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45 Cards in this Set

  • Front
  • Back
What are the major factors that affect growth?
Trauma-separation of epiphysis
Nutrition- vit c,d, ca xu
Hormones- GH, Thyroid
The inactive form of vit d is ___
the active form is ___
it is converted by ____
25 Cholicalciferol
1,25 Dihydrocholicalciferol
converted by KD
in the embryonic stage the
ectoderm forms the ___
the mesoderm forms the ___
the endoderm forms the ____
Skin/nervous sys
skeleton, muscles, ht, kd
Gi, respiratory sys
bone starts budding the what time during gestation?
when does ossification begin?
4th week
9th week
What is the pathology of Osteogenesis Imperfecta?
what causes this?
defective synth of connective tissue and bone matrix
caused by autosomal dominant or recessive gene
how does osteogenesis imperfecta manifest in the recessive type?
dominant type?
recessive type: stillbirth, iu multiple fractures usually during 3rd trimester

dominant: onset during childhood when child becomes active- mistaken as child abuse
what is the pathology of developmental dysplasia of the hip?

this is best to manage if detected during ____. how is it treated?
congenital dislocation of the hip causing a delay in maturation, size and dvlpment of the femoral head and acetabulum

best management if detected in the first 6 months (most growth)
immobilize the hip in abduction to manage
list the manifestations and warning signs of dvlpmntl hip dysplasia
Asymentry of hip/gluteal fold
shortening of thigh- 1 knee higher than other
ltd abduction of affected hip-inability to open
+Barlow/Ortolani Sign
Baby sleeps with a straight leg
Toeing-in occurs during ___dvlpmnt
and it is due to ______

Explain Toeing-out
Caused during normal devlpmnt
it is inversion of the foot/leg usually due to uneven dvlpmnt of muscles in the lower leg

eversion of foot/leg, external femoral roation
Toeing-in/out can or cannot be fixed?
can be fixed
What is Genu-valgum
What causes this?
deformity causing decreased space btwn the knees

Lax medial collateral ligament of the knee
what are the warning signs of osteoporosis?
there are no warning signs unless you fracture a vertebrae/hip/distal radius causing pain
vertebrae may collapse causing height loss and/or kyphosis
explain the difference between osteoporosis and osteomalacia
porosis: increase porosity of bones due to a loss of bone mass the rate of resorption is great than rate of formation

malacia: bone softening due to a mineral xu
what are the pathologic changes that occur with osteoporosis?
marrow canal widens making cortical bone thinner
more porous/spongy bone due to loss of trabeculae
what pathologic change occurs with osteomalacia?
demineralization of bone causes softening
what are the manifestations of osteomalacia?
bone PAIN!
muscle weakness
bone deformitites (kyphosis, bowleg)
secondary hyperthyroidism (result of osteomalacia- increase blood Ca)
pathologic fracture
what are the pathologic changes of Pagets Disease?
rapid bone resorption(osteoclasts-too fast)) followed by production of abnormal bone that is rough and pitted- often precursor to osteosarcoma
what are the manifestations of Pagets Disease?
nerve pasly/compression
cardiovascular disorder-tachycardia causing death
ventilation failure
what are the test results needed that will diagnos pagets disease?
xrays
blood test- increased alkaline phosphatase
urine test- increased hydroxyproline
what is the tx for Pagets Disease?
anti-inflammatory drugs
Calcitonin- antagonist to osteoclast function
Mithramycin- anti-metabolite cancer drug
How can Osteoporosis be prevented?
exercise
1500mg Ca/day
400-800 IU Vit D
HRT
Calcitonin
Biphosphonates (prevent resorption of bone)
what are tophi and when do they appear?
=accumulation of uric acid in a joint/ear that manifests outward and is filled with a pasty/chalky white substance that is easy to rupture

occurs in cases of CHRONIC Gout
Genu Varum vs Genu Valgum
Varum=bowleg
Valgum=knock knees - lax medial collateral ligament
what is the pathology of scoliosis?
lateral deviation of the spinal clum
what are the manifestations of scoliosis?
high shoulder
prominent hip
projecting scapula
pain/sob
what are the causes of structural classifications of scoliosis?
congenital-strctrl anomolies during embyronic dvlpmnt
neuromuscular- neuropathic/myopathic diseases
idiopathic
What is the pathology of Coxa PLana Leg-Calve-Perthes? what groups are most affected by this disease?
avascular necrosis of bone and marrow of the epiphyseal growth center in the femoral head
affects mostly white boys between 2-13yrs
what are the stages of Coxa PLana Leg-Calve-Perthes?
Synovitis (1-3 weeks)
Avascular necrotic (months-year)
Re-vascularization-resorb necrotic
bone
Healing-mature cell replacement
what are the manifestations of Coxa PLana Leg-Calve-Perthes?
Pain in groin/thigh/hip- causing limping
Ltd Abduction/internal rotation
progressive onset and prolonged course
What is the pathology of Osgood Schlatter disease?

what is the cause?
tendonitis/tearing of the tibial tubercule due to pulling on tendon

caused by stress placed on the knee during critical growth period-quick growth
what groups are most likely to experience Osgood Schlatter Disease?
boys 11-15yrs ***
girls 8-13yrs
what are the manifestions of Osgood Schlatter Disease?
knee pain upon exercise
resolves after closure of tibial growth plate
what is the pathology of gout?
accumulation of uric acid in blood that precipitates in the joints/periphery causing uric a in the synovial fluid or in tophaceous deposits
gout is more likely to occur in men-or-women? what age range?
men >40yrs
what causes gout?
overproduction of uric acid- metabolic waste product of purine
underexcretion of uric acid by the KD
what drugs can interfere with the excretion of uric acid?
salicylate and thiazide drugs
uric acid is excreted via the ____
KDs
describe the pathogenesis of Gout
rise in uric acid-> precipitates in joints->chemotaxis of PN->phagocytosis of uric acid-> death of PN->lysosomes released-> destruction of cartilage and subchondral bone
what are the cardinal s/s of acute gout?
inflammation/severe pain in big toe for few days/weeks
what is intercritical gout?
similar to remission
clinical manifestations disappear and affected joints seem normal (however- uric acid levels in blood will still be hi)
what is the principle behind treating gout?
try to preserve joints - chronic inflammation will cause destruction
T/F
hi uric acid levels in blood (hyperuricemia) = gout
F
in order to be gout there must be swollen/tender joints in addition
what drugs can be used to treat gout?
NSAIDS, colchichine, corticosteroids- treat pain/inflammation

Allopurinol- treat hyperuricemia by blocking xanthine oxidase enzyme needed to convert xanthin/purine to uric acid
what is the ezyme needed to convert purine to uric acid?
xanthine oxidase
what are some lifestyle and dietary options to help treat/prevent gout?
maintain ideal weight
reduce alcohol
avoid LV, KD, Sardine, Anchoive