Unit 6: Chapter 49 Flashcards

(33 cards)

1
Q

Skeletal System Generation

A

From mesodermal and neural crest cells of the developing embryo.
Vertebra of axil skeleton beings 4th week in utero, limbs buds of lower extremities.
Ossification begins during 9th week of lower thoracic and upper lumbar vertebrae.
Hand pads days 33-36
Fingers days 41to 43

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2
Q

Bone Growth

A

The epiphyseal plates, there is continuous cartilage synthesis, calcification, erosion, and osteoblast invasion so that there is always active bone formation.
This process allows bone growth to proceed without changing the shape of the bone or causing disruption of the articular cartilage.
The cells in the growth plate stop dividing at puberty, at which time the epiphysis and metaphysis fuse.

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3
Q

Epiphyseal Growth Plates

A

Specialized structures of long bones that allow for rapid growth.

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4
Q

Chondrocytes

A

Involved in synthesizing the art oil age of the epiphyseal plate.

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5
Q

Long Bones Growth

A

As long bones grow in length, the deeper layers of cartilage cells in the growth plate multiply and enlarge and ultimately calcify.
The embedded cartilage cells then die, attracting the osteoblasts to migrate into the area.
Osteoid is secreted from the osteoblasts, which assists the mature bone in forming
End of long bones that allow growth at the age of 20 with plate closes

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6
Q

Horome for Normal Growth

A

TSH
Insulin like growth factors
Insulin
Alteration in these hormones affect greowht

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7
Q

Metatarsus Adductus (Toeing In)

A

Or pigeon toes
Common congenital foot deformity

The forefoot commonly is adducted and gives the foot a kidney-shaped appearance, whereas the hindfoot is normal.
Caused by torsion in the foot, lower leg, or in the entire leg.
Toeing-in because of adduction of the forefoot usually is the result of the fetal position maintained in utero.
It may occur in one foot or in both feet.

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8
Q

Metatarsus Grading System

A

Grade I is a supple deformity that can be passively manipulated into a straight position and requires no treatment.
grade II deformity corrects only to a straight lateral border
grade III deformity is more rigid and may require further treatment.
Treatment consisting of serial long leg casting or a brace that pushes the metatarsals (not the hindfoot) into abduction usually is required in a fixed (rigid) deformity

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9
Q

Genu Varum (Bowlegs)

A

is an outward bowing of the knees greater than 1 inch when the medial malleoli of the ankles are touching

As children grow, lower limb alignment usually follows a predictable pattern
Most infants and toddlers have some bowing of their legs up to 18 months of age.
If there is a large separation between the knees (>15 degrees) after 2 years of age, the child may require bracing.
The child also should be evaluated for diseases such as rickets or tibia vara

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10
Q

Genu Valgum (Knock Knees)

A

is a deformity in which there is decreased space between the knees.
The medial malleoli in the ankles cannot be brought in contact with each other when the knees are touching. Valgus gradually develops after age 24 months and is most apparent between 3 and 4 years of age.
The condition usually is the result of lax medial collateral ligaments of the knee.
Obesity is also associated with the development

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11
Q

Knock Knees Issues

A

Can be ignored up to age 7 unless is a larger angle
Usually resolves spontaneously.

can cause gait awkwardness and increased risk for sprains and fractures.
Uncorrected genu valgum may cause subluxation and recurrent dislocation of the patella, with a predisposition to chondromalacia and joint pain and fatigue.
New challenges such as obesity need to become a priority management outcome in pediatric orthopedics

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12
Q

Osteogenesis Imperfecta

A

is a hereditary disease characterized by defective synthesis of type I collagen.
It is one of the most common hereditary bone diseases.
OI is usually transmitted as an autosomal dominant trait.
type III form ,which is the most progressively deforming type with multiple life-threatening defects, is sometimes, although rarely, inherited as an autosomal recessive trait.
Mutainsns in the genes impacts the development of bones, joints, ears, ligaments, teeth, sclera and skin.

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13
Q

Osteogenesis Imperfecta Manifestations

A

include a spectrum of disorders marked by extreme skeletal fragility.
Thin and poorly development bones that are prone to #
Four major subtypes
1. Post birth: mildest; multiple #, blue sclerae, hearing and dental issues
2. Perinatal: lethal, infant is stilborn or dies within a few days
3. Perinatal and post birth: most progressive and severely deforming; multiple #, growth reparation, severe deformities
4. Post birth; white sclera, fractures, dental and hearing issues

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14
Q

Development of Dysplasia of the Hip

A

formerly known as congenital dislocation of the hip, is an abnormality in hip development that leads to a wide spectrum of hip problems in infants and children, including hips that are unstable, malformed, subluxated, or completely dislocated.
In less severe cases, the hip joint may be unstable, with excessive laxity of the joint capsule, or subluxated, so that the joint surfaces are separated and there is a partial dislocation
the head of the femur is located outside of the acetabulum.

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15
Q

Leg-Calve-Perthes Disease

A

an idiopathic osteonecrotic disease of the proximal (capital) femoral epiphysis. A vascular necrosis of the bone and marrow involving the growth plate center of the femoral head.
It occurs in mostly boys, between ages 3 and 12 years, with a median age of 7 years.
Much more common in whites.
No definite genetic pattern has been established, it occasionally affects more than one family member.
Unknown cause, maybe associated with acute trauma.

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16
Q

Scoliosis

A

lateral deviation of the spinal column commonly in the coronal or frontal plane that may or may not include rotation or deformity of the vertebrae.
A three-dimensional deformity of the spine, often affects the entire skeletal torso.
It can be classified with regard to age of onset and etiology. Girls are affected.
The majority of deformities are idiopathic.
Others can be congenital, associated with neuromuscular disorders (cerebral palsy or muscular dystrophy), a result of intraspinal deformities, or caused by uneven lower limb length

17
Q

Idiopathic Scoliosis Types

A
  1. Infantile: When the deformity curve is manifested before 3 years of age. This type is rare.
  2. Juvenile: When the curve(s) present between 4 and 9 years of age. This type is uncommon.
  3. Adolescent: When the deformity manifests after 10 years of age until the end of growth. This type represents approximately 80% of scoliosis cases.
    MTNR1B gene
18
Q

Congenital Scoliosis

A

is caused by disturbances in vertebral development during the sixth to eighth weeks of embryologic development.
Divided into failures of formation and failures of segmentation.
Failures of formation indicate the absence of a portion of the vertebra, such as hemivertebra (absence of a whole side of the vertebra) and wedge vertebra (missing only a portion of the vertebra).
Failure of segmentation is the absence of the normal separation between the vertebrae.

19
Q

Osteopenia

A

Or low bone density
Condition that is common to all metabolic bone diseases.
It is characterized by a reduction in bone mass greater than expected for age, race, or sex that occurs because of a decrease in bone formation, inadequate bone mineralization, or excessive bone deossification.
Caused by osteoporosis, osteomalacis, malignancies, endocrine disorders

20
Q

Osteoporosis

A

metabolic bone disease characterized by a loss of mineralized bone mass causing increased porosity of the skeleton and susceptibility to fractures.
Guideline:

  1. Those who have a hip or vertebral fracture
  2. Those who have T scores less than −2.5 at the neck of the femur or spine after appropriate evaluation to exclude secondary causes
  3. Those who have a 10-year probability of a hip fracture greater than 3% and a T score between −1.0 and −2.5 at the spine or neck of the femur
  4. Those who have a 10-year probability of a major osteoporosis-related fracture greater than 20%
    Often age related
21
Q

Risk Factors with Osteoporosis

A

Personal Characteristics:
Advanced age
Female
White (fair, thin skin)
Small bone structure
Postmenopausal
Family history
Lifestyle:
Sedentary
Calcium deficiency (long term)
High-protein diet
Excessive alcohol intake
Excessive caffeine intake
Smoking
Drug and Disease Related:
Aluminum-containing antacids
Anticonvulsants
Heparin
Corticosteroids or Cushing disease
Gastrectomy
Diabetes mellitus
Chronic obstructive lung disease
Malignancy
Hyperthyroidism
Hyperparathyroidism
Rheumatoid arthritis

22
Q

Osteomalacia and Rickets

A

In contrast to osteoporosis, which causes a loss of total bone mass and results in brittle bones, osteomalacia and rickets produce a softening of the bones but do not involve a loss of bone matrix.3
Approximately 60% of bone is mineral content, approximately 30% is organic matrix, and the remainder is living bone cells.

23
Q

Osteomalacia

A

is a generalized bone condition in which there is inadequate mineralization of bone.
two main causes of osteomalacia:
1. Insufficient calcium absorption from the intestine because of a lack of dietary calcium or a deficiency of or resistance to the action of vitamin D
2. Phosphate deficiency caused by increased renal losses or decreased intestinal absorption
Vitamin D deficiency is caused most commonly by reduced vitamin D absorption as a result of biliary tract or intestinal diseases that impair fat and fat-soluble vitamin absorption.

24
Q

Osteomalacia Manifestations

A

Bone pain
Tenderness and fractures
Severe cases: fatigue
Treamtment: treating the underlying cause, nutrition, calcium and vitamin D supplements
Dignose SL x yay, bone scan and biopsy

25
Rickets
metabolic bone disease characterized by a failure or delay in calcification of the cartilaginous growth plate in children whose epiphyses have not yet fused. Also manifested by widening and deformation of the metaphyseal regions of long bones and a delay in the mineralization of trabecular, endosteal, and periosteal bone surfaces. There are several forms of rickets, including nutritional rickets, vitamin D–dependent rickets, and vitamin D–resistant rickets.
26
Rickets Manifestations
haracterized by changes in the growing bones of children with overgrowth of the epiphyseal cartilage because of inadequate provisional calcification and failure of the cartilage cells to disintegrate. Bones become deformed; ossification at the epiphyseal plates is delayed and disordered, resulting in widening of the epiphyseal cartilage plate. Any new bone that does grow is unmineralized.
27
Piagets Disease
Second most common bone diease after osteoporosis occur in people in their fourth decade and is characterized by local areas of excessive bone turnover and disorganized osteoid formation. is a focal process with considerable variation in its stage of development in separate sites. onset, is marked by regions of rapidly occurring osteoclastic bone resorption, followed by a period of hectic bone formation with increased numbers of osteoblasts rapidly depositing bone in a chaotic manner such that the newly formed bone is of poor quality and is disorganized rather than lamellar. The poor quality of bone accounts for the bowing and fractures that occur in bones affected by the disease.
28
Piagets Disease Manifestations
varies in severity from a simple lesion to involvement of many bones. It may be present long before it is detected clinically. many people have no symptoms and their disease is found when managing another health problem. The clinical manifestations depend on the specific area involved. Involvement of the skull can cause headaches, intermittent tinnitus, vertigo, and eventual hearing loss. In the spine, collapse of the anterior vertebrae causes kyphosis of the thoracic spine. The femur and tibia become bowed. Softening of the femoral neck can cause coxa vara Coxa vara, in combination with softening of the sacral and iliac bones, causes a waddling gait.
29
Physiologic Basis of Fatigue
includes factors such as diaphragmatic, motor, and neurologic mechanisms. Diaphragmatic fatigue occurs in both acute and chronic respiratory conditions where the force and duration of muscle work exceeds muscle energy stores. Neuromuscular fatigue involves the loss of maximal capacity to generate force during exercise.
30
Physiologic and Psychological Measures of Fatigue
Subjective symptom The most important aspect of quality of life was the amount of daily activity the person was able to perform. is the sensation that comes with having exhausted energy reserves. It is a state experienced by everyone at some time in life. Can be a normal physical response, such as that following extreme exercise in healthy people, or it can be a symptom experienced by people with limited energy reserve, such as people with cardiac or respiratory disease, anemia, or malnutrition, or those on certain types of drug therapy. also may be related to lack of sleep or mental stress.
31
Mechanism of Fatigue
Origin or cause of fatigue can be physiologic, psychological, pathologic, or unknown (e.g., CFS or ME). It can be caused by environmental factors (e.g., excessive noise, temperature extremes, changes in weather), drug-related incidents (e.g., use of tranquilizers, alcohol, toxic chemical exposure), treatment-related causes (e.g., chemotherapy, radiation therapy, surgery, anesthesia, diagnostic testing), physical exertion (e.g., exercise), and psychological factors (e.g., stress, monotony)
32
Chronic Fatigue
Not a protective function, differs from acute fatigue in terms of onset, intensity, perception, duration, and relief. is much more complex and difficult to diagnose. There are several possible causes such as hypothyroidism, anemia, heart disease, Lyme disease, fibromyalgia, lung disease, electrolyte dysfunction, tuberculosis, hepatitis, and cancer. It is a common problem experienced by people with chronic health problems. With HF or emphysema is accepted given the pathophysiology of these conditions.
33
Low Bone Density
Or osteopenia Oocytes hen bones loose minerals malting them esker but not yet having osteoporosis. Primary cause is lack of calcium Other: hormal imbalances, smoking, excessive alcohol or long term steriod use Risk factors: females, over 50, family history