lecture 85 Calcium, PTH and Metabolic Bone disorders Flashcards
(37 cards)
in the post op ICU a patient is noted to have low serum calcium levels, is this normal?
Yes – post op patients may have low albumin; therefore less protein bound calcium and lower serum calcium measurement
when you measure a total serum calcium, what components are you measuring?
what factors might alter these values?
□ Protein Bound Calcium
□ Diffusible Non Ionized
□ Ionized Calcium
Low albumin – lower protein bound calcium; lower total Calcium
Alkalosis – more protein bound calcium, but same Ca overall
Acidosis – lower protein bound calcium, but same Ca overall
if there is low albumin , how do you measure calcium levels ?
“Corrected Ionized Calcium” = Total Calcium + Correction Factor
Correction Factor = (4 - Albumin) x .8
Normal albumin: 3.5 -5.5
what organs control the level of serum calcium?
what hormones control the level of calcium ?
Intestines, bones, kidneys
PTH
1, 25 OH2 Vit D
Calcitonin, PTHRP
describe the generation of the active form of vit D?
function of this active form?
Skin: UV Light converts 7 Dehydroxycholesterol –> Vit D3
Liver: D3 —> 25 OH Vit D
Kidney: 25 OH Vit D –> 1,25 OH2 Vit D (Calcitriol); under control of PTH
§ Gi Tract: Increased Absorption of Ca2+ and PO4
§ Bone – Stimulates Bone breakdown
§ Maintains serum Ca and P
§ Negative Feedback on PTH glands
what form of vit D is measured when measuring vit D values ?
25 OH Vit D (not 1,25 bc the body readily converts this when it needs to)
Effect of PTH on the Kidney
□ Increases conversion of 25 vit D to 1,25 Vit D
□ Reabsorption of Ca2+ increased
□ Decreased Reabsorption of PO4
effect on PTH on bone
§ Bone – Two Opposite Effects – Anabolic and Catabolic – KNOW THIS
□ If Brief Stimulus (eg PTH injection) — bone Formation
® Osteoblasts – make new bone and stimulate Osteoclast activation
□ Prolonged Stimulus — Bone Breakdown
® Stimulation of osteoclast differentiation and Function (increasing blood calcium)
what is the most abundant anion in the body?
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too much of this anion in the serum can lead to____
PO4
vascular calcification
how is phosphorous regulated in the body?
§ High Phosphorous –
□ Increased PTH —> Phosph excretion from the kidney
□ FGF23 (made in osteocytes) —> Causes phosph excretion from the kidney
what is the most common cause of outpatient (asymptomatic) Hypercalcemia ?
what is the most common etiology of this ?
at what serum concentration may symptoms begin?
Primary Hyperparathyroidism –
□ 85% – single adenoma
□ 10% hyperplasia
Ca > 12 mg/dl
Signs and Symptoms of primary Hyperparathyroidism
Bones, Stones, Moans, Groans, Psychological Overtones
Asymptomatic – Most
Bones – Osteroporsis, pain and fracture
Stones – kidney stones, polyuria, azotemia
Moans – Neuromuscular weakness, fatigue, Chondrocalcinosis
Groans – constipation/N/V/peptic ulcers
Psychological Overtones -- Mild - depression Severe -- obtundation, coma Other -- eye (band keratopathy) Common cause of death in cancers (PTHRP)
what are three inherited forms of Primary hyperPTH
Rare form: FHH (familial hypocalciuric hypercalcemia) – AD mutation to calcium sensing receptor
MEN1
MEN 2
three non PTH mediated forms of hypercalcemia
what is the most common form of inpatient hypercalcemia
PTH levels are normal
Vit D Mediated - eg VIt D intoxication
PTHRP – most common form of inpatient (symptomatic)hypercalcemia
Other – Milk alkali syndrome, Immobilization, rhabdo
3 REQUIREMENTS for the dx of primary HyperPTH
® Elevated Serum Calcium
® Elevated or Inappropriately Normal PTH
® Elevated or normal Urine Calcium
Treatment of HyperPTH
Mild – none
Symptomatic:
Surgery – Localization of PTH glands by US and Sestamibi Scan, and removal of the glands.
For Poor Surgical Candidates – Cincalcet (calcimimetic agent) that tricks the PTH gland into thinking Calcium levels are sufficient
Treatment of Hypercalcemia
Acute Treatment –
Saline, Loop Diuretics,
IV Bisphosphonates (stbilize bone)
Treat the underlying cause –
Surgery, chemorads, glucocorticoids
what is secondary HyperPTH
Most common etiologies
Complications –
Parathyroid glands are reacting to something else such as low Calcium or Excess Phosphorous
etiologies –
CKD (most common); Hypercalcicuria, Vit D Deficiency
Bone Loss
what is tertiary HyperPTH
§ General: Same as primary hyperPTH, but in a patient who has been through a bout of Secondary HyperPTH
Eg CKD patient who then develops PTH Adenoma == Hypercalcemia
main causes of hypoPTH
Post op (thyroidectomy, head and neck surgery)
Auto Immune
AD CASR Mutaiton which perceives high levels of calcium
Digeorge Syndrome
requirements for dx of hypoPTH
□ Low PTH (Or inappropriately normal)
□ Low serum Ca
High Phosphorous
Hallmark and other symptoms of Hypocalcemia
Symptomatic if acute/severe rate of rise –
® Tetany – HALLMARK (neuromuscular irritability, paraesthesias, Seizures, larygospasm, cardiovascular collapse)
® Widened QT
® Mental Status – Fatigue, anxiety, depression, psychosis
® Intracranial – calcification of the basal ganglia
® Ocular – Cataracts
® Dental – early development = defective enamel
Two bedside signs for hypocalcemia
Chvostek Sign – tap along facial nerve –> ipsilateral twitch
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Trousseau Sign – BP cuff –carpal spasm
what is Pseudo-Hypoparathyroidism
Rare resistance to PTH (eg at the level of the kidey)
aka Albright’s Hereditary Osteodystrophy
