RT 208 Pathology Flashcards

1
Q

Vitamin D

A

Absorption of calcium in the intestine. Activated by ultraviolet radiation

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2
Q

Vitamin A

A

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

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3
Q

Vitamin C

A

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

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4
Q

Pituitary Gland

A

Human Growth Hormone

Stimulates reproduction of cartilage cells in epiphyseal plates

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5
Q

Thyroid Hormone

A

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

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6
Q

Calcitonin

A

calcium storage in bone

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7
Q

Sex hormones

A

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

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8
Q

Parathyroid Gland

A

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

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9
Q

Minerals

A
Calcium 25%
Phosphorus 12%
Magnesium 0.37%
Potassium 0.7%
Zinc .009%
Copper .0009%
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10
Q

Protein

A

for Osteoid production

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10
Q

Etiology:

A

Vitamin C deficiency leading to inadequate production of collagen

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11
Q

S/S

A

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

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12
Q

Tx

A

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

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13
Q

Etiology:

A

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

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14
Q

Lack of estrogens and androgens in post-menopausal women

A

and androgens in post-menopausal women

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15
Q

Nutritional disorders

A

not enough protein or calcium in diet

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16
Q

Disuse

A

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.

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17
Q

Osteoporosis Treatment

A
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
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18
Q

Symptoms of Osteomalacia - Rickets

A

Etiology:
Sunlight stimulates ergosterol
Renal Rickets

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19
Q

Etiology

A

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

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20
Q

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

A

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

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21
Q

Renal Rickets

A

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.

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22
Q

Osteomalacia

A

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

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23
Q

Hyperparathyroidism - Primary

A

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

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24
Q

Hyperparathyroidism - Secondary

A

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.

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25
Q

S/S

A

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

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26
Q

Osteitis DeformansPaget’s Disease

A

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).

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27
Q

Osteitis DeformansPaget’s Disease - Etiology

A

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.

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28
Q

Paget’s Disease

A

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.

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29
Q

Treatment - Paget’s Disease

A

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)

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30
Q

Tumors of the Bone -Primary

A

originate in bone or bone components

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31
Q

Tumors of the Bone - Secondary

A

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.

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32
Q

Primary tumor of the bone - Osteoma

A
Benign
Age of patient - any
Common site -Skull, ear, sinuses
Etiology -Bony outgrowth in EAM. Bilateral, multiple lesions
Tx: Surgical Excision
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33
Q

Primary tumor of the bone - Fibroma

A

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

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34
Q

Primary tumor of the bone - Osteochondroma

A

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

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35
Q

Primary tumor of the bone - Chondroma

A

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

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36
Q

Primary Malignant Bone Tumors -Osteosarcoma

A
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

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37
Q

Primary Malignant Bone Tumors -Fibrosarcoma

A

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
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38
Q

Primary Malignant Bone Tumors -Chondrosarcoma

A

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

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39
Q

Primary Malignant Bone Tumors -Ewings Sarcoma

A

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

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40
Q

Primary Malignant Bone Tumors -Giant Cell Tumor

A

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

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41
Q

Inflammatory Lesions of the Bone - Osteomyelitis

A

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:

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42
Q

Hematogenous dissemination

A

bacteremia

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43
Q

Traumatic implantation

A

GSW, compound fx

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44
Q

Osteomyelitis -Most common bacteria

A

Staph Aureus, E. Coli, Proteus vulagaris Pseudomonas Aeruginosa

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45
Q

Sequestrum

A

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

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46
Q

Involucrum

A

Necrotic bone stimulates periosteum to create new

bone at the site of the infection.

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47
Q

Osteomyelitis: S/S

A

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

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48
Q

Osteomyelitis: Dx:

A

History of injury

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49
Q

Legg-Calve Perthes – Coxa Plana

A

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.

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50
Q

Osteomyelitis: Blood Tests

A

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

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51
Q

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

A

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.

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52
Q

Legg-Calve Perthes – Coxa Plana Etiology

A

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

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53
Q

Legg-Calve Perthes S/S

A

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.

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54
Q

Legg-Calve Perthes – Coxa Plana - DX

A
  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
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55
Q

Inflammatory Lesions of the Bone - Osgood-Schalatter Disease

A

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.

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56
Q

Osgood-Schalatter Disease - Etiology

A

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.

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57
Q

Osgood Schlatter Disease - S/S

A

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

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58
Q

Osgood Schlatter Disease - DX

A

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

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59
Q

Inflammatory Lesions of the Bone -Aseptic Necrosis

A

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

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60
Q

Aseptic Necrosis - Etiology

A

Death of bone with secondary irritation and low grade inflammation

(a) Idiopathic: no known cause
(b) Associated trauma

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61
Q

Aseptic Necrosis - S/S

A

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.

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62
Q

Aseptic Necrosis - common sites

A

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
Q

Aseptic Necrosis - Treatment

A

Treatment: Immobilization
Treatment: Immobilization and analgesics

64
Q

Inflammatory Lesions of the Bone Traumatic arthritis (osteoarthritis)

A

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
Q

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

A

(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
Q

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

A
  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
Q

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

A

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
Q

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

A

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
Q

Arthroplasty

A

joint replacement

70
Q

Arthrodesis

A

Surgical fusion (laminectomy)

71
Q

Osteoplasty

A

Scraping deteriorated bone from joint

72
Q

Osteotomy:

A

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

73
Q

Inflammatory Lesions of the Bone Septic Arthritis

A

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
Q

Inflammatory Lesions of the Bone Septic Arthritis Etiology

A

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
Q

Inflammatory Lesions of the Bone Septic Arthritis DX

A

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
Q

Inflammatory Lesions of the Bone Septic Arthritis TX

A

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
Q

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

A

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

78
Q

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

A

for Penicillin resistant bacteria

79
Q

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

A

for H. Influenzae

80
Q

Inflammatory Lesions of the Bone Septic Arthritis

TX(4) Gentamicin

A

for Gram negative bacilli

81
Q

Inflammatory Lesions of the Bone Gouty Arthritis

A

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
Q

Primary Gout

A

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

83
Q

Secondary Gout

A

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

84
Q

Gouty Arthritis - DX

A

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
Q

Gout Treatment

A

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
Q

Allopurinol

A

reduces uric acid formation

87
Q

Colchicine

A

prevents recurrent attacks

88
Q

Probenecid and Sulfinpyrazone

A

promote uric acid excretion

89
Q

Inflammatory Lesions of the Bone Rheumatoid ArthritisAutoimmune Disorder

A

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
Q

Rheumatoid ArthritisAutoimmune Disorder Pathogenic Process

A

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

91
Q

Rheumatoid Arthritis -Pathogenic Process

A

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
Q

Rheumatoid Arthritis - S/S

A

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
Q

Rheumatoid Arthritis - DX

A

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
Q

Rheumatoid Arthritis Treatment TX

A

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
Q

Muscle and Connective Tissue Disorders

A
  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
Q

Tendonitis:

A

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

97
Q

Tendonitis:

Typical sites include:

A

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

98
Q

Tendonitis: Etiology

A

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

99
Q

Tendonitis: Bursitis:

A

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
Q

Muscle and Connective Tissue Disorders -Tendonitis - S/S

A

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
Q

Muscle and Connective Tissue Disorders -Bursitis - S/S

A

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

102
Q

Tendonitis- Diagnosis: X-rays

A

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
Q

Bursitis- Diagnosis: X-rays

A

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
Q

Treatment – Bursitis and Tendonitis

A
  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
Q

Epicondylitis (tennis elbow)Epitrochlear Bursitis

A

Inflamation of the forearm extensor, supinator tendon.

106
Q

Epicondylitis (tennis elbow)Epitrochlear Bursitis -Etiology

A

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
Q

Epicondylitis (tennis elbow)Epitrochlear Bursitis - S/S

A

Elbow pain that worsens and radiates to forearm and hand.

108
Q

Epicondylitis DX

A

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
Q

Carpal Tunnel Syndrome

A

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
Q

Carpal Tunnel Syndrome -Etiology

A

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
Q

Carpal Tunnel Syndrome -Causes

A

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
Q

Hallux Valgus - Bunion

A

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
Q

Hallux Valgus - Bunion - Etiology

A

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
Q

Hallux Valgus - Bunion - S/S

A

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

115
Q

Hallux Valgus - Bunion - Traetment

A

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
Q

Congenital Disorders

A

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
Q

Talipes Treatment

A
  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:
  4. forefoot adduction then varus (inversion) and finally equinus (plantar flexion)
118
Q

Congenital Hip Dysplasia

A

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
Q

Congenital Hip Dysplasia- Etiology:

A

Unproven theories suggest:

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

120
Q

Congenital Hip Dysplasia - DX

A

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
Q

Spinal Disorders

A

Kyphosis
Lordosis
Scoliosis
Herniated Nucleus Pulposes

122
Q

Scoliosis

A

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
Q

Scoliosis -Causes

A

(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
Q

Scoliosis - Diagnosis

A

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
Q

Scoliosis - Diagnosis

A

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
Q

Scoliosis - Diagnosis

A

Measuring the degree of curvature using the Cobb Method

127
Q

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

A

Monitor every three months

128
Q

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

A

spinal exercise and brace

129
Q

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

A

may require spinal fusion

130
Q

Herniated Nucleus Pulposes

A

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
Q

HNP

A

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
Q

HNP Etiology

A
  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
Q

HNP - Signs/Symptoms

A

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

134
Q

HNP Diagnosis

A

(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

135
Q

HNP Treatment: Usually conservative

A

(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

136
Q

Fractures and Dislocations

A

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

137
Q

Fracture

A

Loss of integrity of the bone structure

138
Q

Fractures and Dislocations S/S

A

the “5 P’s” for arm and leg fractures:

(1) Pain and point tenderness
(2) Pallor
(3) Pulse loss
(4) Paresthesia
(5) Paralysis

139
Q

Fracture Incomplete:

A

break partially extends through bone (Greenstick)

140
Q

Fracture Complete:

A

Bone breaks into two or more pieces

141
Q

Fracture Simple (closed):

A

overlying skin is not broken

142
Q

Fracture Compound (open):

A

overlying skin is broken with risk of infection

143
Q

Fracture Non-displaced:

A

fractured bones remain in alignment

144
Q

Fracture Displaced:

A

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

145
Q

Fracture Transverse:

A

break runs transversely across bone

146
Q

Fracture Oblique:

A

break runs at an angle across the bone

147
Q

Fracture Spiral

A

break winds around bone like a coil

148
Q

Fracture Linear:

A

Break runs the length of the bone

149
Q

Fracture Comminuted:

A

bone is shattered or compressed in fragment

150
Q

Fracture Impacted:

A

Bone ends are driven into each other

151
Q

Fracture Compression:

A

Bone collapses (vertebrae) under pressure

152
Q

Fracture Avulsion:

A

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

153
Q

Fracture Depression:

A

Trauma drives bone fragments inward

154
Q

Dislocation

A

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

155
Q

Subluxation

A

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

156
Q

Disolocation and Subluxations Etiology

A

May be congenital or occur as a result of trauma