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12 Cards in this Set

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Explain normal Ca++ metabolism:
GI absorption:
serum:
reservoir:
primary regulator

PTH secretion is stimulated when Ca++ < ____:

How does PTH increase serum Ca?
GI absorption - 200 mg/day
serum - 50% free, 45% protein bound, 5% complexed
reservoir - bones
primary regulator - PTH

<7.5 mg/dl

kidney reabsorption, active vit-D in kidney, bone resorption
Effect of serum albumin, tourniquet, pH, and serum P on Ca++:
albumin - decrease of 1g/dl --> serum Ca++ decrease 0.8 mg/dl
tourniquet - transudation of plasma water elevates total serum Ca
pH --> changes in pH --> changes Ca-protein binding (0.1 pH --> 0.12 mg/dl Ca)
serum P - increased serum P --> lowers ionized Ca, then total serum Ca as CaPO4 deposited in bone
Major causes in differential of hypocalcemia:

S/S of hypocalcemia:
decreased PTH
PTH resistance (pseudohypoPTH)
decreased vit D
increased deposition
pancreatitis
increased bone mineralization

carpopedal spasm, paresthesia, muscle cramps, tetany, psychosis, prolonged QT, cardiac changes
Signs of hypocalcemia:

What is pseudohypoPTH:
Chvostek's sign, Trousseau's sign, hyperreflexia, dry skin, brittle hair, transverse ridging of nails, dental enamel hypoplasia

hormone resistant hypoPTH, short stature, round face, short neck, brachydactyly, retarded
first step in hypocalcemia dx:

How to R/O pseudo-hypoCa, acute respiratory alkalosis:

Next step in eval:
check serum ionized Ca

check serum albumin, pH

check serum PTH
if low - +hypoPTH (duh)
if high - check serum P; low P = vit D deficiency, pancreatitis, bone mets disease
When do you see high serum P?

Tx of hypocalcemia:

Acute symptomatic hypocalcemia requires:
rhabdomyolysis, CRF, pseudohypoPTH

correction of disease
Ca++ supplementation - IV, PO
vit D supplementation

immediate 10-15 mEq Ca++ IV
Who usually gets primary hyperPTH?

75% are due to what:

Explain high PTH effect on serum Ca:

Most common presentation:
post-menopausal women

single adenomas

increased bone resorption, GI absorption, increased vit D stimulation

asymtomatic hypercalcemia
PTH, pancreas, pituitary, AD:

PTH, medullary thyroid, pheo, AD:

Effect of sarcoid, histoplasmosis:

ARF and hypercalcemia:
MEN 1

MEN 2a

increased active vit D

polyuric recovery phase --> elevated PTH, active vit D, dissolution of ectopic CaPO4 deposits
Meds that can cause hypercalcemia:

Malignancies and hypercalcemia:
vit D intox - dialysis patients, women being tx'ed for OP
Milk-alkali - ingestion of large amounts of Ca, alkali products
TZ diuretics

most common - secondary to osteolytic lesions - breast ca, MM
lymphomas - too much active vit D
squamous, renal, bladder, ovarian - PTHrP type proteins
defect in familial benign hypocalciuric hypercalcemia:

When should it be suspected?

Clinical features of hyperPTH:

features of sarcoid:
mutation in PTH calcium receptors

urinary Ca/creatinine ratio <0.01

nephrolithiasis, hyperchloremic acidosis, hyperP, pseudogout, osteitis fibrosa cystica

hilar adenopathy, rash, lymphadenopathy, EKC conduction abnormalities
Features of malignancies and hyperCa:

thyrotoxicosis:

Tx of acute hypercalcemia:
serum Ca > 15, anorexia, weight loss

hyperreflexia, systolic HTN

fluids, induce calciuria - saline diuresis
anti-resorptive therapy:
1st line - pamidronate disodium IV
adjunct - calcitonin
2nd line - etidronate, gallium nitrate
Drug more potent than pamidronate, rapid onset, relapse time twice as long:

Indications for surgery in primary hyperPTH:
zoldronic acid

serum Ca >11.5
nephrolithiasis
compromised renal fxn
hypercalciuria
OP
age <50