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Calcium Metabolism - Coggle Diagram
Calcium Metabolism
Parathyroid Hormone
Function
Maintains ionized Ca+ within narrow rangles, stimulates calcium reabsoprtion, stimulates bone resorption (release of calcium from bone), and conversion of calcifediol to calcitriol
Kidney
Increase Ca resoprtion
Increases phosphate excretion
Increases hydroxylation of Vitamin D which increases intestinal CA absorption
Bone
Increases bone respoiption -> decrease cortical bone mass
Primary Phase: Increased permebaility of sotecytes and other cells of bone membrane allows Ca to move into extracellular fluid
Secondary Phase: Widespread resorption of mineral and organic compoennts of matrix, in trabecular bone
Physiological Action
Characteristics
Synthesized as larger preprohormone that undergoes cleavage, continuously synthesized, and metabolized by liver and kidneys
Regulators
Hypocalcaemia -> Increase PTH
CA binding to Ca-snesing receptor: Decreases PTH synthesis and secretion
Calcitriol: Decrease PTH gene transcription, but hypocalcaemia will override this
Feedback loop
PTH -> Increase bone release of calcium and kidney reabsorption -> Increase Ca2+ ECF -> Inhibit PTH
PTH -> Increase Kidney secretion of Calcitriol -> INcrease GI reabsopriton of Ca2+ -> Inhibit PTH
Calcium
99% of total calcium is in bone
Extracellular
50% is ionized, 40% is protein bound, 10% is complexed with anions
Homeostasis
Increase in PTH will increase calcium blood levels
ECF Calcium
Secrete and absorb from bone, from kidneys which will excrete into urine, from diet which will excrete into feces
Disorders
Hypercalcemia
Causes
Increased bone resorption, increased GI absorption, Decreased renal excretion
PTH Dependent
Primary Hyperparathyroidism
Excessive PTH secretion (In MEN1, Men2a and isolated familial hyperparathyroidism)
Tertiary hyperparathyroidism
PTH independent
Malignancy associated, vitami D excess, Thyrotoxicosis, adrneal insuffieciency, immobilization, paget's disease
Malignancy associated
Mostly secondary effects of increased tumor derived factor which lead to bone resorption and kidney calcium reabsorption
Treatment
Fluids, Furosemide, Calcitonin, Steroids, Biphosphonates, dialysis
Clinical Signs: Weakness, hypertension, valve and arterial calcificatin, Constipatient, stones, bone pain, altered mental status (bones, groans, stones, psychiatric overtones)
Hypocalcemia
Clinical Features: Paresthesia, laryngospasm, seizures, carpopedal spasm, Chvostek's Sign, Trousseau's sign, hyperreflexia
Causes
Low PTH, Vitamin D deficiency, Pseudohypoparathyroidism, drugs
Hypoparathyroidsm
Lack of PTH leads to low ECF Ca2+
Treatment
ABCs, Replace calcium, treat hypomagnesemia, may require vitamin D
Secondary Hyperparathyroidsm
Increased in PTH caused by another condition, Vitamin D disorders (deficiency or malabsoprtion), phosphate disorders, calcium deficiency
Chronic Kidney disease
Low calcium, unabel to reabsorp which leads to increase feedback and high PTH levels
Vitamin D
Regulation
Metabolism
Calciferol (vitamin D) from plant sources and UV exposure is produced into calcitriol
Action
Increase in Ca and phosphorus absoprtion, decrease cell proliferation in parathyroid gland, decrease in PTH gene transcription
Calcitonin
Action
Inhibits osteoclast mediated bone resportion
Renal Effects: Inhibits phosphorus reabsooption, and has some natriuretic effect (increased Ca excretion)
Therapeutic Uses
Hypercalcaemia - Administration quickly lowers serum Ca throguh reduced osteoclast activitiy
Disorders