Post on 23-Dec-2015
description
Bones = insoluble salts• Protect, weight, levers
ECF = soluble ions (1%)• Ionized• Protein bound
PTH secretion – regulated by free Ca2+
PTH Kidney
Bone
A 17 year-old female with a history of total thyroidectomy was sent to the emergency department (ED) for an abnormal lab study.
The patient reported a previous history of electrolyte problems with which she felt "twitchy," yet reported no symptoms during this ED evaluation.
A blood pressure cuff was placed on the patient's right arm and inflated to a pressure above the patient's systolic blood pressure.
After approximately 2 minutes, the patient's right hand developed a contracted position. Within seconds of release of the cuff, the patient's hand returned to a normal position.
Etiology:• Renal failure: 1,25-hydroxy Vit D deficiency Vit D
deficiency (nutritional)
• Hypomagnesemia: failure of release of PTH
• Hypoparathyroidism: from surgery and stunned hypoparathyroidism, neck radiation, autoimmune destruction or Ca-sensing receptor auto-Ab
• Drug induced: Phenytoin – damages vitamin DFoscarnet, Cinacalet – inhibits PTH release
Pseudohypoparathyroidism• Peripheral tissue resistance to PTH
Primery site = renal tubules Bone osteitis fibrisa cystica
• Ia and Ib: end organ resistance• Ia:• serum PTH • skeletal abnormalities• Mental retardation• Short stature
Hypoproteinemia:• nephrotic syndrome, • chronic illness, • malnutrition, • cirrhosis• volume overexpansion.
• Corrected Calcium:[N(Alb) – P(Alb)] x 0.8 + (Ca)
Each 1.0 Alb = 0.8 Ca
Vit D deficiency:1. Crohn’s disease2. Celiac sprue3. Pancreatic insufficiency4. Nutritional/Sunlight
• PTH levels are high • Alk phos can be elevated
Hyperphosphatemia:• Excessive enteral or parenteral
phosphate administration
• The tumor lysis syndrome
• Rhabdomyolysis- induced acute renal failure
Pancreatitis• Libereted FA chelate Ca2+
Sepsis:• Hypocalcemia is associated with a
worse prognosis.
• Most often reported with gram-negative sepsis
• Has occurred in toxic shock syndrome caused by staph
• The pathophysiology of hypocalcemia in this setting is unknown.
Clinical manifestations• Neuromuscular irritability: • perioral paresthesias, • cramps, • + Chvostek’s,• + Trousseau’s, • laryngospasm• irritability, depression,• psychosis, • ICP, seizures, • QT interval
Clinical manifestations:• Rickets and/or osteomalacia: • Chronic vit D low Ca2+,
low PO43- low
bone/cartilage mineralization
• growth failure, • bone pain, • muscle weakness
Clinical manifestations:• Renal osteodystrophy • ( vit D & PTH in renal failure)
• osteomalacia • ( mineralization of bone due to
Ca and 1,25-(OH)2D)
• osteitis fibrosa cystica • (due to PTH)
Diagnostic studies• Ca• alb• PTH• 25-(OH)D• 1,25(OH)2D (if renal failure or rickets)• Mg• PO4
• Alk phos• UCa
Treatment
• Symptomatic: intravenous Ca gluconate (1–2 g IV over 20 mins) + calcitriol* (most effective in acute hypocalcemia, but takes hrs to work)
• Asymptomatic and/or chronic: oral Ca (1–3g/d) & vitamin D (ergocalciferol* 50,000 IU PO q wk x 8-10wks)
• Chronic renal failure: phosphate binder(s), oral Ca, calcitriol or analog
Resources
• Fischer, Conrad; Internal medicine clerkship: Survive clerkship & ace the shelf. 1st Edition. Kaplan Publishing. Hypocalcemia, pages: 86-87.
• Sabastine, Mark; Pocket medicine: The massachsetts General Hospital Handbook of Internal Medicine. Fourth Edition. Lippincott Williams & Wilkins. Calcium disorders, page: (7-12)
• Goldman's Cecil Medicine: Expert Consult Premium 24th Edition. Saunders. Hypocalcemia, pages 1113 - 1119