
• fat fibrosis connective tissues eventually replace skeletal muscle fibers, progressively weakening muscles
69
MD types
• some types are rare, others are common
• most types are inherited, but some occur due to spontaneous genetic mutation
• some types cause tremendous disability and rapid decline while others have minimal symptoms and hardly noticeable progression
• some types present in childhood, others in late adulthood
• **Duchenne MD is most common and severe type affecting only males (*X-linked recessive*)**
70
MD complications
• cardiomyopathy
• recurrent respiratory infections
• respiratory compromise
• death
71
MD Manifestations
**vary on type; all of muscles may be affected or only selected group**
• intellectual disability (*some types*)
• muscle weakness that slowly worsens to hypotonia
• muscle spasms
• delayed development of muscle motor skills
• difficulty using 1+ muscle groups
• poor coordination
• drooling
• ptosis
• frequent falls
• problems walking
• gowers maneuver
• unilateral calf hypertrophy
• scoliosis/lordosis
• progressive loss of joint mobility and contractures (*clubfoot and foot drop*)
72
Bone tumors
majority are malignant and occur as secondary tumors from other cancers (rarely occur as primary)
**exact cause of primary tumors unknown; more common in *men and whites*; Paget disease is a risk factor**
73
Osteochondroma (benign bone tumor)
develops adjacent to growth plates; **MOST COMMON BENIGN BONE TUMOR**
occurs most often between 10-20 yrs old
74
Osteosarcoma (malignant bone tumor)
begins in bone cells, usually in femur, tibia, fibula
occurs most often in children and YAs
75
Condrosarcoma (malignant bone tumor)
slow growing; begins in cartilage cells that are commonly found on ends of bones
most frequently affects older adults
76
Ewing sarcoma (malignant bone tumor)
origin unknown; may begin in nerve tissue within the bone
occurs most frequently in children and YAs
77
Bone tumor manifestations
**often asymptomatic in early stages**
• pathologic fractures
• bone pain
• palpable mass
• fatigue
• unintended weight loss
