Calcium and Phosphate Disorders Flashcards
what hormones are released in response to hyper/hypo calcemia?
- high blood Ca++: causes release of calcitonin
- calcitnon promotes deposition of blood Ca++, thus lowering blood Ca++
- low blood Ca++: promotes release of PTH
-
PTH promotes:
- Ca+ reabsorption at the distal tubule
- Ca++ absorption from bone/gut
- relase of calitriol, which:
- increases synthesis of CPB
- promotes Ca++ absorption from gut/bone
-
PTH promotes:
what would increase Ca++ absorption from the gut?
- puberty
- pregnancy/lactation
- Vitamin D excess
- acromegaly
what would decrease Ca++ absorption of gut?
High vegetable & high fat diet
Steroids
Senescence
Gastrectomy
Malabsorption
Diabetes
Renal Failure
how does acidosis/alkalosis effect presence of calcium in the urine
- acidosis: hypercalciuria
- alkalosis: hypercalciuria
which diruetic corresponds to which level urine Ca++ level
Loop - hypercalciuria
Mannitol – hypercalciuria
Thiazides – hypocalciuria
Amiloride - hypocalciuria
false hypercalcemia vs true hypercalcemia
False Hypercalcemia: Increase total Ca++ resulting from increase total proteins
True Hypercalcemia: Increase in free plasma Ca++. This leads to clinically relevant hypercalcemia
- if free plasma Ca++ not known: obtain plasma albumin level to estimate total calcium
what are the major causes of hypercalcemia?
“chimpanzees”
-Calcium supplementation
- Hyperparathyroidism
- Idiopathic
- Milk-alkali syndrome
- Paget’s disease
- Addison’s disease
- Neoplastic disease
- Zollinger-Ellison syndrome
- Excessive vitamin A
- Excessive vitamin D
- Sarcoidosis-think granulomatous disease
what are major clinical manifestations of hypercalcemia?
- bones, stones, grones, psychiatric overtones
- bones = abnormal bone remodeling/fracture risk
- stones = increased risk for kidney stones
- groans = abdominal cramping, nausea, ileus, coonstipation
- psychiatric overtones
treatments for hypercalcemia:
- Saline Infusion (0.9% NS)
- Loop Diuretics once rehydrated
- Dialysis
- Calcitonin (promotes calcium deposition) – short term effects
- for cancer:
- Steroids – beneficial in cancer
- IV Bisphosphonates – treatment of choice in cancer
- Inhibit bone reabsorption, inhibits calcitriol synthesis (calcitriol synthesis is usually stimulated by PTH and increases plasma Ca++)
major causes of hypocalcemia
Chronic and acute renal failure
Vitamin D deficiency-can lead to osteoporosis
Magnesium deficiency
Acute pancreatitis
Hypoparathyroidism and pseudohypoparathyroidism
Infusion of phosphate, citrate, or calcium-free albumin
nueromuscular manifestations of hypocalcemia
- troesseu’s sign: pt is unable to control finger movements when a blood pressure cuff is placed on their arm
- Chostek’s sign: facial switch
cardiovascular manifestations of hypocalcemia
- Hypotension
- Decreased Cardiac Output
- Ventricular ectopic activity
- QT interval prolongation - monitor this patient with an EKG closeley
symptoms of hypocalcemia
Most patients will be asymptomatic or report symptoms of intermittent paresthesia (numbness and tingling) of the hands and feet or perioral numbness
general treatment for hypocalcemia
- leafy greens
- calcium supplements (1-3 g/day)
- IV
- only indicated in patients with symptomatic hypocalcemia OR ionized calcium levels below 0.65 mmol/L
major causes of hyperphosphatemia:
- enhanced metabolism
- hemolysis
- rhabdomyolysos
- malignant hyperthermia
- neoplastic disease
- leukemia, lymphoma
- renal failure
- hypothyroidism, psuedohypothyroidism
major clinical manifestations of hyperphosphatemia
- formation of insoluble calcium-phosphate complexes that deposit in:
- soft tissues
- joints (should in picture)
- kidneys
- hyperphosphatemia can actually cause acute hypocalcemia, resulting in:
- seizures
- tetany
treatment for hyperphosphatemia
- Oral phosphate binders
- Aluminum Salts (up to 3gms/daily)
- Calcium Salts (up to 8gms/daily) - dont give in someone with hypercalcemia
- PhosLo
- Non-Calcium Binders
- Renagel of Fosrenal
- Magnesium Salts (up to2-3gms/day) - dont give in someone with hypermagnesemia
what is considered severe moderate/severe hypophosphatemia
- moderate: decrease of 2.5- 1 mg/dl
- severe: decrease of less than 1.0 mg/dl
causes of hypophosphatemia
- low intake
- this is rarely due to patients diet.
- if patient does have hypophosphatemia due to low diet, is it likely indicative of a malabsorption issue
- increased excretion:
- likely due to PTH
- (in phys we learned that the combined effects of PTH leads ot no change in plasma phosphate, idk)
- likely due to PTH
clinical manifestations of hypophosphatemia
Metabolic Encephalopathy
2) RBC dysfunction – may cause hemolysis
3) Leukocyte dysfunction
4) Thrombocytopenia
5) Decreased muscle strength and myocardial contractility.
treatment of hypophosphatemia
1) 2)
Oral phosphate salts Neutraphos
IV phosphorus
a) Severe (<1.0mg/dl) in critically ill – 0.08-0.16mmol/kg IV over 2-6 h
b) Moderate (1.0-2.5mg/dl) on ventilator – 0.08-0.16mmol/kg IV over 2-6 h
c) Moderate (1.0-2.5mg/dl) not on ventilator – oral treatment with 1,000 mg/day
d) Mild – treat with oral 1,000 mg/day
major causes of hypermagnesemia
- renal insufficiency
- hemolysis
- concentration in erythrocytes - 3x greater than the serum
- will rise 0.1/ mEqL for every 250 mL of erythrocytes
- expected only in massive hemolysis
clinical manifestations of hypermagnesemia
- cardiac conduction delays
- depressed contractility
- vasodilation
- early symptoms include loss of deep tendon reflexes (hyporeflexia) and can progress to flacid paralysis
