1479713317-hypocalcemia in medicine .ppt

Hypocalcemia

1. HYPOCALCEMIA

2. Normal values
 Total plasma or serum calcium :
8.5 – 10.5 mg/dl
 Ionized calcium :
4.6 – 5.3 mg/dl
 Adjusted Sr. Calcium levels = 8 + 0.8(4- Sr.Alb)

3. A) B)
C) D)
Which of these hand posturing is
seen in hypocalcemia ?

4. CLINICAL FEATURES
•ACUTE PRESENTATION :
NEUROMUSCULAR IRRITABILITY
•TETANY
1)APPARENT
2)LATENT

5. TETANY
•APPARENT
 General fatigue and muscle weakness
 Twitching in muscles
 Paresthesia & Numbness
 Circumoral Paresthesia & peripheral tingling
Muscle cramps
Carpopedal spasms

6. TETANY
•LATENT

7. •Trousseau sign/ Main de accoucheur sign
BP cuff > 15 mmhg above SBP
• Extension of elbow
• Flexion wrist & MCP jt
• Extension of IP jt
• Adduction of fingers
•Chvostek sign
facial spasms/twitching produced by lightly tapping over the facial
nerve just in front of the ear on masseter near angle of mandible .

9. •Albumin is the major reservoir of protein-bound calcium.
•Disorders that alter plasma pH or serum albumin
concentration must be considered when circulating calcium
concentrations are being evaluated.
•The fraction of ionized calcium is inversely related to plasma
pH; alkalosis can precipitate hypocalcemia by lowering
ionized calcium without changing total serum calcium.
•Alkalosis may result from hyperpnea caused by anxiety or
from hyperventilation related to physical exertion.

10. •A decrease in albumin concentration of 1 g/dl results in a
decrease in protein-bound and hence total calcium
concentration of about 0.8 mg/dl.
•Binding of calcium to albumin is strongly pH-dependent
between pH 7 and pH 8; an acute increase or decrease in pH of
0.1 pH units will increase or decrease, respectively, protein
bound calcium by about 0.12 mg/dl.
•Thus, in hypocalcemic patients with metabolic acidosis, rapid
correction of acidemia with sodium bicarbonate can precipitate
tetany, due to increased binding of calcium to albumin and a
consequent decrease in the ionized calcium concentration.

11. •Hypoproteinemia may lead to a false
suggestion of hypocalcemia because the
serum total calcium level is low even though
the ionized Ca
2+
remains normal.

•It is best to measure serum ionized calcium if
hypocalcemia or hypercalcemia is suspected.

12. ETIOLOGIC CLASSIFICATION OF
HYPOCALCEMIA
•PARATHYROID HORMONE DEFICIENCY
•PARATHYROID HORMONE RECEPTOR DEFECTS
(PSEUDOHYPOPARATHYROIDISM)
•MITOCHONDRIAL DNA MUTATIONS
•MAGNESIUM DEFICIENCY
•EXOGENOUS INORGANIC PHOSPHATE EXCESS
•VITAMIN D DEFICIENCY
 
 

14. PARATHYROID HORMONE
DEFICIENCY
•Aplasia or hypoplasia of parathyroids
•Suppression of neonatal PTH secretion due to
maternal hyperparathyroidism
•Preproparathyroid hormone gene mutation
•Ca
2+
-sensing receptor activating mutation
•Autoimmune parathyroiditis
•Infiltrative lesions

15. •Primary hypoparathyroidism causes
hypocalcemia, but does not cause rickets.

16. Etiology of primary
hypoparathyroidism
•Congenital malformation (e.g., DiGeorge syndrome or
other complex syndromes) resulting from
developmental abnormalities of the third and fourth
branchial arches
•Surgical procedures, such as thyroidectomy or
parathyroidectomy, in which parathyroid tissue is
removed either deliberately or as a complication of
surgery for another goal
•Autoimmunity (autoimmune polyglandular syndrome
type 1), which may destroy the parathyroid gland

17. Pseudohypoparathyroidism
•Pseudohypoparathyroidism may occur in one
of four forms, all with hypocalcemia and
hyperphosphatemia.

18. Pseudohypoparathyroidism
•Type Ia-an abnormality of the G
sα protein linking the PTH
receptor to adenylate cyclase; biologically active PTH is
secreted in great quantities but does not stimulate its
receptor
•Type Ib-normal phenotype, normal G
sα
with abnormalities in
the production of adenylate cyclase
•Type Ic-abnormal phenotype, normal production of adenylate
cyclase, but a distal defect eliminates the effects of PTH
•Type II-normal phenotype, normal production of adenylate
cyclase, with a postreceptor defect, close to type Ib

19. •Pseudohypoparathyroidism is an autosomal
dominant condition that may present at birth or
later.
•Other clinical manifestations of
pseudohypoparathyroidism associated with Albright
hereditary osteodystrophy include short stature,
stocky body habitus, round facies, short fourth and
fifth metacarpals, calcification of the basal ganglia,
subcutaneous calcification, and, often,
developmental delay.

20. •Albright hereditary osteodystrophy may be
inherited separately so that a patient may
have a normal appearance with hypocalcemia
or may have the Albright hereditary
osteodystrophy phenotype with normal serum
calcium, phosphate, PTH, and response to
PTH.

21. •During the first 3 days after birth, serum
calcium concentrations normally decline in
response to withdrawal of the maternal
calcium supply via the placenta.
•Sluggish PTH response in a neonate may result
in a transient hypocalcemia.

22. •Hypocalcemia caused by attenuated PTH
release is found in infants of mothers with
hyperparathyroidism and hypercalcemia; the
latter suppresses fetal PTH release, causing
transient hypoparathyroidism in the neonatal
period.

23. •Normal serum magnesium concentrations are
required for normal parathyroid gland
function and action.
•Hypomagnesemia may cause a secondary
hypoparathyroidism, which responds poorly
to therapies other than magnesium
replacement.

24. •Neonatal tetany is most often noted in
premature or asphyxiated infants and infants
of diabetic mothers.

25. •Excessive phosphate retention, as occurs in
renal failure, also produces hypocalcemia.

26. •The etiology of hypocalcemia usually can be
discerned by combining features of the clinical
presentation with determinations of serum
ionized calcium, phosphate, alkaline
phosphatase, PTH (preferably at a time when
the calcium is low), magnesium, and albumin.

28. •If the PTH concentration is not elevated
appropriately relevant to low serum calcium,
hypoparathyroidism (transient, primary, or
caused by hypomagnesemia) is present.

29. •Vitamin D stores can be estimated by
measuring serum 25-hydroxyvitamin D.

30. •Renal function is assessed by a serum
creatinine measurement or determination of
creatinine clearance.

31. Treatment
•Treatment of severe tetany or seizures
resulting from hypocalcemia consists of
intravenous calcium gluconate (1-2 mL/kg of a
10% solution) given slowly over 10 minutes,
while cardiac status is monitored by
electrocardiogram (ECG) for bradycardia,
which can be fatal.

32. •Long-term treatment of hypoparathyroidism
involves administering vitamin D, preferably
as 1,25-dihydroxyvitamin D, and calcium.
•Therapy is adjusted to keep the serum calcium
in the lower half of the normal range to avoid
episodes of hypercalcemia that might produce
nephrocalcinosis and to avoid pancreatitis.

33. Important Physiologic Changes in
Bone and Mineral Diseases
•Condition Calcium Phosphate Parathyroid Hormone 25(OH)D
Primary hypoparathyroidism ↓ ↑ ↓
Nl Pseudohypoparathyroidism ↓ ↑ ↑
Nl Vitamin D deficiency Nl(↓) ↓ ↑
↓ Familial hypophosphatemic rickets Nl ↓ Nl (sl↑)
Nl Hyperparathyroidism ↑ ↓ ↑
Nl Immobilization ↑ ↑ ↓
Nl

34. RICKETS
•Rickets is defined as decreased or defective
bone mineralization in growing children;
osteomalacia is the same condition in adults.
•The proportion of osteoid (the organic portion
of bone) is excessive.
•As a result, the bone becomes soft and the
metaphyses of the long bones widen.

35. Clinical manifestations
•Most manifestations of rickets are due to
skeletal changes.
•Craniotabes
•Rachitic rosary
•Growth plate widening is also responsible for
the enlargement at the wrists and ankles.
•Harrison groove

40. •Very low birth weight infants have an increased
incidence of rickets of prematurity.
•In older infants, poor linear growth, bowing of
the legs on weight bearing (which can be
painful), thickening at the wrists and knees, and
prominence of the costochondral junctions
(rachitic rosary) of the rib cage occur.

•At this stage, x-ray findings are diagnostic.

41. •In nutritional vitamin D deficiency, calcium is
not absorbed adequately from the intestine.
•Poor vitamin D intake (food fads or poor
maternal diet affecting breast milk vitamin D)
or avoidance of sunlight in infants exclusively
breastfed may contribute to the development
of rickets.

42. •Fat malabsorption resulting from
hepatobiliary disease (biliary atresia, neonatal
hepatitis) or other causes (cystic fibrosis) also
may produce vitamin D deficiency because
vitamin D is a fat-soluble vitamin.

43. •Defects in vitamin D metabolism by the kidney
(renal failure, autosomal recessive deficiency
of 1α-hydroxylation, vitamin D-dependent
rickets) or liver (defect in 25-hydroxylation)
also can cause rickets.

44. •In familial hypophosphatemic rickets, the
major defect in mineral metabolism is failure of
the kidney to reabsorb filtered phosphate
adequately so that serum phosphate decreases,
and urinary phosphate is high.
•The diagnosis of this X-linked disease usually is
made within the first few years of life.
•Disease typically is more severe in males.

45. •The etiology of rickets usually can be
determined by assessment of the mineral and
vitamin D status (25-hydroxyvitamin D < 8
ng/mL suggests nutritional vitamin D
deficiency).
•Further testing of mineral balance or
measurement of other vitamin D metabolites
may be required.

46. •Several chemical forms of vitamin D can be
used for treatment of the different rachitic
conditions, but their potencies vary widely.
•Required dosages depend on the condition
being treated .

47. •Rickets usually is treated with 1,25-
hydroxyvitamin D and supplemental calcium.
•In hypophosphatemic rickets, phosphate
supplementation (not calcium) must
accompany vitamin D therapy, which is given
to suppress secondary hyperparathyroidism.

48. •Adequate therapy restores normal skeletal
growth and produces resolution of the
radiographic signs of rickets.
•Nutritional rickets is treated with vitamin D in
one large dose or multiple smaller
replacement doses.
•Surgery may be required to straighten legs in
untreated patients with long-standing disease.