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Flashcards in RT 208 Pathology Deck (157):
1

Vitamin D

Absorption of calcium in the intestine. Activated by ultraviolet radiation

2

Vitamin A

Needed for bone resorption that occurs during normal development. Retarded development of bone occurs without it.

3

Vitamin C

needed for synthesis of collagen which is used by osteoblasts to make osteoid.

4

Pituitary Gland

Human Growth Hormone
Stimulates reproduction of cartilage cells in epiphyseal plates

5

Thyroid Hormone

Thyroid Gland -T3 and T4 stimulates the replacement of cartilage in epiphyseal plates. Excessive secretion halts bone growth. A deficiency causes stunted growth.

6

Calcitonin

calcium storage in bone

7

Sex hormones

Androgens (testosterone), and Estrogens . Testes, ovaries and adrenal gland (zona reticularis of adrenal cortex).

8

Parathyroid Gland

parathormone. Stimulates osteoclasts to release calcium into the blood stream.

9

Minerals

Calcium 25%
Phosphorus 12%
Magnesium 0.37%
Potassium 0.7%
Zinc .009%
Copper .0009%

10

Protein

for Osteoid production

10

Etiology:

Vitamin C deficiency leading to inadequate production of collagen

11

S/S

Internal bleeding into joints, periosteum and mucus membranes, petechiae, ecchymoses, anemia, pallor, bleeding gums and loose teeth.

12

Tx

Restore vitamin C intake. 100-200 mg p.o. daily

13

Etiology:

Rate of bone resorption increases while rate of bone formation slows down causing loss of bone mass.

14

Lack of estrogens and androgens in post-menopausal women

and androgens in post-menopausal women

15

Nutritional disorders

not enough protein or calcium in diet

16

Disuse

Lack of exercise which is necessary for osteoid formation. “Atrophy”of disuse.
Example: patient’s whose extremities have been in a cast for six weeks.

17

Osteoporosis Treatment

Basically symptomatic and try to prevent additional fractures
Estrogens to decrease bone resorption
Fluoride to stimulate bone formation
Calcium and Vitamin D
Teach patient good body mechanics

18

Symptoms of Osteomalacia - Rickets

Etiology:
Sunlight stimulates ergosterol
Renal Rickets

19

Etiology

Vitamin D deficiency either due to inadequate dietary intake, malabsorption in gastrointestinal tract or too little sunlight.

20

Sunlight stimulates ergosterol in the skin and makes vitamin D active.

Vitamin D is necessary for the absorption of calcium and phosphorus in the GI tract.

21

Renal Rickets

kidney injury causes retention of phosphorus in the body which stimulates the parathyroid gland to release parathormone and increase calcium levels in the blood by removing calcium from the bone.

22

Osteomalacia

There is plenty of osteoid but no calcium to provide strength. Bow legs, knock knees result

23

Hyperparathyroidism - Primary

is where one or more of the parathyroid glands enlarge and increase the secretion of PTH (parathormone). Parathyroid adenoma accounts for 80% of this problem

24

Hyperparathyroidism - Secondary

Excessive compensatory production of PTH because of high levels of phosphorus in the blood due to renal problems. Hypocalcemia from inadequate dietary calcium can cause it too.

25

S/S

Kidney stones, chronic back pain from fx, neuromuscular and CNS (personality disturbances, depression, psychosis, and coma)

26

Osteitis Deformans Paget’s Disease

a slowly progressive metabolic disorder characterized by an initial phase of bone resorption (osteoclastic phase), followed by a reactive phase of abnormal bone formation (osteoblastic phase).

27

Osteitis Deformans Paget’s Disease - Etiology

exact cause is unknown but it is thought that viral infection (mumps) may trigger it years after the exposure. 5% of patient’s with Paget’s disease develop osteosarcoma.

28

Paget’s Disease

Paget’s disease occurs worldwide but is rare in Asia, Middle East, Africa and Scandinavia.

In United States approximately 2.5 million people over the age of 40, mostly men have the disease
.
S/S: Early stages patient may be asymptomatic. Pain may occur from impingement of abnormal bone on spinal cord. Cranial enlargement (frontal and occipital bones) involved.

Pagetic sites are warm, tender and susceptible to pathologic fracture.

29

Treatment - Paget’s Disease

Drug therapy: Calcitonin given sc or IM or etidronate given p.o. to retard bone resorption

Mithramycin (cytoxic antibiotic) to decrease calcium loss, urinary hydroxypoline and serum alkaline phosphatase

Surgery: to repair fracture sites or correct deformities

Other tx: aspirin, ibuprofen for pain (symptomatic)

30

Tumors of the Bone -Primary

originate in bone or bone components

31

Tumors of the Bone - Secondary

metastatic tumors from other cancers (breast, prostate, etc.) that spread to the bone via the blood stream (nutrient artery and branches) or by direct invasion (proximity). The cancer usually will appear in the metaphysis (area between diaphysis and epiphysis) where the nutrient artery enters the bone. Cancer cells get trapped in the capillary beds of the bone and start growing.

32

Primary tumor of the bone - Osteoma

Benign
Age of patient - any
Common site -Skull, ear, sinuses
Etiology -Bony outgrowth in EAM. Bilateral, multiple lesions
Tx: Surgical Excision

33

Primary tumor of the bone - Fibroma

Benign
Age of patient - any
Common site -Fibrous bone tissues
Etiology -Displaces bone cells

34

Primary tumor of the bone - Osteochondroma

Benign
Age of patient - Age 15 to 25
Common site Lower femur
Etiology -Most common benign tumor

35

Primary tumor of the bone - Chondroma

Benign
Age of patient - any
Common site = Phalanges of hands and feet
Etiology = Develops from cartilage

36

Primary Malignant Bone Tumors -Osteosarcoma

Age of patient - 10-25
Location - Metaphysis of long bones
Femur
Tibia
Humerus

Comments - Most common
15% 5 year survival rate

Treatment - 1. Surgery:
(a) resection
(b)Amputation
2. XRT
3. Chemo

37

Primary Malignant Bone Tumors -Fibrosarcoma

Age of patient -Males
30 to 40

Location - Fibrous tissue surrounding bone
1. Flat bones

Comments - Vary rare tumor
Nonosseous origin


Treatment -
1. Surgery:
a. Amputation
2. XRT
3. Chemo

38

Primary Malignant Bone Tumors -Chondrosarcoma

Age of patient -Males
30 to 50

Location -
Pelvis
Femur
Ribs
Shoulder

Comments - Develops From cartilage Painless, slow growing


Treatment -
Surgery
XRT for palliation
Chemo

39

Primary Malignant Bone Tumors -Ewings Sarcoma

Age of patient -Males 10 to 20

Location -
Lower ext.
Femur
Pelvis
Tib/Fib
Vertebrae

Comments -Bone marrow Poor Px Mets to lung

Treatment -
Surgery
XRT
Chemo

40

Primary Malignant Bone Tumors -Giant Cell Tumor

Age of patient - Females 18-50

Location -
Long bones
Knee area

Comments -Benign tumor that becomes malignant

Treatment -
Surgery
Curettage
Scraping away material from cavity or surface

41

Inflammatory Lesions of the Bone - Osteomyelitis

a pyogenic infection of bone that may be acute or chronic.
Etiology:
(a) Complication of an acute localized infection
(b) Hematogenous dissemination- bacteremia
(c) Traumatic implantation: GSW, compound fx
Most common bacteria is Staph Aureus, E. Coli, Proteus vulagaris Pseudomonas Aeruginosa
Terms:
(a) Sequestrum: dead bone that collects and drains
its way out through an abscess or sinus tract
(b) Involucrum: Necrotic bone stimulates periosteum to create new
bone at the site of the infection.
S/S: Patient may have pain, tenderness, heat, swelling and restricted movement in the infected bone.
Dx: History of injury
Blood Tests: leukocytosis, elevated Erythrocyte Sedimentation Rate (ESR)
Blood cultures:

42

Hematogenous dissemination

bacteremia

43

Traumatic implantation

GSW, compound fx

44

Osteomyelitis -Most common bacteria

Staph Aureus, E. Coli, Proteus vulagaris Pseudomonas Aeruginosa

45

Sequestrum

dead bone that collects and drains its way out through an abscess or sinus tract

46

Involucrum

Necrotic bone stimulates periosteum to create new
bone at the site of the infection.

47

Osteomyelitis: S/S

Patient may have pain, tenderness, heat, swelling and restricted movement in the infected bone.

48

Osteomyelitis: Dx:

History of injury

49

Legg-Calve Perthes – Coxa Plana

Etiology: Spontaneous vascular interuption causes necrosis of femoral head in 1-3 weeks
New blood supply causes bone resorption and deposition of new bone cells. Deformity may result from pressure on weakened area (6 mo)
New bone replaces necrotic bone (2-3 years)
S/S: Persistent limp that becomes more severe especially during second stage of disease.
Mild pain (hip, thigh or knee) that is aggravated by activity and relieved by rest. Severely restricted abduction and rotation of hip.

50

Osteomyelitis: Blood Tests

leukocytosis, elevated Erythrocyte Sedimentation Rate (ESR) Blood cultures:

51

Inflammatory Lesions of the Bone - Legg-Calve Perthes Disease (Coxa Plana)

It is a disease where vascular interruption of the blood supply to a bone causes ischemic necrosis of the head of the femur. This causes the femoral head to flatten. It occurs most frequently in boys aged 4 to 10. The disease runs it’s course in 3 to 4 years. It may lead to premature osteoarthritis in later life due to misalignment of the acetabulum and flattened femoral head.

52

Legg-Calve Perthes – Coxa Plana Etiology

Spontaneous vascular interuption causes necrosis of femoral head in 1-3 weeks

53

Legg-Calve Perthes S/S

Persistent limp that becomes more severe especially during second stage of disease. Mild pain (hip, thigh or knee) that is aggravated by activity and relieved by rest. Severely restricted abduction and rotation of hip.

54

Legg-Calve Perthes – Coxa Plana - DX

1. Physical exam and history
2. Hip x-ray taken every 3-4 months
3. Aspiration and culture of synovial fluid
to rule out joint sepsis
Tx: Protect femoral head from further damage by containing it within the acetabulum.
3 months of bed rest with reduced weight traction then hip abduction splint or cast

55

Inflammatory Lesions of the Bone - Osgood-Schalatter Disease

Is a painful, incomplete separation of the epiphysis of the tibial tubercle from the tibial shaft. It is most common in adolescent boys and affects both knees.

56

Osgood-Schalatter Disease - Etiology

Trauma before the complete fusion of the epiphysis to the main bone. It may be a single violent trauma or repeated knee flexion against a tight quadraceps muscle or a deficient blood supply and or caused by genetic factors.

It occurs between the ages of 10 to 15 years old.

57

Osgood Schlatter Disease - S/S

Constant aching, pain and tenderness below the knee cap which worsens during any activity that causes forceful contraction of the patellar tendon on the tubercle.
Soft tissue swelling, heat and tenderness may be present

58

Osgood Schlatter Disease - DX

Physical exam: examiner forces the tibia into internal rotation while slowly extending the patient’s knee from a 90 degree flexion. At about 30 degrees flexion there is pain that subsides immediately with external rotation of the tibia

X-rays may be normal or show epiphyseal separation and soft tissue swelling for up to six months after onset.

TX: 6 to 8 weeks of immobilization through reinforced elastic knee support, plaster cast or splint. This allows revascularization and
re-ossification of the tubercle and minimizes the pull of the quadriceps muscle.
(2) Supportive treatment may include activity restrictions and cortisone injections into the joint to relieve tenderness.
(3) Surgery in extreme cases. It may be necessary to remove or “fix” the epiphysis or drill holes through the tubercle of the main bone for form vascular channels

59

Inflammatory Lesions of the Bone -Aseptic Necrosis

Etiology: Death of bone with secondary irritation and low grade inflammation
(a) Idiopathic: no known cause
(b) Associated trauma
S/S: The age group is between 5 to 15 years old.
Symptoms: pain, muscle spasm, and postural disorders. It is usually self limited and spontaneously regenerates. It is a slow process.
Common sites: Small bones of the wrist and ankle
NOTE: Scaphoid bone of the wrist is most common which is why we do a PA wrist with ulna deviation.
Treatment: Immobilization
Treatment: Immobilization and analgesics

60

Aseptic Necrosis - Etiology

Death of bone with secondary irritation and low grade inflammation
(a) Idiopathic: no known cause
(b) Associated trauma

61

Aseptic Necrosis - S/S

The age group is between 5 to 15 years old.
Symptoms: pain, muscle spasm, and postural disorders. It is usually self limited and spontaneously regenerates. It is a slow process.

62

Aseptic Necrosis - common sites

Small bones of the wrist and ankle

NOTE: Scaphoid bone of the wrist is most common which is why we do a PA wrist with ulna deviation.

63

Aseptic Necrosis - Treatment

Treatment: Immobilization
Treatment: Immobilization and analgesics

64

Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis)

The most common form of arthritis. It is a chronic condition causing deterioration of the joint cartilage and formation of reactive bone at the margins and subchondral areas of the joint.
Generally it begins at age 40 and progresses through middle age. Disability depends on the site and severity of involvement. It can range from minor limitations of the fingers to severe disability in persons with knee or hip involvement.

65

Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis) - Etiology

(1) Primary: A normal part of aging from metabolic, genetic, chemical and mechanical factors (wear and tear).
(2) Secondary: develops following a predisposing event such as trauma (sprain, fracture or congenital deformity)

66

Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis) - S/S

1. Joint pain after exercise or weight bearing that is relieved by rest. Stiffness in the morning
(2) Grating of the joint during motion and limited movement
(3) Osteoarthritis of the interphalangeal joints produces irreversible changes in the distal joints (Heberden’s nodes) and proximal joints (Bouchard’s nodes). These may be painless at first but eventually become red, swollen and tender

67

Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis) - DX

Thorough physical exam will confirm symptoms, and a lack of systemic symptoms rules out inflammatory joint disorders such as rheumatoid arthritis.
X-rays: PA, Lateral and oblique views confirm:
(1) Narrowing of joint space
(2) Joint deformity due to degeneration or articular damage
(3) Bony growths at weight-bearing areas
(hips and knees)

68

Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis) - TX

Pallative through medication and therapy
(1) Analgesics: aspirin, phenylbutazone, ibuprofen
(2) Intraarticular injections of corticosteroids
(3) Reduce joint stress by immobilization
(4) Surgery:
(a) Arthroplasty: joint replacement
(b) Arthrodesis: Surgical fusion (laminectomy)
(c) Osteoplasty: Scraping deteriorated bone from joint
(d) Osteotomy: change alignment of bone to relieve
stress by excision of wedge of bone or cutting of bone

69

Arthroplasty

joint replacement

70

Arthrodesis

Surgical fusion (laminectomy)

71

Osteoplasty

Scraping deteriorated bone from joint

72

Osteotomy:

change alignment of bone to relieve stress by excision of wedge of bone or cutting of bone

73

Inflammatory Lesions of the Bone Septic Arthritis

A medical emergency. Septic arthritis is caused by a bacterial invasion of the joint with inflammation of the synovial lining. If the organism enters the joint cavity then effusion and pyogenesis follow with eventual destruction of the bone and cartilage. Septic arthritis can lead to ankylosis and fatal septicemia.

74

Inflammatory Lesions of the Bone Septic Arthritis Etiology

Bacteria spread from a primary site through blood or contiguous extension to the joint.
Common organisms: Gram positive: Staph Aureous, Strep Pyogenes, Strep peumoniae, and Strep Viridans.
Gram Negative: Neiserria gonorrhea and Hemophilus influenzae
Other: E. Coli, Salmonella, and Pseudomonas
Note: Gram Positive usually infect Adults
H. Influenzae infect children

75

Inflammatory Lesions of the Bone Septic Arthritis DX

Laboratory: Gram stain or culture of synovial fluid. Joint fluid analysis shows gross pus or watery, cloudy fluid, decreased viscosity and WBC count of 50,000 per cubic mm.
X-ray: Distension of joint capsule followed by narrowing of the joint space (indicating damage) and erosion of the bone.
Nuclear medicine: 3 phase bone scan

76

Inflammatory Lesions of the Bone Septic Arthritis TX

Antibiotic Therapy Culture and Sensitivity
(1) Penicillin G: Staph Aureous, Staph Pyogenes
Staph Pneumoniae, Staph Viridens, and
N. Gonorrhea
(2) Nafcillin: for Penicillin resistant bacteria
(3) Ampicillin: for H. Influenzae
(4) Gentamicin: for Gram negative bacilli

77

Inflammatory Lesions of the Bone Septic Arthritis TX (1) Penicillin

G: Staph Aureous, Staph Pyogenes Staph Pneumoniae, Staph Viridens, and N. Gonorrhea

78

Inflammatory Lesions of the Bone Septic Arthritis TX (2) Nafcillin

for Penicillin resistant bacteria

79

Inflammatory Lesions of the Bone Septic Arthritis TX (3) Ampicillin

for H. Influenzae

80

Inflammatory Lesions of the Bone Septic Arthritis
TX(4) Gentamicin

for Gram negative bacilli

81

Inflammatory Lesions of the Bone Gouty Arthritis

Gout is a metabolic disease (an error in Purine metabolism) marked by urate deposits in the joint. It mainly occurs in the joints of the lower extremities.

82

Primary Gout

Purine is an amino acid which causes an over production of uric acid with retention in the blood (hyperuricemia).

83

Secondary Gout

Develops during the course of other diseases (obesity, diabetes mellitus, hypertension, sickle cell anemia and renal disease

84

Gouty Arthritis - DX

Presence of monosodium urate monohydrate crystals in the synovial fluid (arthrocentesis) or tophaceous material reveals intracellular crystals of sodium urate.
Increased serum uric acid in primary gout
Increased urinary uric acid in secondary gout
TX: Immobilization of joint
Analgesics: Acetaminophen
Corticosteroids or Corticotropin (IV or IM) Joint Aspiraton

85

Gout Treatment

TX: Reduce hyperuricemia
Allopurinol = reduces uric acid formation
Colchicine = prevents recurrent attacks
Probenecid and Sulfinpyrazone = promote uric acid excretion
NOTE: These drugs should not be given to patients with uric acid kidney stones.

86

Allopurinol

reduces uric acid formation

87

Colchicine

prevents recurrent attacks

88

Probenecid and Sulfinpyrazone

promote uric acid excretion

89

Inflammatory Lesions of the Bone Rheumatoid Arthritis Autoimmune Disorder

A chronic, systemic, inflammatory disease that primarily attacks peripheral joints (MCP) and surrounding muscles, tendons, ligaments and blood vessels.
Pathogenic Process: It believed that altered IgG antibodies are not recognized by the body so the body creates antibodies against itself (called RF antibodies).

90

Rheumatoid Arthritis Autoimmune Disorder Pathogenic Process

It believed that altered IgG antibodies are not recognized by the body so the body creates antibodies against itself (called RF antibodies).

91

Rheumatoid Arthritis -Pathogenic Process

Synovitis develops from congestion and edema of the synovial capsule.
Formation of pannus (thickened layers of granulation tissue antigen/antibody) marks the second stage of the disease. Pannus covers and invades the cartilage causing damage
Fibrous ankylosis (fibrous invasion of the pannus and scar formation occludes the joint space) characterized by the third stage of the disease

92

Rheumatoid Arthritis - S/S

RA develops insidiously and produces non-specific symptoms such as fatigue, malaise, anorexia and persistent low-grade fever, and weight loss. Later more specific localized articular symptoms develop at the following joints: PIP, MCP, and metarsophalangeal joints.

93

Rheumatoid Arthritis - DX

X-ray shows demineralization of bone and soft and soft tissue swelling. Later loss of cartilage and narrowing of joint spaces. Finally, bone and cartilage destruction, subluxations and deformities.
Lab: Rheumatoid Factor (RF) positive with a titer of 1:160 or higher
Erythrocyte Sedimentation Rate: elevated
Synovial fluid analysis: increased volume and turbidity but decreased viscosity and C3 & C4 complement. WBC count more than 10,000 per cubic cm.

94

Rheumatoid Arthritis Treatment TX

Salicylates (aspirin) decrease pain and inflammation
Non-Steroid Anti-inflamatory agents (NSAID)
such as Indomethacin, Fenoprofen and
Ibuprofen) are used
Immunosuppressive drugs such as
Cyclophsphamide and Azathioprin are used
* Supportive measures include 8 to 10 hours of sleep, splinting of joints and physical therapy that includes Range of Motion (ROM) exercises

95

Muscle and Connective Tissue Disorders

1. Tendonitis: is an inflammation of the tendons and muscle attachments to bone.
Typical sites include: Rotator cuff, Hip, Achilles tendon and Hamstring
Etiology: Trauma. Strain during sports activity and musculoskeletal disorders such as Rheumatic disease, congenital defects, postural misalignments or hypermobility and abnormal body development
2. Bursitis: usually occurs at middle age from recurring trauma that stresses a joint or from an inflammatory joint disease such as rheumatoid arthritis or gout. Septic bursitis may result from wound infection or bacterial invasion of the skin covering the bursa.

96

Tendonitis:

Tendonitis: is an inflammation of the tendons and muscle attachments to bone.
.

97

Tendonitis:
Typical sites include:

Typical sites include: Rotator cuff, Hip, Achilles tendon and Hamstring

98

Tendonitis: Etiology

Trauma. Strain during sports activity and musculoskeletal disorders such as Rheumatic disease, congenital defects, postural misalignments or hypermobility and abnormal body development

99

Tendonitis: Bursitis:

usually occurs at middle age from recurring trauma that stresses a joint or from an inflammatory joint disease such as rheumatoid arthritis or gout. Septic bursitis may result from wound infection or bacterial invasion of the skin covering the bursa.

100

Muscle and Connective Tissue Disorders -Tendonitis - S/S

restricted movement of joint and localized pain that occurs mainly at night. Fluid accumulation causes swelling.
Calcific tendonitis: calcium deposits in the tendon cause proximal weakness and erosion into the adjacent bursa

101

Muscle and Connective Tissue Disorders -Bursitis - S/S

Fluid accumulation in the bursa causes irritation, inflammation, and sudden or gradual pain with limited movement.

102

Tendonitis- Diagnosis: X-rays

Diagnosis: X-rays: with tendonitis x-rays will be normal at first but may later show bone fragments, osteophyte formation, sclerosis, or calcium deposits.

103

Bursitis- Diagnosis: X-rays

Localized pain and inflammation and a history of unusual strain or injury 2 to 3 days before the onset of pain. During early stages the x-rays are normal except in situations of calicific bursitis.

104

Treatment – Bursitis and Tendonitis

1. Rest the joint. Use immobilization with splint, cast or sling
2. Analgesics
3. Application of cold and warm compresses
4. Ultrasound (diathermy)
5. Injections of corticosteroids/lidocaine

105

Epicondylitis (tennis elbow) Epitrochlear Bursitis

Inflamation of the forearm extensor, supinator tendon.

106

Epicondylitis (tennis elbow) Epitrochlear Bursitis -Etiology

Partial tear of the tendon. It is a common injury in persons whose activities require a forceful grasp, wrist extension against resistance and frequent forearm rotation.

107

Epicondylitis (tennis elbow) Epitrochlear Bursitis - S/S

Elbow pain that worsens and radiates to forearm and hand.

108

Epicondylitis DX

Patient history. Doctor may reproduce pain by wrist extension and supination with lateral movement.
X-rays are negative
TX: Injections of corticosteroids and lidocaine
Aspirin
Supportive treatment includes: immobilization with a splint, heat therapy and short wave diathermy or ultrasound and physical therapy such as manipulation and massage to detach the tendon from the chronically inflammed periosteum.

109

Carpal Tunnel Syndrome

The most common nerve entrapment syndrome.
It involves entrapment and compression of the median nerve at the wrist, within the carpal tunnel.
Other structures passing through the carpal tunnel are: flexor tendons to the fingers and thumb and blood vessels.

110

Carpal Tunnel Syndrome -Etiology

The carpal tunnel is formed by the carpal bones and the transverse carpal ligament. Inflammation or fibrosis of the tendon sheaths that pass through the carpal tunnel cause edema and compression of the median nerve.

111

Carpal Tunnel Syndrome -Causes

may include: rheumatoid arthritis, flexor tenosynovitis, nerve compression, pregnancy, renal failure, menopause, diabetes mellatus, acromegaly, edema following a Colles fracture, hypothyroidism, benign tumors, tuberculosis and other granulomatous disease.
Repetitive motion syndromes have been identified as a causative agent too

112

Hallux Valgus - Bunion

lateral deviation of the great toe at the metarsophalangeal joint. It occurs with medial enlargement of the first metatarsal head and bunion formation (bursa and callus formation at the bony prominency)

113

Hallux Valgus - Bunion - Etiology

It may be congenital or familial but it is most often acquired from degenerative arthritis or prolonged pressure on the foot by shoes that compress the foot.
Congenital hallux valgus occurs as a result of abnormal bone alignment

114

Hallux Valgus - Bunion - S/S

Tender bunion covered by a deformed, hard, erythematous skin and palpable bursa. Pain from pressure caused by shoes is an indication too.

115

Hallux Valgus - Bunion - Traetment

Good footcare and proper shoes. Foam pads to separate first and second toes at night. Severe disease is treated by bunionectomy with corrective immobilization.

116

Congenital Disorders

Tailipes: Clubfoot
Most common congenital disorder of the lower extremities. It is marked by a deformed talus bone and shortened Achilles tendon.
1:1000 births
Talipes equinovarus: foot points downward

117

Talipes Treatment

1. Correct deformity
2. Maintain correction until foot regains normal muscle balance
3. Observe foot for evidence of deformity recurrence
Deformity is corrected in sequential order with:
1. forefoot adduction then varus (inversion) and finally equinus (plantar flexion)

118

Congenital Hip Dysplasia

Abnormality of hip joint that is present at birth and is the most common disorder that affects hip joints of children under 3 years old.

119

Congenital Hip Dysplasia- Etiology:

Unproven theories suggest:
(1) Maternal hormones relax ligaments for preparation of labor
(2) Breech delivery rather than normal cephalic delivery

120

Congenital Hip Dysplasia - DX

1) check skin folds at hip area. Should be equal bilaterally
(2) Place child prone and observe buttock fold. Affected side will be higher
(3) Move patient into positions that would dislocate hip
(4) x-rays show the location of the femur in relation to the shallow acetabulum

121

Spinal Disorders

Kyphosis
Lordosis
Scoliosis
Herniated Nucleus Pulposes

122

Scoliosis

is a lateral curvature of the spine that may be found in the thoracic, lumbar, or thoracolumbar spinal segments. The curve may be convex to the right (most common in T-spine) or to the left (lumbar). Rotation of the vertebral column around it’s axis occurs and may cause rib cage deformity. Scoliosis is most often associated with kyphosis and lordosis.

123

Scoliosis -Causes

(1) Functional (postural) = poor posture
(2) Structural (deformity of vertebral bodies)
(a) Congenital: Wedge vertebra
(b) Paralytic or musculoskeletal due to asymmetric paralysis from polio or cerebral palsy
(c) Idiopathic (most common): may be transmitted as an autosomal dominant or multifactorial trait. Classified as infantile, juvenile or adolescent which generally affects girls between the ages of 10 to skeletal maturity.

124

Scoliosis - Diagnosis

Look at persons back
1. Is one shoulder higher than the other?
2. When child’s arms hang loosely at their side does one arm swing away from the body more than the other?
3. Is one hip higher or more prominent than the other?
4. Does child tend to tilt to one side?

125

Scoliosis - Diagnosis

X-rays in the AP and lateral projections taken with the patient standing upright and bending.
Measuring the degree of curvature using the Cobb Method
Note:
(1) Curve of 25 degrees or less = Monitor every three months
(2) Curve 30-50 degrees = spinal exercise and brace
(3) Curve of 40 degrees or more may require spinal fusion

126

Scoliosis - Diagnosis

Measuring the degree of curvature using the Cobb Method

127

Measuring the degree of curvature using the Cobb Method - Curve of 25 degrees or less

Monitor every three months

128

Measuring the degree of curvature using the Cobb Method - Curve 30-50 degrees

spinal exercise and brace

129

Measuring the degree of curvature using the Cobb Method - Curve of 40 degrees or more

may require spinal fusion

130

Herniated Nucleus Pulposes

This problem occurs when all or part of the nucleus pulposes (the soft gelatinous central portion of the intervertebral disk) is forced through the disk’s weakened or torn outer ring (annulus fibrosis)

131

HNP

The extruded disk may impinge on spinal nerve roots as the exit from the spinal canal or the spinal cord itself. This will result in back pain and other signs of nerve root irritation (tingling, shooting pains etc.).

132

HNP Etiology

1. Severe trauma or strain to the back
2. Intervertebral disk degeneration due to age
(a) 90% occurs in lumber or Lumbar sacral region
(b) 8% in the cervical region
(c) 2% in the thoracic region

133

HNP - Signs/Symptoms

Severe low back pain which radiates to the buttocks, legs and feet, usually unilaterally. Pain may be sudden following the injury and may go away but recur at intervals.
Sciatic pain follows beginning as a dull pain in the buttocks. Valsalva maneuver, coughing, sneezing or bending intensifies the pain.
Sensory and motor loss in the affected nerve root may result in atrophy of leg muscles and weakness

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HNP Diagnosis

(1) X-rays to R/O other abnormalities of spine
(2) Check of extremity pulses including posterior tibial and dorsalis pedis pulses, skin temperature to R/O ischemic disease
(3) Myelography: contrast injection into the subarachnoid space of spinal canal between 3rd and 4th lumbar vertebrae
(4) Computed Tomography
(5) MRI – shows soft tissue swelling and herniation

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HNP Treatment: Usually conservative

(1) Bed rest with pelvic traction, heat, and an exercise program
(2) Aspirin to reduce inflammation and edema
(3) Epidural injections of steroids (cortisone or dexamethasone) and lidocaine as well as muscle relaxants (diazepam or methocarbamol)
(4) Surgery: laminectomy: excision of a portion of the lamina and remove protruding disk. Spinal fusion may be necessary to overcome segmental instability.
(5) Chemonucleolysis: injection of the enzyme Chymopapain to dissolve the disk
(6) Microdiskectomy (laser) removal of fragments of the disk

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Fractures and Dislocations

Fracture: Loss of integrity of the bone structure
(1) Causes: trauma, child abuse, pathologic (metabolic or nutritional), tumors (primary or metastatic), and stress fractures (prolonged standing, walking or running)
S/S: the “5 P’s” for arm and leg fractures:
(1) Pain and point tenderness
(2) Pallor
(3) Pulse loss
(4) Paresthesia
(5) Paralysis

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Fracture

Loss of integrity of the bone structure

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Fractures and Dislocations S/S

the “5 P’s” for arm and leg fractures:
(1) Pain and point tenderness
(2) Pallor
(3) Pulse loss
(4) Paresthesia
(5) Paralysis

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Fracture Incomplete:

break partially extends through bone (Greenstick)

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Fracture Complete:

Bone breaks into two or more pieces

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Fracture Simple (closed):

overlying skin is not broken

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Fracture Compound (open):

overlying skin is broken with risk of infection

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Fracture Non-displaced:

fractured bones remain in alignment

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Fracture Displaced:

Bone ends are not in alignment creating risk of muscle contractures and deformity

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Fracture Transverse:

break runs transversely across bone

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Fracture Oblique:

break runs at an angle across the bone

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Fracture Spiral

break winds around bone like a coil

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Fracture Linear:

Break runs the length of the bone

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Fracture Comminuted:

bone is shattered or compressed in fragment

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Fracture Impacted:

Bone ends are driven into each other

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Fracture Compression:

Bone collapses (vertebrae) under pressure

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Fracture Avulsion:

overexertion tears a muscle or ligament away from bone with pulling away a piece of the bone

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Fracture Depression:

Trauma drives bone fragments inward

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Dislocation

the bones of the joint totally lose contact with their articulating surfaces

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Subluxation

the bones of the joint partially lose contact with their articulating surfaces

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Disolocation and Subluxations Etiology

May be congenital or occur as a result of trauma