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Musculoskeletal Disorders Flashcards

1
Q

What is osteoporosis?

A

Loss of matrix, porous matrix, atrophy of bone.

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2
Q

What is a complication of OP because of the fragile bone?

A

Fracture (minimal force).

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3
Q

What are 3 etiologic factors for OP? 2 major risk factors?

A

Ageing, genetic predisposition (PBM), endocrine changes. RF: low PBM, post-menopause (loss of E)

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4
Q

What role does E play in maintaining bone health?

A

Limits bone breakdown/osteoclast activity

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5
Q

What is the patho for OP? When does one reach PBM? When does longitudinal bone growth stop?

A

30 years. 20 years. Architectural changes inside bone + microscopic damage sets in. Basically more matrix is being removed than is being laid, therefore the matrix becomes porous and bone density is reduced.

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6
Q

Up until when are manifestations of OP usually silent? What areas of the body are affected by OP (3)?

A

Fracture (acute, severe pain). Damage to vertebrae (change in stature - hunched over), distorted spine (breathing issues), dentition issues.

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7
Q

How can OP be diagnosed?

A

XRAY in advanced cases (substantial porosity), bone density scan (looks at absorption and transmission of light through radius, neck of femur + lumbar spine - lower value = more porous).

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8
Q

What is a major thing we want to avoid in OP? What are 5 treatment methods?

A

Prevent fractures. Pain + disability, weight bearing activities, antiresoprtive agents (osteoclasts), anabolic agents (osteoblasts), adequate Vit D, protein, calcium.

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9
Q

What is OA? Which joints are affected first? What is lost in this disease? How fast is the progression?

A

Degenerative joint disease. Weight bearing joints. Cartilage between bones in joints + sunchondrial bones. Slow.

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10
Q

What are the 2 etiologic factors for primary OA? alte

A

Wear + tear with ageing, genetic predisposition (defective gene coding for protein that maintains cartilage - cartilage injures easily + does not repair properly)

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11
Q

What is the etiologic factor for secondary OA? What two factors does obesity play?

A

Injury, obesity, professional sports (repetitive joint movement). OBESITY: 1. carry more weight therefore more stress on joints (wear + tear) 2. low-grade systemic disease of inflammation - adipose tissue somehow has some metabolic impact on joint.

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12
Q

Normal, physiologic cartilage has what 3 features?

A

Smooth + is surrounded by fluid for a no friction environment, is weight bearing, and will dissipate force to bone by “deforming”

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13
Q

What is the patho for OA?

A

Composition + properties of cartilage, then cytokines are released by chondrocytes triggering the release ++ proteases which destroys cartilage. Chondrocyte damage leads to an impaired ability to heal cartilage.. Cartilage deteriorates - the bone makes contact with bone - sclerosis of bone (inc density to make stronger so it doesn’t erode) - then cysts and fissures appear as fluid enters cracks in bones - and bone forms osteophytes (projections) inside joints resulting in joint enlargement + deformity

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14
Q

What is an initial manifestation of OA? Later? Finally, 2 more manifestations?

A

Non-localized aching pain. Activity-related pain to weight bearing joints. Crepitus + stiff, inflamed joints.

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15
Q

How is OA diagnosed (4)?

A

Hx, Px, xray (not always useful), labs (to rule out other joint problems like septic arthritis)

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16
Q

What are 3 treatment methods for OA? 1st line? What are 3 treatments for severe OA?

A

Monotherapy pain meds PRN. Acetaminophen (1st line), COX 2 inhibitors. SEVERE: intra articular steroid injection (is cortisone), PT, Sx (joint replacement).

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17
Q

What 2 things does the enzyme cyclooxygenase 2 do? By giving COX 2 inhibitors what are we achieving?

A

Mediates/advances inflammation + leads to the production of prostaglandin (PG). Preventing both of those from happening.

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18
Q

What is RA? Which joints are affected first? Then later which joints? What type of HS reaction is this? Is this disease systemic or localized to an area of the body?

A

Chronic autoimmune CT disease resulting in inflamed + deformed synovial joints. Non weight-bearing + then weight bearing. Type 3. Systemic.

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19
Q

What is the etiology for RA?

A

Complex trait - viral trigger (EBV?), genetic mutation (MHC/HLA).

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20
Q

Touch on the 3 main patho points for RA.

A
  1. altered T cell response results in targeting of synovial membrane leading to inflm + damage to joint. 2. Altered B cells produce rheumatoid factors (RF) autoantibodies that target tissue. 3. RF forms IC that deposit in synovial membrane resulting in inflm. Repeated inflm - deformity of joint - pannus forms inside joint
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21
Q

In RA, what is a pannus? What 4 issues arise when this is formed?

A

A pannus is granulation tissue that forms within a joint. It: occupies space in the joint, releases enzymes that destruct the cartilage, has damaging inflammatory cells, and reduces the joints mobility.

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22
Q

What two types of deformities are there in the hands of someone with RA?

A

Swan neck deformity + ulnar drift/shift

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23
Q

Are the manifestations limited to the joints, or are there some unrelated to joints? Which manifestations appear subtly (2) in RA? What are 3 other articular manifestations? What body systems/structures are also affected in RA (5), and why?

A

Both. SUBTLE: low grade fever, malaise. Increased fatigue, AM joint pain (stiffness), and stiffness after activity. NON ARTICULAR: heart, BVs, skin, eyes, lungs. Because there is CT distributed throughout the body.

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24
Q

How is RA diagnosed? (5)

A

Hx, Px, exclude other diseases of the skeleton, X-ray (not revealing early on), labs (RF antibodies).

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25
What is an issue with the validity of testing for RF antibodies in RA?
Not everyone tests positive for these Ab, only about 75% of people do, especially in early stages of RA.
26
What is important to remember about the treatment of RA? What pain management can we do? Other meds? What if the immunomodulatory doesn't work, what's next?
Limit progression. Meloxicam or naproxen (NSAID). Immunomodulatory (Plaquenil). Maintain pain meds + Sulfasalazine (anti-inflammatory + immunomodulatory) + methotrexate
27
What is an issue with using Plaquenil as a drug for RA? What class of drug is this? What 2 properties does this drug have?
Antimalarial. The drug deposits in the eye so need an eye exam every 6-12 months. It is an anti-inflm + immunomodulatory.
28
If someone is receiving methotrexate for RA, what are some important diagnostics to get?
CBC (antifolate), liver Es (hepatotoxic), creatinine monthly.
29
What is gout? What compound causes this?
Crystal-induced joint disease. Uric acid crystal deposit in joints from building up in circulation.
30
For primary gout, who does it most commonly affect? What is the main cause?
95% men. Metabolic issue.
31
For secondary gout, what are 4 etiologic factors?
Excessive cell turnover/destruction, renal problem, alcohol ingestion (beer), and chemo.
32
What is the patho for primary gout?
Altered purine (adenine + guanine) breakdown which leads to asymptomatic hyperuricemia. Later: crystals deposit in synovial joints, WBC influx + complement action occurs - WBC phagocytize the crystals resulting in WBC necrosis and enzyme release resulting in inflammatory joint damage - recurrent acute attacks happen and tophi form
33
What is a tophi/tophus?
Accumulation of uric acid crystal, the lesion present in gout.
34
What are the stages one progresses through in gout?
1. Asymptomatic hyperuricemia. 2. acute inflm (over night - usually in one joint like big toe and usually following alcohol binge or heavy meal, drugs, or excessive exercise). 3. issue subsides in about a week. 4. asymptomatic hyperuricemia maintains and joints are affected more frequently + different joints now affected too.
35
Why is the big toe often a place for the first gout occurrence? Why overnight?
Its in the periphery, so there is decreased temperature to the area (compounds easier to precipitate out) and there is reduced activity over night = decreased temperature too.
36
Is uric acid more soluble in blood or synovial fluid?
Blood. In synovial fluid = crystals.
37
Do people with hyperuricemia always have gout?
No
38
How is gout diagnosed?
Uric acid in serum + urine, XRAY showing uric acid in joints.
39
How is gout treated? Acute attacks (3 different methods)? Long term (4)?
NSAIDS, cholchicine or steroids. LONG TERM: reduce hyperuricemia, increase uric acid exrection (increase fluid intake), no alcohol (especially beer - purine) + decrease protein diet (decrease purine intake)
40
What is MD? What cell changes occur? What 4 things differentiate the different types of MD?
Genetic disease causing progressive skeletal muscle degeneration. Atrophy + necrosis of muscle cells + then pseudohypertrophy. 1. groups of muscles. 2. age of onset (0-60). 3. rate of progression/deterioration. 4. mode of inheritance.
41
Which is the most common form of MD?
Duchennes
42
What is pseudohypertrophy?
Untrue hypertrophy, deposits adipose tissue into muscle that causes enlargement, not actual muscle.
43
What is the etiologic factor for MD?
Recessive x-linked trait (mother to son), genetic defect with gene on short arm of X chromosome.
44
What is the patho for MD?
Gene on short arm of X chr. mutation - altered dystrophin - poor attachment of contractile proteins - fibre necrosis with use - poor repair + regeneration - further necrosis - Ca+ influx + Es release (CK- damage muscle) - body tries to increase muscle size - pseudohypertrophy (fibrofatty CT replaces muscle).
45
What is the function of dystrophin? When this is defective what occurs?
Provides attachment of contractile proteins to membrane. Contractile proteins are incorrectly attached + movement is considered to be endurious as it causes damage + inflm damage
46
When is an individual with MD usually asymptomatic until in terms of muscle usage? What is a manifestation of MD? Which body system's muscles are affected? What does an individual with MD usually die from? How long is their life span?
2-3 years. Progressive muscle weakness. Respiratory + cardiac muscles. Usually die from resp +/or cardiac complications. 20-25 years.
47
How is MD diagnosed? Which diagnostics are important (4)? What types of screens/early diagnosis can we do?
Hx, Px (important). In Px we are looking for voluntary movement which will be abnormal. Serum creatinine kinase (CK), biopsy of muscle to look for pseudohypertrophy + dystrophin. Carrier screening (mom), and prenatal Dx (12 weeks gestation + onward).
48
Is there a cure for MD? What things will we want to do as far as treatment is concerned?
No. Supportive care (braces, breathing exercises, Sx if muscle affects joints), symptomatic tx, increase comfort + fx.
49
What is systemic lupus erythematosus (SLE)? Who is it more common in?
Chronic inflammatory disorder that affects virtually every organ system. Females + African, Hispanic + Asian population.
50
What is the etiology for SLE? What is thought about imbalance of sec hormones playing a role in SLE?
Complex trait = genetic predisposition (MHC/HLA) + environmental trigger. Androgens protect against SLE whereas E favours development of SLE (heightened T helper cell + dec suppressor T cell leading to development of autoAb?)
51
What is the patho for SLE?
B cell hyperactivity - autoAb production - directly damage tissue or combine with corresponding Ag to form tissue-damaging IC
52
What autoAb are involved in SLE?
Antinuclear Ab (ANA) including antideoxyribonucleic Ab (antiDNA), autoAb directed against elements of blood + plasma proteins.
53
What are 2 MS mnfts of SLE? 2 integ? 2 renal? 2 resp? 2 cariac? 3 blood? 2 CNS?
MS: Arthritis, OP. INTEG: Malar (butterfly) rash on nose + cheeks, hair loss. RENAL: GN, RF. RESP: pleural effusion, pneumonia. CARDIAC: pericarditis, myocarditis. BLOOD: anemia, neutropenia, thrombocytopenia. CNS: strokes, altered LOC.
54
How is SLE diagnosed (4)?
4/11 indicated criteria (manifestations), immunofluorescence (test for ANA), antiDNA, serum tests (reveal anemia etc)
55
What are 4 major things we want to accomplish with treatment?
1. Prevent progressive loss of organ fx 2. dec poss of exacerbations. 3. dec disability. 4. prevent complications.
56
What are some treatment methods for SLE (4)?
NSAIDS, hydrochloroquine (antimalarial), corticosteroid, immunosuppressant (cyclophosphamide).
57
What are 2 benefits for using cholchicine as a treatment for gout? Can this be used long term?
Limit migration of leukocytes to joint + minimize inflammation and enzymatic damage to joint. No long term use.
58
Which type of cancer is more common to occur in the bone, primary or secondary?
Secondary
59
Primary tumors will most commonly affect which part of the bone? Why?
Metaphysis. The metaphysis is where growth occurs, therefore cell division is much higher in that area of the bone.
60
What is the most common type of primary bone tumor? Which area of the skeleton does this most commonly occur? Will this cancer mets? To where? 75% of cases will be found in people before age ____, why is this? The other 25% are found in those with _________, why is this?
Osteosarcoma. Knee. Yes, to the lungs. Age 20 because their bones are still growing therefore ++ cell division. Paget's disease because of ++ bone formation and resorption that occurs with this disease.
61
What percentage of cancers will spread to the bone? Over 85% of what cancers will spread to the bone?
50. Breast, lung + prostate.
62
Secondary bone malignancies will have lytic or blastic lesions. What does this mean?
The tumor needs to invade + destroy normal bone (lytic) in order to make room for malignant cells (blastic).
63
What 2 manifestations are common for bone cancer? What is a serious complication?
Pain + swelling (inflammation). Fractures.
64
How is bone CA diagnosed?
CT, MRI, XRAY, biopsy, bone density scan.
65
What is the treatment for bone cancer? What must we prevent?
Chemo, radiation, sx (amputation or block excision + restorative grafting), pain meds. Fractures.
66
What is the most common type of bone lesion?
Fracture
67
What is a fracture defined as?
A break in the continuity of the bone.
68
What things do we use to classify fractures?
Cause, location, pattern, type.
69
What is a simple fracture? Compound fracture?
Closed - bone does not break through skin Open - bone breaks skin.
70
What is a greenstick fracture (type)? Who is this fracture most common in, and why?
A bone that has one broken and one bent surface. Children. Their bones are not yet mature and therefore are more flexible.
71
What is a pathologic fracture (type)?
A fracture that results because of a bone disorder (OP)
72
What is a comminuted fracture (type)?
Multiple fragmented breaks at one site.
73
What is an oblique fracture (pattern)?
Break at 45 degree angle because of a twisting force (like twisting your ankle)
74
What is a longitudinal fracture (pattern)?
Longitudinal break line.
75
What is a burst fracture (appearance)?
AKA comminuted. Bone breaks into multiple pieces at one point, usually at end of bone.
76
What is a chip fracture (appearance)? Common location for this?
Small fragment chips off. Joint.
77
What is a displaced fracture (appearance)?
When the bone separates at the fracture.
78
Et/patho for a fracture?
+++ force on bone leads to fracture.
79
What are 4 manifestations of a fracture?
Pain, l/o function, hemorrhage and deformity.
80
What are the 4 stages of healing a fracture?
Hematoma formation, fibrocartilaginous (soft) callus formation, bony callus formation + remodelling.
81
What important things occur in the hematoma formation phase? How many hours until a hematoma is formed?
Formation of a fibrin meshwork. 48 - 72 hours.
82
What 4 important roles does the fibrin meshwork formation do in the hematoma formation phase?
1. framework for inflammatory cells. 2. ingrowth of fibroblasts. 3. development of capillary buds. 4. molecular signalling to initiate cellular events.
83
What benefit does the hematoma play during the first phase of fracture healing?
Holds fractured bones in place to prevent further displacement (to some degree).
84
What are the main features of the fibrocartilaginous (soft) callus formation phase?
Granulation tissue (procallus) forms to give rise to new BVs. Fibroblasts produce fibrocartilaginous soft callus bridge that connects bone fragments. No weight bearing.
85
What are the main features of the bony callus formation?
Conversion of fibrocartilaginous cartilage to bony callus. Osteoblases produce spongy bone.
86
What are the main features of the remodelling phase of fracture healing?
Dead bone is removed by osteoclasts. Spongy bone is changed to compact bone. Remodelling of the bone to resemble original shape + strength.

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