Calcium Flashcards
Pth Increases the plasma calcium and decrease plasma phosphate by acting on ?
Bone : increase resorption
Kidney:increase ca+2 resorption ,decrease phosphate resorption
Gut:activation of vitamin d
Calcitonin decrease calcium and decrease phosphate by acting on
Bone: Decrease bone resorption
Kidney: Decrease calcium reabsorption and Decrease phosphate reabsorption
Gut :decreased postprandial calcium reabsorption
Vitamin D: increase calcium and phosphate by acting on
Bone : high bone resorption
Symptoms of hypocalcemia
- Asymptomatic ( sever symptomatic< 7.5 mg/dl )
- Rickets and osteomalacia
- Increased neuromuscular irritability
a. Numbness/tingling
b. Tetany
• Hyperactive deep tendon reflex
• Chvostek sign- tapping on facial
nerve leads to a contraction (twitching) of facial
muscles
• Trousseau sign - Inflate Bp culf to a pressure higher than the patient’s systolic
BP for 3 minutes This elicits carpal
spasms.
c. Seizures - Basal ganglia calcifications
- Cardiac manifestations
a. Arrhythmias
b. Prolonged QT interval on ECG
Diagnosis of hypocalcemia
obtain the following: BUN, Cr, magnesium
albumin, and ionized calcium. Amylase, lipase, and liver function tests may also be
warranted.
2. Serum PO(phosphate)high in renal insufficiency and in hypoparathyroidism, low in primary
vitamin D deficiency
- PTH
a. Low in hypoparathyroidism
b. Elevated in vitamin D deficiency, CKD)
C. Very high in pseudohypoparathyroidism
Ca+2
Normal level : 8.5- 10.5 mg/dl
Affected by albumin and ph
Calcium in plasma exist in two forms:
1.Protein bond ( albumin)
2.free ionized ( physiologically active controlled by PTH, independent of albumin levels)
So hypoalbuminemia causes decrease in total calcium, but ionized calcium is normal and estimated by this formula :
total calcium- ( serum albumin*0.8)
Ph and calcium
Increase in pH increases the binding of calcium to albumin so in alkalemic states ( acute Risp Alkalosis)
Total calcium is normal, but I don’t know it’s calcium is low, and the patients frequently manifests the signs and symptoms of hypocalcemia
Causes of hypocalcemia
- Hypoparathyroidism (most common cause) -usually due to surgery so damage to parathyroid gland
- Renal insufficiency -mainly due to decreased production of
1,25-dihydroxy, vitamin D. - Vitamin D deficiency
- Hyperphosphatemia resulting in calcium phosphate deposition
- Hypomagnesemia results in decreased PTH secretion/ Malabsorption–for example, short bowel syndrome, leading to low vitamin D or magnesium
- Pseudohypoparathyroidism–autosomal recessive disease causing congenital end-organ resistance to PTH (so PTH levels are actually high); also characterized by mental retardation and short metacarpal bones
7.Hypoalbuminemia-clinically irrelevant as ionized (metabolically active) component is normal. - Alkalemia-as above, increase in pH causes increased calcium binding, serum levels will be normal but clinically important as ionized fraction is low
- Acute Pancreatitis deposition of calcium deposits lowers serum Ca
- Blood transfusion (with citrated blood )calcium binds to citrate
- Osteoblastic metastases
- DiGeorge syndrome- caused by a deletion on chromosome 22. Absence of thymig shadow on chest x ray
Hypercalcemia ( emergency) endocrinopathies
a. Hyperparathyroidism- increased Ca, low PO,, usually due to an adenoma
(most common cause in outpatients)
b. Renal failure- usually results in hypocalcemia, but sometimes secondary hyperparathyroidism elevates PTH levels high enough to cause hypercalcemia (this is known as tertiary hyperparathyroidism)
c. Paget diseaseof the bone due to osteoclastic bone resorption
d. Hyperparathyroidism, acromegaly, Addison disease
Malignancies that causes hupercalcemia
(most common cause in inpatients)
a. Metastatic cancer- bony metastases result in bone destruction due to osteoclast. activity. Most tumors that metastasize to bone cause both osteolytic and osteoblastic activities (prostate cancer, mainly osteoblastic; breast and kidney carcinoma usually osteolytic)
.
- b. Multiple myeloma secondary to two causes
• Lysis of bone by tumor cells
• Release of osteoclast-activating factor by myeloma cells
C. Tumors that release PTH -like hormone (e.g., squamous cell cancers such as lung head, and neck)
d. Tumors that release PTH (lung, ovarian cancers)
e. Tumors that release vitamin D (e.g., lymphomas)
Drugs that cause hypercalcemia
a. Vitamin D intoxication- increased GI absorption of calcium
b. Milk-alkali syndrome- hypercalcemia, alkalosis, and renal impairment due to excessive intake of calcium and certain absorbable antacids (calcium carbonate milk
c. Drugs-
thiazide diuretics (inhibit renal excretion),
lithium (increases PTH leves
Some patients, e.g., squamous cell carcinoma)
Other Causes of hypercalcemia
Sarcoidosisincreased GI absorption of calcium
Familial hypocalciuric hypercalcemia-distinguished from primary hyperparatis roidism by a low urine calcium excretion versus & normal or high urine calcium excretion in primary hyperparathyroidism
Rx of hypocalcemia
. If symptomatic, provide emergency treaument
wide IV calcium gluconate ,
For long term management, use oral calcium supplements (calcium carbonate)and vitamin D,
For PTH deficiency:
a. Replacement therapy with vitamin D or (calcitriol) plus a high oral calcium intake
b. Thiazide diuretics
-lower urinary calcium and prevent urolithiasis
It is also important to correct hypomagnesemia. It is very difficult to correct the ca level if the magnesium is not replaced first.
Clinical features of hypercalcemia
Stones
bones( bone aches, and pain, osteitis fibrosis cystica
grunts, and groans :
Muscle pain and weakness
Pancreatitis
Peptic ulcer
Gout
Constipation
Psychiatric : depression, fatigue, anorexia, and anxiety, sleep disturbances
Polydepsia , polyuria
Hypertension
Weight loss
Hypercalcemia and hypocalcemia on ECG
• In hypercalcemia, ECG shows shortening of the QT interval.
• In hypocalcemia, ECG shows a prolongation of the QT interval.
