Dasar - Dasar Radiologi Metabolik
Transcript of Dasar - Dasar Radiologi Metabolik
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Dr. Donny Susilawardhono SpRad
Bagian Radiologi RSAL Ramelan
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Secara tidak langsung, sebagian masih bisamemakai plain foto musculoskeletal
Secara langsung untuk melihat morfologi darikelenjar dengan USG
CT Scan
MRI
Scintigraphy
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Secara langsung, dengan melihat kelenjaratau struktur anatomis primer tertentu tgtpatofisiologinya,
Secara tidak langsung dengan melihat efekyang ditimbulkan
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Tulang mengandung : Ekstraseluler material :
Matriks organik atau jaringan osteoid (collagenfibril yang mangandung mucopolysaccharide
ground subastance) Inorganic crystalline component (hydroxyapatite
atau calcium phosphat)
Celluler material : Osteoblast (induced bone formation) Osteoclast (induced bone resorption)
Osteocyte (inactive cell)
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Increased Radiodensity Increased Radiolucency
Secondaryhyperparathyroidism
Osteoporosis
Renal osteodystrophy
Osteomalacia
Hyperphosphatasia Rickets
Idiopathic hypercalcemia Scurvy
Paget disease
Primaryhyperparathyroidism
Osteopetrosis* Hypophosphatasia
Pycnodysostosis* Hypophosphatemia
Melorheostosis*
Acromegaly
Hypothyroidism Gaucher disease
Mastocytosis Homocystinuria
Myelofibrosis
Osteogenesis imperfecta*
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Increased Radiodensity Increased Radiolucency
Myelofibrosis Osteogenesis imperfecta*
Gaucher disease(reparative stage)
Fibrogenesis imperfecta
Fluorine poisoning Cushing syndrome
Intoxication with lead,bismuth, or phosphorus
Ochronosis (alkaptonuria)
Osteonecrosis Wilson disease(hepatolenticulardegeneration)
Hypogonadism
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Osteopenia
Osteoporosis
Deficient matrix
Normal
mineralization
Osteomalacia
Normal matrix
Deficient
mineralization
Hyperparathyroidism
Normal matrix and
mineralization
Increased resorption
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Kualitatif Imaging Techniques forMeasurement Bone Mineral Density
Foto polos CT Scan
Scintigraphy
MRI
Radionuclide and X-RayTechniques Single Photon
Absorptiometry
Dual PhotonAbsorptiometry
Computed TomographyTechnique Quantitative Computed
Tomography Quantitative Ultrasoud
Techniques
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Radioluscent defect pada cortical bone yang
mencerminkan akumulasi nonmineralizedosteoid tissue
Characteristic finding dari osteomalacia
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Generalized metabolic bone disease,characterized by insufficient formation orincreased resorption of bone matrix thatdecreased of bone mass
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Genetic Congenital) Endocrine
Osteogenesis imperfecta, Gonadal dysgenesis,
Turner syndrome (XO),
Klinefelter syndrome (XXY),
Hypophosphatasia,
Homocystinuria,
Mucopolysaccharidosis
Gaucher disease
Anemias:
Sickle-cell syndromes
Thalassemia
Hemophilia Christmas disease
Hyperthyroidism Hyperparathyroidism Cushing syndrome Acromegaly
Estrogen deficiency Hypogonadism Diabetes mellitus Pregnancy
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Deficiency States Neoplastic
Scurvy Malnutrition
Anorexia nervosa
Protein deficiency Alcoholism
Liver disease
Myeloma Leukemia Lymphoma
Metastaticdisease
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Iatrogenic Miscellaneous
Heparin-induced Dilantin-induced
Steroid-induced
Involutional(senescent/postmenopausal)
Amyloidosis Ochronosis Paraplegia Weightlessness
Idiopathic
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Immobilization (cast) Disuse
Pain
Infection
Reflex sympathetic dystrophy syndrome (Sudeckatrophy)
Transient regional osteoporosis: Transient osteoporosis of the hip
Regional migratory osteoporosis Idiopathic juvenile osteoporosis
Paget disease (hot phase)
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Target sitesof
Osteoporosis
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Periarthricular Porosis
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Osteoporosis
with
fracture
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Principal Compressive Group Extend from medial cortex of femoral neck to superior part of femoral head Major weight-bearing trabeculae In normal femur are the thickest and most densely packed Appear accentuated in osteoporosis Last to be obliterated
Secondary Compressive Group Originate at the cortex, near the lesser trochanter
Curve upward and laterally toward the greater trochanter and upper femoralneck Characteristically thin and widely separated
Principal Tensile Group Originate from the lateral cortex, inferior to the greater trochanter Extend in an arch-like configuration medially, terminating in the inferior
portion of the femoral head
Secondary Tensile Group Arise from the lateral cortex below the principal tensile group Extend superiorly and medially to terminate after crossing the middle of the
femoral neck
Greater Trochanter Group Composed of slender and poorly defined tensile trabeculae Arise laterally below the greater trochanter
Extend upward to terminate near the greater trochanter's superior surface
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Ricket (anak-anak) dan osteomalacia(dewasa)
Faulty mineralization (calcification) of bonematrix
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Nutritional Deficiency
Vitamin D Dietary
Insufficient sunlight Impaired synthesis
Calcium Phosphorus
bsorption bnormalities
Gastric surgery
Intestinal surgery (bypass) Gastric disorders (obstruction)
Intestinal disorders (sprue)
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Renal Disorders
Renal tubular disorders Proximal tubular lesions (failure of absorption of inorganic phosphate,
glucose, amino acids) Distal tubular lesions (renal tubular acidosis)
Combined proximal and distal tubular lesions
Renal osteodystrophy
Miscellaneous
Associated with Wilson disease
Fibrogenesis imperfecta
Fibrous dysplasia Neurofibromatosis Hypophosphatasia
Neoplasm
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Target site
OfRickets
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Infantile Rickets Vitamin D resistant Rickets
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6 -18 months Generalized demineralisation of skeleton
Tend to bowing deformities (in weight bearingbones, when begin to stand and walk)
Restless & sleep poorly Closing of fontanella is delayed
Softening of cranial vault (craniotabes)
Enlargement of cartilage at costochondral
junction (rachitic rosary) Serum calcium dan phosphorous low
ALP increased
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Radiologic landmark : Observed in metaphyse and epiphyse
Widening of the growth plate
Cupping and flaring metaphysis, which appear
disorganized and frayed Similar changes seen in secondary ossification
centers of ephypise
Bones become radiolucent
Loss of sharpness at the periphery
Bowing deformities
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8-year-old boy with untreated dietary rickets shows osteopenia of thebones, widening of the growth plates of the distal radius and ulna, and
flaring of the metaphyses, all typical features of this condition
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4-year-old boy shows wideningof the growth plates of thedistal femur and proximal tibiasecondary to lack of
mineralization in the provisionalzone of calcification.
Note also cupping and flaringof the metaphyses.
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3-year-old girl with vitamin D-deficiency rickets showsincreased bone radiolucency,widening of the growth plates,
cupping and flaring of themetaphyses, and blurring of theoutline of the secondaryossification centers, allradiographic hallmarks of thiscondition.
Note also bowing of the tibia andfibula, a frequent feature ofrickets
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Pathofisiologi sama dgn Ricket Proses terjadi setelah pertumbuhan tulang
terjadi
Seringkali terjadi ok faulty absorption arivitamin D larut lemak di GIT yang sekunderok malabsorption syndrome
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Histologically, osteomalacia is characterized by excessive quantities ofinadequately mineralized bone matrix (osteoid) coating the surfaces oftrabeculae in spongy bone and lining the haversian canals in the cortex.
Radiographically, osteomalacia presents with generalized osteopenia,and multiple, bilateral, and often symmetric radiolucent lines are seen inthe cortex perpendicular to the long axis of the bone; they are referredto as pseudofractures or Looser zones.
These defects, which represent cortical stress fractures filled with poorlymineralized callus, osteoid, and fibrous tissue, are common along theaxillary margins of the scapulae, the inner margin of the femoral neck,the proximal dorsal aspect of the ulnae, the ribs, and the pubic andischial rami
The condition, described by Milkman and known as Milkmansyndrome, is a mild form of osteomalacia in which the pseudofracturesare particularly numerous.
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Generalized osteitis fibrosa cystica or Recklinghausendisease of bone Overactivity of the parathormone-producing parathyroid
glands. Increased production of this hormone is secondary to
either gland hyperplasia (9% of cases) or adenoma (90%);
only in very rare instances (1%) does hyperparathyroidismoccur secondary to parathyroid carcinoma. Excessive secretion of parathormone, which acts on the
kidneys and on bone, leads to disturbances in calcium andphosphorus metabolism, resulting in hypercalcemia,hyperphosphaturia, and hypophosphatemia.
Renal excretion of calcium and phosphate is increased,and serum levels of calcium are elevated, while those ofphosphorus are reduced. Serum levels of alkalinephosphatase are also elevated.
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Hyperparathyroidism can be divided into primary,secondary, and tertiary forms. The classic form ofthe disorder,
Primary hyperparathyroidism, is marked byincreased secretion of parathormone resulting
from hyperplasia, adenoma, or carcinoma of theparathyroid glands. S Secondary hyperparathyroidism is caused by
increased secretion of parathyroid hormone inresponse to a sustained hypocalcemic state.
Tertiary hyperparathyroidism represents atransformation from a hypocalcemic to ahypercalcemic state.
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Primary hyperparathyroidism is usuallyassociated with hypercalcemia.
Women are affected about three times asoften as men, and the condition is most often
seen in the patient's third to fifth decade
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The parathyroid glands escape from theregulatory effect of serum calcium levels.
Patients in whom this escape occurs areusually receiving kidney hemodialysis; they
are considered to have autonomoushyperparathyroidism
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Target Site
Of
Hyperparathyroidism
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Generalized osteopenia; subperiosteal,subchondral, and cortical bone resorption;brown tumors; and soft-tissue and cartilagecalcifications.
Intracortical resorption is manifested bylongitudinal striations, a finding known astunneling, which can be most clearlyappreciated on magnification studies
In the skull, there is a characteristic mottlingof the vault, which yields a salt-and-pepperappearance
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loss of the lamina dura around the toothsocket, which normally is seen as a thin sharpwhite line surrounding the peridentalmembrane that attaches the tooth to bone
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Generalized increase in bone density occurs,particularly in younger patients. In the spine, this change is reflected in dense
sclerotic bands seen adjacent to the vertebral endplates, giving the vertebrae a sandwich-likeappearance (rugger-jersey spine)
However, it must be kept in mind in the evaluation ofhyperparathyroidism that osteosclerotic changes mayalso occur as a manifestation of healing,eitherspontaneously or as a result of treatment.
Deposition of calcium in fibrocartilage, articular
cartilage, and soft tissue is common, and vascularcalcifications are much more frequent in patients withsecondary hyperparathyroidism
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Primary
hyperparathyroidism
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Primary
Hyperparathyroidism
Subchondral bone resorption ispresent at the head of the secondmetacarpal (arrow).
Note also subperiosteal resorptionat the proximal and distal phalanges(open arrows).
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Primary
Hyperparathyroidism
resorption of theacromial end of the rightclavicle
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Primary Hyperparathyroidism
decrease in the overall density of the bone and a granular appearance ofthe vaultthe so-called salt-and-pepper skull
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Primary
Hyperparathyroidism
Brown tumor
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Secondary
Hyperparathyroidism
17-year-old boy with chronic
renal failure developedsecondaryhyperparathyroidism
Rugger-Jersey spine
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Secondary Hyperparathyroidism
48-year-old woman shows evidence of soft-tissue and vascularcalcifications, characteristic findings in secondary hyperparathyroidism.
Note also diffuse osteopenia.
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Evaluasi terbaik dengan modalitas MRI Kedua dengan CT Scan
Foto polos : Ballooning sella
Double floor
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Sella Measurement
Children
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Sella Measurement - Adult
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Double floor Baloning sella tursica
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Sisi kiri Sella Sisi kanan Sella
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MRI MRI
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CT Scan CT Scan
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Tidak tampak jelas pada foto polos biasa Dengan foto polos, tampak sebagai soft
tissue area, lihat airway
USG Grayscale dan Powerdoppler - sensitif
MRI Sensitif
CT Scan spesifik
Scintigraphy
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USG dengan doppler Mudah, murah, praktis
Mengevaluasi kista dan nodule dengan baik
CT Scan Evaluasi morfologis dengan baik
MRI Evaluasi morfologis terbaik
Scintigraphy
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ThoracicGoiter
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Sulit ditemukan Modalitas yang paling sensitif adalah MRI
Tampak jelas bila membesar
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Modalitas yang dapat dipakai adalah USG, CTScan, MRI
Perlu diperhatikan ukuran, homogenitasparenchyme dan ductus pancreaticus
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Diterbitkan sebagai buku yang bernama : ARadiographic Standard of Reference for theGrowing Hand and Wrist
Disiapkan untuk : The United States National,
Health Examination Survey Diterbitkan oleh : The Press of Case Western
Reseve University, Chicagi, 1950 Dibuat oleh :
S.Idle Pyle PhD Alice M. Waterhouse MD William Walter Greulich PhD
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Vicente Gilsanz, M.D., Ph.D. Department ofRadiology, Childrens Hospital Los Angeles,, 4650Sunset Blvd., MS#81, Los Angeles, CA 90027
Osman Ratib, M.D., Ph.D., Department of
Radiology, David Geffen School of Medicine atUCLA, 100 Medical Plaza, Los Angeles, CA 90095
ISBN 3-540-20951-4 Springer-Verlag BerlinHeidelberg New York, Library of Congress
Control Number: 2004114078 Springer-Verlag Berlin Heidelberg New York
Terbaru th 2005
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Bone age assessment is frequently performedin pediatric patients to evaluate growth andto diagnose and manage amultitude ofendocrine disorders and pediatric syndromes
Bones in the hand and wrist are the mostsuitable indicators of skeletal maturity duringthe different phases of postnataldevelopment.
Vicente Gilsanz Osman RatibHand Bone Age
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Six major categories and highlighted inparentheses the specific ossification centers thatare the best predictors of skeletal maturity foreach group: 1) Infancy (the carpal bones and radial epiphyses);
2) Toddlers (the number of epiphyses visible in the longbones of the hand);
3) Pre-puberty (the size of the phalangeal epiphyses); 4) Early and Mid-puberty (the size of the phalangeal
epiphyses);
5) Late Puberty (the degree of epiphyseal fusion); and, 6) Post-puberty (the degree of epiphyseal fusion of the
radius and ulna).
Vicente Gilsanz Osman RatibHand Bone Age
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Late Puberty
Females: 13 years to 15 years of age Males: 14 years to 16 years of age
Assessments of skeletal maturity in this stage are primarilybased on the degree of epiphyseal fusion of the distal phalanges.Fusion of the epiphyses to the metaphyses in the long bones ofthe hand tends to occur in an orderly characteristic pattern, asfollows: 1) Fusion of the distal phalanges; 2) Fusion of the metacarpals; 3) Fusion of the proximal phalanges; and, 4) Fusion of the middle phalanges.
Because of their morphologies, the epiphyseal fusion of themetacarpals is poorly depicted by radiographs and greaterattention is, therefore, placed on the degree of fusion at thephalanges. Since all carpal bones have now attained their earlyadult shape, they are of less value for determination of bone age.
Vicente Gilsanz Osman RatibHand Bone Age
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Depiction, from left to right, of the rogressivedegrees of fusion of the epiphyses to themetaphyses,which usually begins at the centerof the physis
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Assessments in latestages of pubertyand sexualmaturityare based on the
degree ofepiphyseal fusion ofthe distal phalanges(first) and on thedegree of fusion ofthe middlephalanges (second)
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8-month-old boy 10-month-old boy
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10-year-old boy 14-year-old boy
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