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Consequences of Vitamin D deficiency

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Consequences of Vitamin D deficiency & Excess By: Prof. M. Y. JAN Hypervitaminosis D DEFINITION: A disorder due to the excessive ingestion of Vitamin D resulting in ... – PowerPoint PPT presentation

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Title: Consequences of Vitamin D deficiency


1
Consequences of Vitamin D deficiency
Excess
By Prof. M. Y. JAN
2
Hypervitaminosis D
  • DEFINITION
  • A disorder due to the excessive ingestion of
    Vitamin D resulting in neurologic,
    gastrointestinal, and renal manifestations.
  • Alternative Name Vitamin D Toxicity
  • EPIDEMIOLOGY
  • incidence ?
  • age of onset any
  • risk factors
  • patients on vitamin D for chronic
    hyperphosphatemic states

3
Hypervitaminosis D
  • Pathogenesis
  • 1. Chronic Hypervitaminosis
  • may occur after the ingestion of excessive
    amounts of vitamin D over weeks (gt500 ug/d) or
    months (gt45 ug/d)
  • may lead to (malignant) calcification of soft
    tissues
  • heart - aortic valvular stenosis
  • blood vessels - hypertension
  • renal tubules - nephrocalcinosis -gt secondary
    nephrogenic DI -gt polyuria, polydipsia
  • stomach - anorexia, nausea and vomiting, etc

4
Hypervitaminosis D
  • CLINICAL FEATURES
  • Neurological Manifestations
  • hypotonia

  • irritability
  • Gastrointestinal Manifestations
  • anorexia
    with weight loss

  • constipation or diarrhea
  • nausea and
    vomiting
  • Renal Manifestations
  • polydipsia

  • polyuria/nocturia /- dehydration
  • Ocular Manifestations
  • conjunctiva
    - clouding
  • cornea
    clouding
  • retinopathy

5
Hypervitaminosis D
  • Other Manifestations
  • aortic valvular stenosis
  • hypertension
  • pallor
  • Fanconi Syndrome
  • episodes of vomiting, dehydration, weakness,
    and unexplained fever anorexia, constipation
    polydipsia, polyuria failure to thrive growth
    failure rickets

6
Hypervitaminosis D
  • INVESTIGATIONS
  • 1- Serum
  • hypercalcemia
  • evidence of dehydration - elevated BUN,
    creatinine
  • 2- Urine
  • hypercalciuria
  • proteinuria

7
Hypervitaminosis D
  • Imaging Studies
  • 1- Renal Ultrasound
  • nephrocalcinosis /- metastatic calcification
  • 2- Skeletal X-Rays
  • metastatic calcification of long bones
  • generalized osteoporosis
  • 3- 2D Echo
  • aortic valve stenosis

8
Hypovitaminosis D
  • Children
  • Vitamin D Deficiency Rickets
  • Adults
  • Osteomalacia

9
  • Rickets is the most common form of metabolic bone
    disease worldwide.

10
  • Clinical features
  • Abnormal gait, hypocalcemic tetany/ seizures,
    developmental delay, failure to thrive
  • Skeletal findingsgtgtgt

11
  • Skeletal and Radiological findings
  • Bowing or widening of physis
  • Costochondral beading (rachitic rosary)
  • Craniotabes
  • Delayed closure of anterior fontanel
  • Dental abnormalities
  • Flaring of ribs at diaphragm level (Harrison's
    groove)
  • Flaring of wrists
  • Fractures
  • Fraying and cupping of metaphysis
  • Frontal bossing of skull
  • Genu valgum or varum
  • Lordosis/kyphosis/scoliosis
  • Osteopenia
  • In addition, the anteroposterior diameter of the
    pelvis can shrink,
  • resulting in a flat pelvis, in girls may
    lead to obstructed labor

12
  • Nonskeletal effects of vitamin D deficiency
  • Hypocalcaemic seizures secondary to vitamin D
    deficiency occur
  • typically in infants under 6 months, usually
    before radiological
  • features are apparent.
  • Hypocalcaemic tetany, apnea and stridor may also
    present.
  • Hypocalcaemic cardiac myopathy may lead to
    potentially dilated or
  • hypertrophic cardiomyopathy, arrhythmias,
    hypotension, and heart
  • failure.

13

Biochemistry and Physiology of Vitamin D
Endocrine System
14
  • In the skin, photo-conversion of
    7-dehydrocholesterol to vitamin D3 or dietary
    intake of vitamin D3

15
  • Metabolism of vitamin D3 by the liver to
    25(OH)D3, which is the major form of vitamin D
    circulating in the blood compartment.

16
  • Conversion by the kidney of 25(OH)D3 to
    produce the two principal dihydroxylated
    metabolites, namely 1a,25(OH)2D3 and
    24R,25(OH)2D3.

17
  • Systemic transport of the dihydroxylated
    metabolites 1a,25(OH)2D3 and 24R,25(OH)2D3 to
    distal target organs.

18
  • Binding of the dihydroxylated metabolites,
    particularly 1a,25(OH)2D3, to a nuclear receptor
    at the target organs followed by the subsequent
    generation of appropriate biological responses.

19
  • An additional key component in the operation
    of the vitamin D endocrine system is the plasma
    vitamin D binding protein (DBP) that carries
    vitamin D3 and all of its metabolites to their
    various target organs

20
  • Apart from Vitamin D two other Hormones share
    in the regulation of Calcium and Phosphate
    Metabolism
  • Parathormon
  • Calcitonin

21
Renal osteodystrophy is a global term applied to
all pathologic features of bone in patients with
renal failure. Primary retention of phosphate
? hyperphosphatemia ? hypocalcemia ?
secondary hyperparathyroidism Therefore, the
spectrum of clinical and radiographic findings in
renal osteodystrophy .
22
What are the sources of vitamin D for humans?
23
Salt water fish
Small quantities of vitamin D3 are also found in
eggs, veal, beef, butter, and vegetable oils -
while plants, fruits, and nuts are extremely poor
sources of vitamin D.
24
Factors affecting dermal synthesis (sun exposure)
of vitamin D 1- season and latitude 2- Only
locations 30 or closer to the equator have
consistently intense UV-light. 3- duration of
UV sunlight 30 min per week for an
infant wearing only a nappy (diaper)
or 2 h a week fully clothed without a head cover
4- darker skin requires longer sun exposure,
however, as melanin competes with
7-dehydrocholesterol for UV-B photons 5- use of
sunscreens
25
increased indoor activities, and industrial
pollution means inadequate skin exposure, means
deficient resource on Vit D.
26
Treatment of Rickets
  • Preventive 400 1000 IU/day
  • Nutritional Rickets 3000 -6000 IU/day
  • Resistant Rickets 1alpha Calcitriol
  • Calcium supplemetation
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