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253-Green Patho > Muculoskeletal > Flashcards

Flashcards in Muculoskeletal Deck (59):
1

Describe the layers of bone

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

2

Describe key cells of bone

What do the bone cells do?

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

3

Osteoporosis

• Low Bone Mass (loss of matrix/components)
• Porous bone
• Bone atrophy
• Bone becomes Fragile -> fractures common complication

4

Describe the Etiology of Osteoporosis

• 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)

5

Describe the two types of bone remodelling

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)

6

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

• 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

7

Describe MNFTS of Osteoporosis.

• 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

8

Dx of Osteoporosis

• 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

9

Tx Osteoporosis

• 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)

10

What is Osteoarthritis

(Areas affected, progression)

• 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

11

Etiology of Osteoarthritis

Differentiate primary and secondary

• 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

12

Describe physiologic joint Fx

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

13

Pathology of Osteoarthritis

 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)

14

MNTFS of Osteoarthritis

• Initial : non localized aching pain
• Later: activity related wt bearing pain (eventually constant)
• Crepitus
• Movement hurts, no movement joint stiffen
• Stiff Inflm joints

15

Dx of Osteoarthritis

• 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)

16

Tx of Osteoarthritis

Differentiate common vs severe

• 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

17

What is Rheumatoid arthritis

• Chronic autoimmune CT disease
o Inflm, deformed synovial joints

18

Etiology of Rheumatoid arthritis

• Multifactorial (complex trait)
• Genetic predisposition and Viral trigger? (Epstein Barr) (MHC/HLA + Trigger)

19

What is a type 3 Hypersensitivity

• 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

20

Patho of Rheumatoid arthritis

Do B cells or T cells cause Inflm? How?

• 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)

21

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

• 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)

22

Examples of joints deformity cause by rheumatoid arthritis?

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

23

MNFTS of Rheumatoid arthritis

• 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

24

Dx of rheumatoid arthritis

• 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