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18 Rickets Of Vitamin D Deficiency,Tetany Of Vitamin D Deficiency
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18 Rickets Of Vitamin D Deficiency,Tetany Of Vitamin D Deficiency

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  • 1. Rickets of Vitamin D Deficiency Tetany of Vitamin D Deficiency
    • MBBS.weebly.com
  • 2. Rickets
  • 3.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 4.
    • Rickets ---failure in mineralization of
    • growing bone or osteoid tissue (children)
    • the end of long bone, shaft
    • Osteomalacia --mature bone (adults)
    • Rickets of Vitamin D deficiency ---
    • chronic systemic nutrition-deficient disease
    • (<2y)
  • 5.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 6.
    • * VitD ( Vitamin D )
    • important in mineralization of newly
    • formed osteoid
    • * PTH ( parathormone ,甲状旁腺素)
    • * CT ( calcitonine, 降钙素)
    Factors associated with Ca ,P metabolism and bone development
  • 7.
    • Physiological function of VitD
    • * antirachitic function facilitation
    • intestinal absorption of Ca , P(CaBP)
    • reabsorption of Ca & P in the kidneys
    • direct effect on mineral metabolism of bone
    • (deposition and reabsorption)
    • * nonantirachitic function
    • cell proliferation, differenciation, immunity
  • 8. Metabolism and regulation of VitD
    • 7-dehydrocholesterol irradiated ergosterol
    • Provitamin (skin) (plant)
    • photochemically activation
    • diet cholecalciferol calciferol
    • (VitD 3 ) (VitD 2 )
    • 25-hydroxylase in liver
    • 25(OH)D 3
    • 1α-hydroxylase in kidney 24- hydroxylase
    • 1,25-(OH) 2 D 3 24,25-(OH) 2 D 3
    • active inactive
    PTH↑ Ca ↓ , P↓ ( - ) ( + ) Ca ↑ CT↑
  • 9.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 10.
    • Etiology
    • * Inadequate gain of VitD from mother
    • * Inadequate direct exposure
    • to ultraviolet rays in sunlight (296-310 nm)
    • * Rapid growth low-birth weight infants
    • * Inadequate intake of VitD
    • The diets of infants may contain only small amounts of VitD
  • 11.
    • Predisposing factors to VitD deficiency
    • disorders interfere with absorption and
    • utilization of Vit D or Ca or P
    • celiac disease , steatorrhea, disorders of gastrointestine, biliary duct, pancrea, liver or kidney
    • drugs administration
    • * anticonvulsant therapy- (phenytoins, phenobarbital)
    • interfere with the metabolism of VitD
    • * Glucocorticoids--antagonistic to VitD in Ca transport
  • 12.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 13.
    • normal osteogenesis : cartilagenous
    • intramembraneous
    • cartilage cells’ normal cycle--( Fig )
    • zone of resting cartilage
    • zone of proliferating cartilage
    • zone of calcifying cartilage
    • zone of ossication: zone of preparatory
    • calcification(ZPC, 临时钙化带 )
    Pathology
  • 14. Fig.1 Levels of growth plate zone of resting cartilage zone of proliferating cartilage zone of calcifying cartilage zone of preparatory calcification
  • 15.
    • In Ricket cartilage cells fail to complete their normal
    • cycle of proliferation and degeneration;
    • subsequent failure of capillary penetration
    • occurs in a patchy manner(Fig)
  • 16.
    • enlarged costochondral
    • junction
    *Non-calcified, hypertrophied growth plate in rickets (R), compared to a normal growth plate (L).
  • 17. Pathology
    • Disturbance of sclerotic calcification
    • osteomalacia (骨质软化)
    • osteoid deposition( 骨样组织堆积 )
  • 18.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 19. Pathogenesis
    • can be conceptualized to be
    • the body’s attempt to maintain
    • normal serum calcium levels
  • 20.
    • VitD deficiency
    • ↓ Ca, P absorption from the intestine
    • ↓ serum Ca level
    • parathyroid gland
    • ↓ P reabsorption ↑PTH PTH
    • in the kidney
    • ↑ mobilization of
    • Ca ,P from the bone ↓serum Ca
    • ↓ serum P serum Ca->,↓
    • tetany
    • ↓ Ca,P in ECF
    • failure in mineralization of osteoid tissue
    • and cartilaginous matrix
    • rickets Pathogenesis
  • 21.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 22.
    • Clinical manifestations
    • Incidental age 3 m-2 yr
    • osseous changes in growing bone
    • relaxation of muscles and ligaments
    • nonspecific neuropsychatic symptoms
    • Severe case systemic
  • 23. Clinical manifestations
    • Stages
    • Early stage
    • Progressing stage
    • Convalescent stage (恢复期)
    • Sequelae stage (后遗症期)
  • 24. Early stage (1)
    • Symtoms <6(3)m
    • nonspecific neuropsychiatic---
    • irritability
    • restless day and night(unstable sleeping)
    • increased sweating--particularly around
    • the head, no relation with weather
    • bare occiput( 枕秃 )
    • Signs no obvious osseous change
  • 25. bare occiput
  • 26. Early stage (2)
    • biochemical changes
    • serum Ca -> or ↓, P ↓,
    • ALP (Alkaline phosphatase) ↑(500μ/L)
    • 25-(OH)D 3 ↓ , 1,25-(OH) 2 D 3 ↓
    • Roentgenographic examination
    • Normal
    • or ZPC becomes unclear
  • 27. Progressing stage
    • * symptoms in early stage
    • * osseous changes
    • * retardation of development (movement)
  • 28. Progressing stage osseous change
    • * Head
    • craniotabes( 颅骨软化 )(3~6 m)
    • boxlike appearance ( Caput quadratum) (7~8m)
    • larger anterior fontanel , delayed closure(2y)
    • delayed eruption of the temporary teeth,
    • defects of the enamel and extensive caries,
    • calcifying permanent teeth’s being affected
  • 29. boxlike appearance
  • 30. Progressing stage osseous change
    • * Chest (about 1yr)
    • beading of the ribs (rachitic rosary 佝偻病串珠 ) (Fig)
    • Harrison groove ( 赫氏沟 ) (Fig)
    • funnel-like chest ( 漏斗胸 ) (Fig)
    • pigeon breast deformity ( 鸡胸 ) (Fig)
  • 31. rachitic rosary
  • 32. Harrison groove Funnel-like chest L: pigeon breast
  • 33. Progressing stage osseous change
    • * Extremities
    • *thickening of the wrists and ankles(Fig )
    • (Rachitic bracelets 佝偻病手镯、脚镯 )
    • *bowlegs or knock-knees(Fig)
    • ( O 型腿、 X 型腿)
  • 34. R. thickening of the wrists L. thickening of the ankles
  • 35. Thickening of the wrist Thickening of the ankles
  • 36. R. bowlegs L. knock-knees
  • 37. Progressing stage osseous change
    • * others
    • spinal column (kyphosis 脊柱后突, s scoliosis 脊柱侧弯 )
    • concomitant deformity of the pelvis,
    • ec flat pelvis
  • 38. kyphosis & scoliosis
  • 39. Progressing stage
    • muscle and ligament
    • poorly developed and lack tone
    • (late in sitting, standing and walking)
    • overextension of the great joint
  • 40. Clinical manifestations
    • summarized as following table
    • Histological osteomalacia osteoid
    • Pathology (骨质软化) deposition
    • Head Craniotabes Caput
    • quadratum
    • chest Harrison groove, funnel Rachitic
    • -like chest ,Pigeon breast rosary
    • Spinal Kyphosis, Scoliosis
    • column
    • pelvis Flat pelvis
    • extremities Bowlegs, Knock-knees Rachitic
    • bracelets
  • 41. Progressing stage
    • Biochemical changes
    • serum Ca↓, P↓,
    • serum ALP (Alkaline phosphatase)↑↑
    • serum 25-(OH)D↓ 1,25-(OH) 2 D 3 ↓
    • urine cyclic AMP↑
  • 42. Progressing stage
    • Roentgenographic examination (Fig)
    • * rachitic metaphysis
    • (deposition of nonrigid tissue)
    • * at the end of the shaft
    • (widdened, cupping, fraying)
    • ** ZPC becomes unclear even disappear
    • * rarefied cortical bone (↓density )
  • 43. Upper limp Normal X rays Rachitic metaphysis
  • 44. Lower limp Normal X rays Rachitic metaphysis
  • 45. Convalescent stage
    • (after adequate antirachitic treatment)
    • * Clinical manifestation improved---
    • soon regain muscle tone, mentally improved
    • several days serum Ca, P ↑ ->N
    • 4-6w ALP ↓-> N
    • * roentgenographicly improved----
    • 2-3w - ZPC reappears, bone density↑
    • 4w - ZPC, rachitic metaphysis and shafts
    • becomes united
  • 46. Sequelae stage
    • >2-3 yr
    • Severe rachitic child leave osseous deformities
    • — bowleg or knock-knee,
    • pigeon chest, funnel-like chest,
    • kyphosis, scoliosis,
    • head deformity, etc.
    • Biochemical change and Roentgenographic examination normal
  • 47. Sequelae stage
  • 48.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 49.
    • based on
    • a history of inadequate gain of VitD
    • Clinical observation
    • Confirmed by
    • biochemical test 25 - (OH)D↓(11~60 μ g/ml)
    • serum Ca↓, P↓,
    • serum AKP ↑↑
    • roentgenograghic examination
    Diagnosis
  • 50.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 51.
    • * Other rickets
    • # familiar hypophosphatemia ( 家族性低磷血症)
    • or X-linked hypophosphatemia(XLH)
    • # VitD-dependent rickets
    • or Ca ++ deficient form of rickets
    • # Renal tubular acidosis
    • rickets, metabolic acidosis, polyuria, alkaluria
    • # Renal Osteodystrophy
    • # Hepatic diseases associated with rickets
    Differential diagnosis
  • 52.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • & Tetany of VitD Deficiency
  • 53.
    • * pregnant and lactating mothers
    • adequate sunlight; VitD 800U/d;
    • diet rich in Ca, P, VitD
    • * Infant
    • exposure to ultraviolet light
    • daily VitD supplementation
    • Term infant 400 U/d(2w~2yr)
    • premature infants 800 U/d(2w~3m),
    • 400 U/d(3m~2yr)
    • *summer !
    Prevention
  • 54.
    • & Rickets of Vitamin D Deficiency
    • Introduction
    • Physiological function and regulation of VitD
    • Etiology
    • Pathology
    • Pathogenesis
    • Clinical manifestations
    • Diagnosis
    • Differential diagnosis
    • Prevention
    • Treatment
    • &Tetany of VitD Deficiency
  • 55.
    • To control the progressive stage
    • prevent osseous deformity
    • N atural and artificial light
    • Nutrition
    • VitD analogue administration
    • Prevent and treat complication
    Treatment
  • 56.
    • VitD analogue administration
    • Orally VitD 2,000~4,000 IU/d × 2~4 W
    • 1,25(OH) 2 D 3 0.5 ~ 2 μg/d × 2~4 W
    • then VitD 400 IU/d (10ug/d)
    • Single dose im VitD 3 200,000-300,000 IU
    • 2-3m later VitD 400 IU/d
    • reevaluation q1m
    Treatment
  • 57.
    • & Rickets of Vitamin D Deficiency
    • & Tetany of VitD Deficiency
    • Introduction
    • Chemical Pathology
    • Prediposing factor
    • Clinical manifestations
    • Diagnosis & Differential diagnosis
    • Treatment
  • 58.
    • R achitic tetany
    • Incidental age <6m( 4m-3yr)
    • Form of plasma Ca
    8~10% 40% 45~50% IONIZED active form— PH 、 serum P BOUND protein COMPLEXED
  • 59.
    • & Rickets of Vitamin D Deficiency
    • & Tetany of VitD Deficiency
    • Introduction
    • Chemical Pathology
    • Prediposing factor
    • Clinical manifestations
    • Diagnosis & Differential diagnosis
    • Treatment
  • 60.
    • VitD deficiency
    • ↓ Ca, P absorption from the intestine
    • ↓ serum Ca level
    • parathyroid gland
    • ↓ P reabsorption ↑PTH PTH
    • in the kidney
    • ↑ mobilization of
    • Ca ,P from the bone ↓serum Ca
    • ↓ serum P serum Ca->,↓
    • tetany
    • ↓ Ca,P in ECF
    • failure in mineralization of osteoid tissue
    • and cartilaginous matrix
    • rickets Pathogenesis
  • 61.
    • serum Ca 2+ <0.75~1mmol/L
    • serum Ca<1.75~1.88 mmol/L
    • the loss of the inhibitory control that
    • Ca exert on the neuromuscular junctions
    • muscular irritability
    Chemical Pathology
  • 62.
    • & Rickets of Vitamin D Deficiency
    • & Tetany of VitD Deficiency
    • Introduction
    • Chemical Pathology
    • Prediposing factor
    • Clinical manifestations
    • Diagnosis & Differential diagnosis
    • Treatment
  • 63. Prediposing factor
    • VitD deficiency
    • accompany with dull parathyroid response
    • Relative Ca deficiency
    • *enough exposure to sunlight (spring, summer)
    • or VitD administration
    • *concomitant inadequate Ca absortion
    • from the intestine
    • Pathological condition
    • fever, infection, neonatal asphyxia, high P level diet
  • 64.
    • & Rickets of Vitamin D Deficiency
    • & Tetany of VitD Deficiency
    • Introduction
    • Chemical Pathology
    • Prediposing factor
    • Clinical manifestations
    • Diagnosis & Differential diagnosis
    • Treatment
  • 65. Clinical manifestations
    • tetany and concurrent rickets
    • Manifest Tetany (serum Ca 2+ <0.75mmol/L
    • serum Ca<1.75 mmol/L)
    • latent tetany (serum Ca 2+ <0.75~1mmol/L
    • serum Ca<1.75~1.88 mmol/L)
  • 66.
    • Manifest Tetany
    • Convulsions brief but recurrent,
    • conscious between seizures
    • Laryngospasm inspiratory obstruction
    • high-pitched inspiratory crow apnea
    • Carpopedal spasm (Fig )
    Clinical manifestations
  • 67. Fig. Carpopedal spasm The wrist are flexed, the finger extended, the thumbs adducted over the palms, the feet extended and adducted.
  • 68.
    • latent tetany
    • symptoms are not evident, but can be elicited
    • by ischemia
    • or mechanical
    • or electrical
    • Chvostek sign, Peroneal sign, Trousseau sign
    Clinical manifestations stimulation of motor nerves
  • 69. Latent tetany
    • Chvostek sign facial spasm
    • tapping anterior to external auditory meatus
    • 7th(facial) cranial nerve
    • Contraction of the orbicularis oris occurs with
    • a twitch of the upperlip or entire mouth
    • Peroneal sign pedal spasm
    • tapping the head of fibula
    • peroneal nerve
    • dorsiflexion and abduction of the foot
  • 70. Latent tetany
    • Trousseau sign carpospasm
    • A blood pressure cuff on the arm is inflated
    • above the systolic blood pressure for 5 min
    • Ischemia of motor nerves by reducing the blood supply
    • Carpopadal spasm
  • 71.
    • & Rickets of Vitamin D Deficiency
    • & Tetany of VitD Deficiency
    • Introduction
    • Chemical Pathology
    • Prediposing factor
    • Clinical manifestations
    • Diagnosis & Differential diagnosis
    • Treatment
  • 72.
    • bases on
    • Clinical manifestations
    • manifest tetany, latent tetany
    • Biochemical changes
    • serum Ca 2+ <0.75~1mmol/L
    • serum Ca<1.75~1.88 mmol/L
    • The combined presence of rickets
    Dagnosis
  • 73.
    • Afebrile convulsion
    • H ypoglycemia (Glu ↓ )
    • Hypom agnesemia (Mg ↓ )
    • I nfantile spasms
    • Primary hypoparathyroidism(P ↑ )
    • Infection of central nervous svstem
    • acute laryngitis
    Differential diagnosis
  • 74.
    • Prognosis
    • good unless treatment is delayed,
    • death rarely occurs
    • (may result from laryngospasm and cardiac dilation)
    • Prevention
    • identical to that of VitD deficient rickets
  • 75.
    • & Rickets of Vitamin D Deficiency
    • & Tetany of VitD Deficiency
    • Introduction
    • Chemical Pathology
    • Prediposing factor
    • Clinical manifestations
    • Diagnosis & Differential diagnosis
    • Treatment
  • 76.
    • Anticonvulsive treatment
    • * oxygen inhalation
    • * drugs
    • 10% Chloral hydrate 0.4~0.5 ml/kg
    • r.e (retention enema)
    • Valium 0.1-0.3 mg/kg im. iv.
    Treatment
  • 77.
    • * Active treatment —
    • ↑ serum Ca > tetany level
    • Calcium gluconate (10%) 5~10 ml in
    • GS(10%~25%) 10~20 ml
    • iv ( >10 min ) cardiac arrest !
    • not im or s.c. Local necrosis!
    • * Treatment for rickets
    Treatment
  • 78. Mbbs.weebly.com