1) Bone mineral metabolism is tightly regulated by the intestine, kidney, bone, and hormones like PTH, vitamin D, and calcitonin. Calcium levels can be affected by changes in plasma proteins and acid-base balance.
2) Hypercalcemia has various causes like primary hyperparathyroidism and malignancy, and results in symptoms across multiple organ systems. Diagnostic workup to distinguish the causes typically involves testing for PTH and investigating for an underlying malignancy.
3) Hypocalcemia can occur from low or high PTH levels due to conditions like hypoparathyroidism, vitamin D deficiency, or renal failure. It produces neurological symptoms like paresthesias and tet
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
Hypercalcaemia is a common disorder we doctors from all faculties face in day to day clinical practice. This was a presentation done by me to give you an update regarding hypercalcaemia and it's management.
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Magnesium is a very important ion in the body, crucial to over 300 reactions.
Its disorders are underdiagnosed and can help improve healthcare if appropriately treated
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Study Resources:
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2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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4. Calculation of Corrected Calcium
• Because calcium binds to albumin and
only the unbound calcium is biologically
active ,the serum level must be adjusted
as follows
Corrected Ca2+ = [4.5 - Plasma Albumin]*0.8
+ measured S. Calcium
5. Factors affecting Calcium
Concentration
1) Changes in Plasma Protein concentration
- Increased [protein] Increased total [Ca2+]
2) Changes in Anion concentration
- Increased [anion] Increased fraction of Ca2+
that is complexed Decreased ionized [Ca2+]
3)Acid base abnormality
6.
7. Blood calcium is tightly regulated by:
1) Principle organ systems:
Intestine
Bone
Kidney
2) Hormones:
Parathyroid hormone (PTH)
Vitamin D
Calcitonin
12. Neuromuscular
Impaired concentration and memory
Confusion, stupor, coma
Lethargy and fatigue
Muscle weakness
Other
Itching
Keratitis, conjunctivitis
Corneal calcification (band keratopathy)
13. Etiology
I. Parathyroid Related
A. Primary Hyperparathyroidism
B. Lithium Therapy
C. Familial Hypocalciuric Hypercalcemia
II. Malignancy related
A. Solid Tumor (Breast, Lung, Kidney)
B. Hematologic malignancy (Lymphoma, Leukemia)
III. Vitamin D Related
A. Vitamin D Intoxication
B. Increased 1,25(OH)2D (Sarcoidosis)
14. I. Associated with high bone turnover
A. Hyperthyroidism
B. Immobilization
C. Thiazides
D. Vitamin A Intoxication
E. Fat Necrosis
II. Associated with Renal failure
A. Severe Secondary Hyperparathyroidism
B. Aluminium Intoxication
C. Milk-Alkali syndrome
16. Serum Calcium must be corrected for serum
Albumin before labelling it as hypercalcemia.
Among all cases of hypercalcemia, Primary
Hyperparathyroidism and Malignancy are the
most common causes accounting for more
than 90% cases.
Therefore diagnostic approach to
hypercalcemia typically involves
distinguishing between the two.
17.
18.
19. Treatment according to
Calcium Levels
Calcium level <12 mg/dl
Oral Hydration
High salt Diet
Avoid medications that cause hypercalcemia
No treatment at all may be a option
20. Calcium level > 12mg/dl
(Severe or Symptomatic)
Normal Saline: Initially 200-300ml/hr until patient is
euvolemic, then adjust to maintain urine output of 100-
150 ml/hr
Loop diuretics only after volume repletion in patients
with CHF & CKD.
Calcitonin, 4 IU/kg – subcutaneously or intramuscularly;
repeat every 6-12 hours only if patient is responsive
IV Bisphosphonates
Zoledronic acid: 4 mg over 15 minutes; 8 mg if
second dose is required (not FDA approved)
Pamidronate: Given over 2-24 hours, either as 60mg
(Ca level, 12-13.5mg/dl) or 90 mg (Ca level,
>13.5mg/dl)
21. Indications For Hemodialysis
Neurologic Symptoms
Calcium level > 18mg dl
Acute or Chronic Kidney Disease
Congestive Heart Failure
22. Primary Hyperparathyroidism
F:M 3:1
Annual Incidence is 0.2% in patients >60
Includes
a. Adenoma
b. MEN
c. Carcinoma
Presentation:
– Asymptomatic hypercalcemia (>50%)
– Renal stones (20%)
– Decreased bone density
– Symptoms of hypercalcemia (<5%)
23. Images show Subperiosteal Bone Resorption
along the radial aspects of the middle phalanges.
Bone Manifestations in Hyperparathyroidism
25. Osteitis Fibrosa Cystica
(Brown Tumour)
Manifestated in hyperparathyroidism
Represents a reparative cellular process
rather than a neoplastic process.
Histologically identical to giant cell tumour so
it needs to be differentiated.
Commonly seen with Secondary
Hyperparathyroidism.
26. Pathology
In CKD lower serum Ca level lead to a rise in PTH
secretion resulting in mobilisation of skeletal
calcium through rapid osteoclastic turnover of
bone to maintain normal serum calcium levels.
In localised regions where bone loss is
particularly rapid normal marrow contents may
be replaced by haemorrhage, and reparative
granulation tissue, with active, vascular,
proliferating fibrous tissue, resulting in a brown
tumour.
Haemosiderin imparts the brown colour
27.
28. Asymptomatic Primary
Hyperparathyroidism
Most prevalent form of disease
Defined as biochemically confirmed
hyperparathyroidism with the absence of
signs and symptoms typically associated with
more severe hyperparathyroidism such as
features of renal or bone disease.
29. Guidelines for surgery in Asymptomatic
Primary hyperparathyroidism
Serum Calcium >1mg/dl
(above Normal)
24hr Urinary Calcium No Indication
Creatinine Clearance If <60ml/min
Bone Density T score <2.5 at any
of 3 sites (Spine,
distal radius, hip)
Age <50 years
30. FAMILIAL HYPOCALCIURIC
HYPERCALCEMIA
Inherited as Autosomal Dominant Trait
Caused by inactivating Mutation in CaSR leading
to inappropriate secretion of PTH and excessive
reabsorption of Ca in DCT
Patients with primary Hyperparathyroidism have
<99% Ca reabsorption whereas most patients
with FHH have > 99% absorption
Differentiating with Primary hyperparathyroidism
is important as there is no role of surgery in FHH
31. Calcium/creatinine clearance ratio of <0.01 is
suggestive of FHH.
Sequence Analysis of CaSR is commonly
performed for Definitive Diagnosis.
Generally no treatment is required.
32. Secondary Hyperparathyroidism due
to Chronic Renal Failure
Impaired production of 1,25(OH)2D is now thought to be the
principal factor that causes Calcium Deficiency, Secondary
Hyperparathyroidism and bone disease.
Resistance to PTH also contributes to Hypocalcemia.
Recent findings have indicated that increase in FGF23
production by osteocyte occurs in CKD.
FGF23 is potent inhibitor of renal-1alpha hydroxylase so FGF23
dependent reduction in 1,25(OH)2D is important stimulus for
development of secondary hyperparathyroidism.
33. Management of Secondary
Hyperparathyroidism due to CKD
Restriction of phosphate in diet.
Avoidance of Aluminium containing phosphate
binding antacids to prevent problem of aluminium
intoxication.
Adequate Calcium intake by mouth usually 1-2g/day
and supplementation with 0.25-1mcg/d calcitriol.
It is usually recommended to maintain PTH levels
between 150-300pg/ml as high PTH may lead to
progression to Tertiary Hyperparathyroidism and low
PTH levels may lead to Adynamic Bone disease.
34. Tertiary Hyperparathyroidism
Tertiary hyperparathyroidism is a state of excessive
secretion of PTH after a long period of secondary
hyperparathyroidism and resulting in a high blood
calcium level.
It reflects development of autonomous
(unregulated) parathyroid function following a period
of persistent parathyroid stimulation.
• The basis of treatment is still prevention in
chronic kidney failure starting medication and dietary
restrictions long before dialysis treatment is initiated.
• The treatment of choice is surgical removal of three
and one half parathyroid glands.
36. DEFINITION
• Normal Serum calcium: 8.5 mg/dl –
10.5 mg/dl
• A decrease in the calcium levels
below 8.5mg/dl is termed
hypocalcemia
37. LOW PARATHYROID HORMONE LEVELS
1. Parathyroid agenesis
a) Isolated
b)DiGeorge Syndrome
2. Parathyroid destruction
a) Surgical
b)Radiation
c) Infiltration by metastases or systemic diseases
d)Autoimmune
3. Reduced Parathyroid function
a) Hypomagnesemia
b)Activating CaSR mutations
38. HIGH PARATHYROID HORMONE LEVELS ( Secondary Hyperparathyroidism)
1. Vitamin D deficiency or impaired 1,25(OH)2*D production/action
a) Nutritional vitamin D deficiency
b) Renal insufficiency with impaired 1,25(OH)2*D
production
c) Vitamin D resistance
2. Parathyroid hormone resistance syndromes
a) PTH receptor mutations
b) Pseudohypoparathyroidism
3. Drugs
a) Calcium chelators
b) Inhibitors of bone resorption
c) Altered vitamin D metabolism (Phenytoin, Ketoconazole)
4. Miscellaneous
a) Acute Pancreatitis
b) Acute Rhabdomyolysis
c) Hungry bone syndrome
43. Treatment
• Acute, symptomatic hypocalcemia:
– Calcium gluconate, 90 mg or 2.2 mmol IV, diluted in
50 mL of 5% dextrose or 0.9% sodium chloride,
given IV over 5 min
• Continuing hypocalcemia : constant IV infusion
(10 ampules of ca or 900 mg of ca in 1 L of 5%
dextrose or 0.9% sodium chloride administered
over 24 h)
44. Treatment
• Hypomagnesemia: magnesium supplementation
• Chronic hypocalcemia due to
hypoparathyroidism:
– calcium supplements (1000–1500 mg/d elemental
calcium in divided doses) AND
– either vitamin D2 or D3 (25,000–100,000 U daily) OR
calcitriol [1,25(OH)2D, 0.25–2 g/d]
45. Treatment
• Vitamin D deficiency - vitamin D supplementation
• Nutritional vitamin D deficiency:
– low doses of vitamin D (50,000 U, 2–3 times per week
for several months)
• Vitamin D deficiency due to malabsorption:
– higher doses (100,000 U/d or more)
• Goal is to bring serum calcium into the low
normal range and to avoid hypercalciuria, which
may lead to nephrolithiasis
46.
47. VITAMIN D
• major steroid hormone involved in mineral ion
homeostasis regulation.
48.
49. • The 25-hydroxyvitamin D-1α-hydroxylase -
expressed in the proximal convoluted tubule
cells of the kidney.
• PTH and hypophosphatemia are the major
inducers
• Calcium, FGF23, and the enzyme’s product
1,25(OH)2D, repress it
50. • 1α-hydroxylase is produced by macrophages
associated with granulomas and lymphomas.
• Activity of the enzyme is induced by interferon
γ and TNF-α but is not regulated by calcium or
1,25(OH)2D;
• Hypercalcemia,associated with elevated levels
of 1,25(OH)2D, may be observed.
52. Clinical manifestations
• Mild to moderate vitamin D deficiency is
asymptomatic
• Long-standing vitamin D deficiency results in
-Hypocalcemia
-Secondary hyperparathyroidism,
-Impaired mineralization of the skeleton
-Proximal myopathy
53. • RICKETS - In children, before epiphyseal
fusion, vitamin D deficiency results in growth
retardation associated with an expansion of
the growth plate.
• OSTEOMALACIA - The hypocalcemia and
hypophosphatemia that accompany vitamin D
deficiency result in impaired mineralization of
bone matrix proteins.
54. DIAGNOSIS
• Although the normal ranges vary, levels of
25(OH)D <37 nmol/L (<15 ng/mL) are
associated with increasing PTH levels and
lower bone density.
55. • Prolonged vitamin D deficiency results in
hypocalcemia .
• PTH is a major stimulus for the renal 25(OH)D 1α-
hydroxylase, there is increased synthesis of the
active hormone, 1,25(OH)2D.
• Paradoxically, levels of this hormone are often
normal in severe vitamin D deficiency.
• Therefore, measurements of 1,25(OH)2D are not
accurate reflections of vitamin D stores and
should not be used to diagnose vitamin D
deficiency in patients with normal renal function.
56. TREATMENT
• Recommended daily intake –
600 IU from 1 to 70 years of age, and
800 IU for those over 70.
• Toxicity usually is observed only in patients
taking doses in the range of 40,000 IU daily.
57. • Intact activation of vitamin D
– initially (50,000 IU weekly for 3–12 weeks),
followed by maintenance therapy (800 IU daily).
• In patients in whom 1α-hydroxylation is
impaired
– 1,25(OH)2D3 (calcitriol,0.25–0.5 μg/d) and
– 1α-hydroxyvitamin D2 (2.5–5 μg/d).
58. • Pharmacologic doses may be required for
maintenance therapy in patients who are
taking medications, such as barbiturates or
phenytoin,(accelerate metabolism of or cause
resistance to 1,25(OH)2D).
• Calcium supplementation should include 1.5–
2 g/d of elemental calcium.
• 24-h urinary calcium excretion should be in
the range of 100–250 mg/24 h.