Ipapburke Endo Test 2- Study Guide

Front 1

PRIMARY REGULATORS OF SERUM CALCIUM

Back 1

PARATHYROID HORMONE, VITAMIN D, AND CALCITONIN

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DESCRIBE PHYSIOLOGICALLY ACTIVE CALCIUM

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CIRCULATES AS FREE (OR IONIZED)- 50% OF CALCIUM IN THE BLOOD----40% OF THE REST OF CALCIUM IS BOUND TO PROTEINS AND 10% TO BICARB, CITRATE, OR PHOSPHATE

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OSTEOCLASTS

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DISSOLVE BONE

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OSTEOBLASTS

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BUILD NEW BONE

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FUNCTIONS OF PTH

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STIMULATES RESORPTION (OR DISSOLUTION) OF BONE BY OSTEOCLASTS; INCREASES RENAL TUBULAR REABSORPTION OF CALCIUM; AND STIMULATES RENAL ACTIVATION OF VITAMIN D

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JOB OF VITAMIN D

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ENHANCES INTESTINAL ABSORPTION OF CALCIUM AND PHOSPHATE

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WHAT STIMULATES PTH SECRETION?

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FALLING FREE OR IONIZED CALCIUM LEVELS AND SECRETION IS SUPPRESSED BY RISING FREE (IONIZED) CALCIUM LEVELS

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ACTIVE FORM OF VIT D

Back 8

1,25(OH)2D

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WHEN IS CALCITONIN PRODUCED?

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PRODUCED BY THE PARAFOLLICULAR CELLS OF THE THYROID GLAND IN RESPONSE TO AN ELEVATED SERUM CALCIUM LEVEL

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JOB OF CALCITONIN

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INHIBITS CALCIUM RESORPTION FROM BONE (INHIBITS OSTEOCLASTS)

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THREE JOBS OF CALCITONIN

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INHIBITS CALCIUM RESORPTION FROM BONE (INHIBITS OSTEOCLASTS) **; INCREASES CALCIUM STORAGE IN BONE; INCREASES RENAL EXCRETION OF CALCIUM

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NORMALLY, WHEN THE SERUM CALCIUM LEVEL DECREASES, WHAT WILL HAPPEN TO PTH AND CALCITONIN?

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PTH WILL INCREASE AND CALCITONIN WILL DECREASE

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NORMALLY, WHEN THE SERUM CALCIUM LEVEL INCREASES, WHAT WILL HAPPEN TO PTH AND CALCITONIN?

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PTH WILL DECREASE AND CALCITONIN WILL INCREASE

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MAIN USE FOR CALCITONIN AS A DRUG

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FOR USE IN OSTEOPENIA

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HYPERCALCEMIA WITH INCREASED PTH

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PRIMARY HYPERTHYROIDISM

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HYPERCALCEMIA WITH NORMAL OR MINIMALLY INCREASED PTH

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FAMILIAL HYPOCALCUIRIC HYPERCALCEMIA (FHH)

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HYPERCALCEMIA WITH SUPPRESSED PTH

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MALIGNANCY, VIT D EXCESS, HIGH BONE TURNOVER (THYROTOXICOSIS) OR IMMOBILIZATION

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BEST ASSAY FOR EVALUATING SERUM CALCIUM LEVEL

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A FREE (IONIZED) CALCIUM LEVEL

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IF A FREE CALCIUM ASSAY IS NOT AVAILABLE, WHAT DO YOU DO?

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SUBTRACT 0.8 MG/DL PER EACH GRAM OF ALBUMIN OVER A LEVEL OF 4.0 G/DL (CORRECTED TOTAL CALCIUM LEVEL)

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FIVE CLINICAL PRESENTATIONS OF HYPERCALCEMIA

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STONES, BONES, MOANS, GROANS, OVERTONES

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INCLUDED IN "STONES"

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KIDNEY STONES, NEPHROCALCINOSIS, THIRST, POLYURIA, METABOLIC ACIDOSIS

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INCLUDED IN "BONES"

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BONE PAIN AND FRACTURE

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INCLUDED IN "GROANS"

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ANOREXIA, DYSPEPSIA, CONSTIPATION

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INCLUDED IN "MOANS"

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MYALGIA, PROXIMAL MUSCLE WEAKNESS, JOINT PAIN

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INCLUDED IN "OVERTONES"

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DEPRESSION, MEMORY LOSS, CONFUSION, LETHARGY, COMA

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ETIOLOGIES OF PRIMARY HYPERPARATHYROIDISM

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BENIGN PARATHYROID ADENOMA (80%) OR PARATHYROID HYPERPLASIA

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WHY IS THERE HYPERCALCIURIA IN PRIMARY HYPERPARATHYROIDISM?

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EXCESS CALCIUM IN THE GLOMERULAR FILTRATE IS EXCRETED DUE TO IT OVERWHELMING RENAL TUBULAR REABSORPTION CAPACITY (PTH NORMALLY CAUSES THE REABSORPTION OF CA)

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HOW DOES PRIMARY HYPERPARATHYROIDISM CAUSE HYPERCALCEMIA?

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THE PARATHYROID ADENOMA EXCRETES EXCESS PTH WHICH CAUSES THE HYPERCALCEMIA

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S/S OF HYPERPARATHYROIDISM

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MOST PATIENTS ARE ASYMPTOMATIC (NOTICED ON LAB VALUES); MAY SEE A SHORTENED QT INTERVAL ON ECG

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WHAT IS THE ELEVATED CALCIUM AT WHICH PATIENTS GET CONFUSED, WEAK, OR LETHARGIC?

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GREATER THAN 14 MG/DL