Musculoskeletal Pa Tho Physiology A

8/8/2019 Musculoskeletal Pa Tho Physiology A

1/63

1

Review of Musculoskeletal

System

Chapter 36


2/63

2

Skeletal System Function:

Protection

Hematopoiesis

Mineral homeostasis Calcium

Phosphorus

Carbonate Magnesium


3/63

3

Structure

Bone is a connective tissue:

Matrix

Collagen fibers for flexibility andtensile strength

Calcium for rigidity

Hydroxyapatite Ca5(PO4)3OH


4/63

4

Cells:

Osteoblast Form organic components of matrix

Osteocyte

Osteoblasts

From monocytes

Secrete citric and lactic acids

Collagenases and other enzymes

Stimulated by PTH

Inhibited by Calcitonin


5/63

5


6/63

6


7/63

7

Types of Bone

Dense or Compact (85%)

Osteon (Haversian System)

Central (Haversian) canal Lamellae

Lacunae with osteocytes

Canaliculi

Spongy (cancellous) bone (15%)

trabeculae


8/63

8


9/63

9


10/63

10


11/63

11

Periosteum

Outer layer is dense, irregular CT with

nerves and blood vessels

Inner layer Osteoblasts

Anchored to bone by collagen fibers that

penetrate into bone


12/63

12

Bone Formation

Endochondral ossification

Inside hyaline cartilage

Most bones Intramembranous ossification

Forms directly inside membranes

Bones of skull


13/63

13


14/63

14

Growth

Lengthening of bones at epiphyseal plate

Grows from cartilage

Forms epiphyseal line when done growing Undergoing constant remodeling

Adaptation to stress

Healing


15/63

15


16/63

16

Skeleton

206 bones Axial skeleton

Skull and hyoid

Vertebral column Ribs and sternum

Appendicular skeleton

Shoulder girdle Pelvic girdle


17/63

17

Classification

Long bones:Diaphysis

Epiphysis

Metaphysis

Medullary cavity

Endosteum


18/63

18


19/63

19

Classification cont.

Short bones Flat bones

Irregular bones

Sesamoid bones

Wormian bones


20/63

20


21/63

21


22/63

22

Joints

Degree of movement

Synarthrosis immovable joint

Amphiarthrosis slightly movable jointDiarthrosis freely movable joint


23/63

2

3

Synovial joints

Joint capsule Fibrous CT

Tendons and ligaments

Nerves, blood and lymph vesselsSynovial membrane

Loose fibrous CT

Many blood vessels good repairJoint (synovial) Cavity


24/63

2

4


25/63

25

Synovial fluid

Plasma filtrate Synovial cells and leukocytes

phagocytize debris and microbes

Articular cartilageReduce friction

Distribute force


26/63

26


27/63

27

Bone Pathophysiology Inherited conditions:

Osteogenesis imperfecta

Inherited defect in collagen synthesis

Osteopenia and brittle bones

Often- defective tooth formation, bluesclera, faulty hearing

Inheritance can be dominant, recessive or

by new mutation

Several degrees of severity


28/63

28

Achondroplasia

Involves a defect in normal cartilagedevelopment

Epiphyseal plates close early in long bones;

individual has short arms and legs, but normal

spine and skull

Dominant inheritance, but frequent new

mutations

Other organs develop normally Individuals live a normal lifespan


29/63

29

Acquired disorders Osteoporosis porous bone

Most common metabolic bone disease in North

America

Can be attributed to genetics, diet or hormones

Most osteoporosis is idiopathic osteoporosis Bone loss due to an identifiable cause is

secondary osteoporosis

Bone tissue is mineralized normally, but over

time the structural integrity of bone is lost and itbecomes thinner and weaker, and more prone

to fractures.


30/63

30

Key features: bone fracture and the

associated pain. WHO defines osteoporosis by bone

density:

Normal bone > 833 mg/cm2

Osteopenia 833 to 648 mg/cm2

Osteoporosis < 648 mg/cm2

Can be generalized, involving major

portions of the axial skeleton

Can be regional, involving one segment of

the appendicular skeleton


31/63

31


32/63

32

Remodeling is constant

Teen years more bone is laid down than

reabsorbed

Peak bone mass or maximum density

reached at around 30 years of age

After age 30, bone is reabsorbed faster than itis laid down

In women, bone loss is most rapid in the first

years after menopause, but continues

throughout postmenopausal years

Est. 55% of people over 50 have osteoporosis

or low bone mass.


33/63

33

Men also lose bone density, but start out

with more bone mass so takes longer.

By age 90 about 17% of males have had a

hip fracture, vs. 32 % of females

Vertebral fractures also occur kyphosis

Most common in whites, but affects all

races.

African Americans have about half the

fracture rates of whites (higher peak bonemass)


34/63

34


35/63

35


36/63

36


37/63

37

Risk factors Family history

White race

Increased age

Female sex

Small stature

Fair or pale skin

Thin build Early menopause (natural or surgical)

Late menarche


38/63

38

Risk factors cont. Nulliparity

Obesity

Weight below a healthy range

Acidosis

Low dietary calcium and vitamin D High caffeine intake

Sedentary life style

Smoker Excessive alcohol consumption

Liver, kidney disease, rheumatoid arthritis, etc.


39/63

39

Often progresses silently for decades until

fracture occurs

Bones can fracture spontaneously

Most severe in spine, wrist and hips

Estrogens and androgens may be factors

in both sexes

Testosterone is converted into estrogen in

peripheral tissues and decreases bone loss

Rapid bone loss is osteoclast mediated

Slow bone loss is osteoblast mediated


40/63

40

Clinical manifestations Pain and bone deformity

Kyphosis caused by vertebral collapse

Fractures of long bones

Fatal complications include fat or

pulmonary embolism, pneumonia,hemorrhage and shock

20 % die as a result of surgical

complications


41/63

41

Treatment No known cure

Slow bone loss and promote bone

deposition

Calcium and vitamin D supplements

Calcitonin

Hormone replacement therapy

Biophosphates inhibit osteoclasts

Dual x-ray absorptiometry for diagnosis

PREVENTION


42/63

42

Prevention Intake of calcium, vitamin D, magnesium

and possibly boron

Regular, weight-bearing exercise

Avoid tobacco and glucocorticoids

No alcoholism

Hormone replacement?

Parathyroid hormone?

Testosterone for men and possibly women


43/63

43

Rickets and Osteomalacia

Inadequate mineral deposition in

essentially normal organic matrix

Softened bone:

Subject to malformation and distortion pain


44/63

44

Rickets

Dietary vitamin D deficiency causesinadequate mineralization of the

developing skeleton in infants and children

Rarely seen in Western nations Poverty

Ignorance

Bones are soft and easily deformed Tendency to fractures

Therapy: supply vitamin D and calcium


45/63

45

Osteomalacia

Rarely due to vitamin D deficiency

Usually GI malabsorption, renal defect or

chronic kidney or liver diseases.

Elderly often affected due to inadequate

diet or lack of outdoor activity

May accompany and complicate

osteoporosis.


46/63

46

Joint Disorders

Osteoarthritis

Most common joint disease in North America

Minimal inflammatory component

Differentiated from inflammatory disease by:

Absence of synovial membrane inflammation

Lack of systemic signs and symptoms

Normal synovial fluid

Much of the pain and loss of mobility associated

with aging.


47/63

47

Osteoarthritis

Incidence increases with age: 85% of peopleage 65 have some joint degeneration

Incidence similar, but women more severely

affected

Exceptional stress on joints: gymnasts, etc.

Biochemical defect in cartilage

Malformed joint, obesity and postural defects

Genetic component

Torn ACL or meniscectomy


48/63

48

Osteoarthritis When associated with known risk factors it

is secondary OA

No risk factors idiopathic OA

Pathological characteristics:

Erosion of the articular cartilage

Sclerosis of subchondral bone

Formation of bone spurs or osteophytes


49/63

49

Osteoarthritis

Begins in articular cartilage

Yellow-grey or brownish gray

Thin, irregular, frayed

Cracks or fissures develop (fibrillation)

Fluid filled cysts may form

Microfractures of subchondral bone

Formation of fibrocartilage repair plugs

Bone surface exposed Bone responds by becoming dense and hard


50/63

50

Osteoarthritis

Synovial membrane is indirectly affected Fragments of fibrocartilage causeinflammation pain

Fibrous repair of joint capsule restricts motion

Osteophytes form pain and loss of motion

Joint mice


51/63

51

Osteoarthritis

Affects one or more weight-bearing joints Hand, wrist, lower cervical spine, lumbar spine

and sacroiliac, hip, knees, ankles, feet

Aches and stiffness Symptoms increase with activity; diminish with

rest

Usually no swelling or redness of adjacent

tissues

Sometimes nocturnal pain may be referred


52/63


53/63

53

Osteoarthritis

Evaluation made through clinical

assessment and radiologic studies, CT

scan, arthroscopy and MRI

Treatment: Glucosamine may decrease pain and slow

or stop progression 1500 mg/day

Chondroitin sulfate questionableabsorption


54/63

54

Osteoarthritis

Analgesics and antiinflammatory drugs Range of motion exercises

Reduce aggravating factors

Weight loss Use of cane, crutches or walker

Surgical removal of bone spurs

Replacement of joint


55/63

55

Rheumatoid Arthritis

Systemic disease with prominentinvolvement of the joints

Inflammatory joint disease characterized

by:

Inflammatory damage in the synovial

membrane or articular cartilage

Systemic signs of inflammation: fever,

leukocytosis, malaise, anorexia,hyperfibrinogenemia)


56/63

56

Rheumatoid Arthritis Systemic autoimmune disease that causes

chronic inflammation of connective tissue Initially affects synovial membrane

Later articular cartilage, joint capsule,

ligaments and tendons, and bone Affects joints of hands, wrists, ankles, and

feet, but shoulders, hips and cervical spinemay also be involved

Systemic effects on heart, kidney, lungs, skinand other organs


57/63

57

Rheumatoid Arthritis Mild to severe

Destroys and distorts joints

Reduces life expectancy

Remission and exacerbation

1 2% of adult population

Women : men = 3:1

Onset usually in 20s or 30s

Symptoms lessen during pregnancy

Seasonal variation


58/63

58


Idiopathic disease Immune-mediated destruction of joints

Rheumatoid factors (IgM and IgG) target

blood cells and synovial membranesforming antigen-antibody complexes

Genetic predisposition

Possibly bacterial or viral infection(Epstein-Barr)


59/63

59


Chronic inflammation of synovial membrane Cellular proliferation and damage to the

microcirculation

Synovial membrane becomes irregular Swelling, stiffness and pain

Cartilage and bone destruction

Ankylosis or fusing of joint Ligaments and tendons also affected


60/63

60


Systemic effects: Generalized weakness and malaise

Up to 35% develop granulomas called

rheumatoid nodules

Systemic inflammation of blood vessels

rheumatoid vasculitis

Serous membranes may be affected


61/63

61


Evaluation : Physical examination

X-ray

Serologic tests for rheumatoid factor and

circulating antigen-antibody complexes

No cure


62/63

62

Rheumatoid Arthritis Therapy:

Relieve pain and swelling and retain as

much joint function as possible

Resting the joint, or binding or splinting

Use of hot and cold packs

Diet high in calories and vitamins

Strengthening of associated muscles


63/63

63


Drug therapy: Methotrexate

Antimalarial drugs and immunosuppression

Surgical Synovectomy

Correction of deformities

Joint replacement

Documents

Musculoskeletal Pa Tho Physiology A