Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

253-Green Patho > Muculoskeletal > Flashcards

Muculoskeletal Flashcards

1
Q

Describe the layers of bone

A

Periosteum (soft covering with blood vessels)
Cortical, or Hard Bone (osteon)
Cancellous, or Spongy Bone (trabecular)
Bone Marrow (Blood cell producing)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe key cells of bone

What do the bone cells do?

A

Types of bone cell include osteoclasts, which break down bone tissue; osteoblasts, which build new bone tissue; osteocytes, which hold the bone together; and lining cells, which protect the bone.

The bone cells do many things for the skeletal system, such as the development of new bones and continual bone remodeling (the maintenance of bones and the homeostatic regulation of minerals in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Osteoporosis

A
  • Low Bone Mass (loss of matrix/components)
  • Porous bone
  • Bone atrophy
  • Bone becomes Fragile -> fractures common complication
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Describe the Etiology of Osteoporosis

A
  • Ageing
  • Genetic Predisposition
  • Endocrine changes (hormone levels and action change, Estrogen inhibits resorption)

• 2 major Risks
o Low peak bone mass (~30yrs= Max PBM)
o Post Menopause (INC in bone loss r/t E DEC that normally inhibits breakdown)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the two types of bone remodelling

A

Bone remodeling (or bone metabolism) is a lifelong process where mature bone tissue is removed from the skeleton (a process called bone resorption) and new bone tissue is formed (a process called ossification or new bone formation. (Pg 1442)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe Patho (i.e. progression) that lead to Osteoporosis

A
  • Peak mass at ~30yrs
  • Longitudinal bone growth stops at ~20 yrs
  • Imbalance of formation and resorption
  • INC loss post menopause
  • Micro damage sets in from pressure/trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe MNFTS of Osteoporosis.

A

• Often silent until a fracture occurs (XR will show advanced osteo)
o Acute, severe pain

• Damage to vertebrae
o Change in Stature
o Distorted spine
o Breathing problems (r/t position)

Dentation problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Dx of Osteoporosis

A

• Xray (shows later stages)
• Bone density Scan (using light to determine density in different skeletal areas- lumbar, radius and neck of femur key indicators)
o Result shown as a T value (1- 2.5) High = More porous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Tx Osteoporosis

A
  • Prevent fractures
  • Pain and disability
  • Wt bearing activity (avoid injury/overexertion)
  • Antiresorptive agents (osteoclasts)
  • Anabolic agents (osteoblasts)
  • Well balanced nutrition (Ca, Vit D and Calories)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Osteoarthritis

Areas affected, progression

A 
•	Degenerational joint disease (joint wear and tear, but other factors present)
o	l/o cartilage and subchondral bone
•	Weight bearing joints more affected
•	Usually non inflammatory damage
•	Slow progression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Etiology of Osteoarthritis

Differentiate primary and secondary

A

• Primary is idiopathic (but theories exist)
o Wear and tear with aging
• Genetic predisposition
o Suggests there may be genes that impact cartilage maintenance and minor repair proteins in cartilage.
o Easier cartilage dmage and poor repair

• Secondary
o Injury, obesity, repetitive motion, etc.
• NOTE: obesity increases wt bearing impact but also is considered a low grade inflm disease which impacts joint health

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe physiologic joint Fx

A

 Chondrocytes maintain cartilage
 Articular cartilage (smooth cartilage + fluid reduces friction and had ability to withstand force [wt bearing])
• Dissipates force to bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pathology of Osteoarthritis

A

 Composition and properties of cartilage change -> cytokines (TNF and interleukins) -> proteases (excessively) -> destruction of cartilage

Chondrocyte damage -> impaired ability to heal cartilage

Cartilage deteriorates -> unprotected bone -> sclerosis (stiffening/hardening) of bone

Cysts (hollow/fluid) and fissures appear as fluid enters cracks in bone

Osteophytes form (projections/bone lesion) (worsen articulation) -> joint enlarges and deforms (see 59-6 for process)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

MNTFS of Osteoarthritis

A
  • Initial : non localized aching pain
  • Later: activity related wt bearing pain (eventually constant)
  • Crepitus
  • Movement hurts, no movement joint stiffen
  • Stiff Inflm joints
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Dx of Osteoarthritis

A
  • Hx and Px (no single test)
  • X ray (not always useful)
  • Labs (Inflm markers?, more simply eliminating other possibilities like septic arthritis, gout or other forms)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tx of Osteoarthritis

Differentiate common vs severe

A

• Cartilage is not replaceable
• Monotherapy PRN (One at a time)
• Tylenol (1rst choice)
• Cox 2 inhibitors (inhibits enzyme cyclo-oxygenase)
( Cox 2 mediates/advances Inflm and leads to production of prostaglandins (pain)

  • Severe: intra articular injection (often quick short term relief, but side effects means minimal long term use)
  • Rehabilitation (physio)
  • Sx- joint replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Rheumatoid arthritis

A

• Chronic autoimmune CT disease

o Inflm, deformed synovial joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Etiology of Rheumatoid arthritis

A
  • Multifactorial (complex trait)

* Genetic predisposition and Viral trigger? (Epstein Barr) (MHC/HLA + Trigger)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is a type 3 Hypersensitivity

A
  • Type3 H- IC are not destroyed by enzymes as normal-> into blood stream-> enter cap-> embed in Cap wall (throughout body)
  • Impedes filtration + abnormal deposit (macrophage will destroy deposit) =Inflm
  • Type 3 H is proceeded by infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Patho of Rheumatoid arthritis

Do B cells or T cells cause Inflm? How?

A
  • Altered T cell response -> targets synovial membrane (initially) -> inflammation and joint damage
  • Altered B cells -> Abs production (rheumatoid factors RF) -> target tissues (connective in joints, later connective elsewhere in body)
  • RF form IC’s -> deposit in synovial membrane -> Inflm

IGG (ab) - IGRF (Ag)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What does repeated inflm in joint bring about in Rheumatoid arthritis?

A

• Repeated Inflm -> deformity (granulation tissue – not normal in joint, more harm then good)

• Pannus (vascular, granulation tissue)
o Releases destructive enzymes
o Source if damaging Inflm cells
o Dec joint mobility (less space, more Inflm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Examples of joints deformity cause by rheumatoid arthritis?

A

EX: Swan neck deformity, Ulnar drift/shift (Other MNFTS 59-2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MNFTS of Rheumatoid arthritis

A

• Subtle onset
o Low grade fever malaise
• Increasing fatigue
• AM joint pain
• Stiffness after inactivity
• Non articular (as it progresses…could take decades)
o Heart, blood vessels, skin, lungs, eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Dx of rheumatoid arthritis

A
  • Hx, Px (exclude other diseases)
  • Xray and labs (like ANA… but limited use)
  • Rheumatoid factor (only 75% of those with RA are positive in test)
25
Tx of rheumatoid arthritis
• Limit progression • Pain (eg meloxicam or naproxen (NSAID) • Start with plaquenil (eye exam q 6-12m- related to side effect) (its anti Inflm and immunomodulatory (anti malarial pill normally) • Usually combination therapy e.g. o Sulfasalazine( seen in IBD) and methotrexate (also used in IBD, CA Tx) (CBC, liver Es (liver damage) and Creatinine monthly)
26
What is Gout
crystal induced joint disease R/t Uric Acid deposits in joints (by product of protein break down. Inflm occurs during removal by defense cells
27
Differentiate Primary and Secondary Gout
• Primary o 90% of gout o Metabolic (Purines-Adenine and Guanine) o Mostly in Men • Secondary o Cell destruction (cell turnover… malignancies etc) o Impaired Renal fx (poor excretion of by product) o Others (beer and alcohol consumption, chemo)
28
Patho of Gout
* Altered purine metabolism -> Asymptomatic hyperuricemia * Later: crystals deposit in synovial joints * WBC influx and complement activation * WBC phagocytize crystals -> WBC necrosis -> E release -> Inflm joint damage * Recurrent acute attacks -> Tophi lesions (Tophus formed by accumulation of uric acid crystals, space occupying lesions)
29
Outline 5 Stages of Gout
1) Asymptomatic Hyperuricemia 2) acute Inflm and pain (overnight, 1 joint – usually large toe) • uric acid crystalizes in synovial fluid not blood • Toe also colder, plus inactivity overnight = crystallization • Often following heavy meal or alcohol binge (high (purine content in beer) High intensity exercise (r/t protein breakdown) 3) Subsides in a week (with anti infm treatment) 4) Asymptomatic for months to years after) 5) Frequent recurrent attacks -> Permanent damage
30
Dx of Gout
Dx • Serum and urine uric acid • Uric acid in joints (Xray- more specific)
31
Tx of Gout
• Acute attacks: Pain and Inflm o NSAIDS o Colchicine (limits leukocyte migration to joint) o Steroids * DEC hyperuricemia * INC Uric acid excretion * Eliminate alcohol * Dec protein in Diet
32
What is Muscular Dystrophy
• Skeletal Muscle degeneration (progressive) (later other muscle- Ex: heart) o d/t atrophy, necrosis and pseudohypertrophy • Not true muscle tissue, but instead adipose tissue
33
What are the types of muscular dystrophy based on? What is the most common type?
• Types Based on o muscle group, Age (0-60yrs) o Rate of progression o mode of inheritance • Duchenne MD is most common o 1 in 35000 (mainly males)
34
Et of Muscular Dystrophy
• Recessive, x linked trait o (Male has only one X, only need one to cause disease, female other X will override disease...i.e. recessive) o Mother is carrier to son Note: Gene is on short arm of X chromosome
35
Where is the affected gene in Muscular dystrophy and what does it code for?
Gene is on short arm of X chromosome Codes for DYSTROPHIN (Protein on membrane of muscle) o Provides attachment of contractile filaments
36
Patho fo Muscular dystrophy
* Mutation-> altered protein -> poor contractile proteins attachment -> fiber necrosis with use -> poor repair and regeneration -> more necrosis -> Ca influx (into muscle) and E release (i.e. Creatine Kinase CK) * Fibrofatty CT replaces muscle tissue * More muscle use, increases Inflm damage
37
MNFTS of Muscular Dystrophy
* Asymptomatic until 2-3 yrs * Progression of muscle weakness * Respiratory and Cardiac muscle affected * Usually death associated with resp or Cardiac complications
38
Dx of Muscular Dystrophy
* Hx * Voluntary movement limited * Serum CK (muscle damage marker) * Biopsy (looking for dystophin) * Carrier screening for gene
39
Tx for muscular dystrophy
* No cure * Supportive and symptomatic care * Provide for comfort and fx
40
What intake cause INC in Nitrogenous compounds?
Protein catabolism
41
Are secondary or primary bone cancers more common?
Secondary- large well vascularized
42
Describe some different kinds of Bone CA. How are they categorized? Which is the most common?
Osteosarcoma (most common) • A Bone forming tumor (Bone cells) Chondrosarcoma (cartilaginous cells) Fibrosarcoma (fibrous cells) (Osteoclastoma or Ewings) Based on cell type (and aggression)
43
Where and in whom does Osteosarcoma generally present? Is it Aggressive or slow progression?
• Usually in vicinity of knee o Often in metaphysis of nearby long bone • 75% before age of 20 o Older individuals with CA will general have other bone diseases • Aggressive (metastasis to lung)
44
Describe Secondary Bone CA | Incidence, Types of Lesions and common Primary sites
• Bone is common secondary site o ~50% of all CA spreads to bone o > 85% from breast, lung and prostate • lytic or blastic lesions o Lytic- Malignant cells release enzyme/mediators that breakdown tissue • Pain, swelling, fractures
45
Diagnosis of Bone CA
• X ray, CT, MRI o Xray requires substantial bone change/damage to be visualized • Biopsy • Bone Scan (will only tell you density)
46
Tx of Bone CA
* Triad of Tx * Block excision (tumor plus surrounding tissue) AND Restorative Grafting * Amputations * Deal with pain and prevent fractures
47
Describe the basic of how fractures are classified
``` • Most common bone lesion, break in continuity of bone • Many classifications o Cause, location, pattern, type • Simple (closed) • Compound (open) (pushes through skin) ```
48
Fraction descriptions by type
• Greenstick o 1 broken and 1 bent surface o In children (why?) -> Bone not fully matured, more flexible • Pathologic o d/t bone disorder (eg osteoporosis) • Comminuted o Multiple breaks at single site (fragments)
49
Fractures by pattern
``` • Oblique o (break at around 45 degrees) o d/t twisting force (e.g twisted ankle) • Longitudinal o Longitudinal break line ```
50
Fractures by appearance
• Burst fracture o Bone breaks into multiple pieces o Usually at end of bone • Chip o Often Small fragment near joint • Displaced o Bone separates at fracture line
51
Other common fracture names we discussed in class
Colees- wrist Potts, distal fibula Compression fracture on vertebrae
52
What causes a fracture (etiology)
Force overload on bone
53
MNFTS of Fracture
* PAIN (+swelling) * Deformity * l/o fx * Hemorrhage (always bleed if not seen it’s in the bone, also first step of healing process * Soft tissue injury
54
Fracture Tx
* Reduction (align bones) * Immobilization and healing * Preserve and restore Fx (physio)
55
State 4 stages of Fracture healing | Descriptions later
Hematoma formation Soft Callus formation Bony Callus Formation Remodeling
56
Describe Hematoma Formation
AKA Blood clot • 48 to 72hrs • Gelatenous, provides some stability and begins alignment on bone ends • Provide a framework/medium for cellular signaling through mediators • Seals the fracture site • Inflm cells appear (physiologic) • Necrosis and removal of bone
57
Describe Soft Callus formation
* Characterized by appearance of fibrocartilage * Granulation tissue (physiologic) to allow formation of new blood vessels Angiogenesis * Appearance of Fibroblast and collagen * Capillary buds give rise to new vessels
58
Bony Callus Formation
* Cartilage changes to spongy bone. * Bone trabeculae * Not yet weight bearing * Osteoblasts appear in higher number
59
Remodelling
* Secondary remodeling builds bone back to original appearance (likely still some deformity) * Extra material removed, spongy bone to compact bone

253-Green Patho (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions