lecture 85 Calcium, PTH and Metabolic Bone disorders Flashcards

1
Q

in the post op ICU a patient is noted to have low serum calcium levels, is this normal?

A

Yes – post op patients may have low albumin; therefore less protein bound calcium and lower serum calcium measurement

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2
Q

when you measure a total serum calcium, what components are you measuring?

what factors might alter these values?

A

□ 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

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3
Q

if there is low albumin , how do you measure calcium levels ?

A

“Corrected Ionized Calcium” = Total Calcium + Correction Factor

Correction Factor = (4 - Albumin) x .8

Normal albumin: 3.5 -5.5

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4
Q

what organs control the level of serum calcium?

what hormones control the level of calcium ?

A

Intestines, bones, kidneys

PTH
1, 25 OH2 Vit D
Calcitonin, PTHRP

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5
Q

describe the generation of the active form of vit D?

function of this active form?

A

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

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6
Q

what form of vit D is measured when measuring vit D values ?

A

25 OH Vit D (not 1,25 bc the body readily converts this when it needs to)

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7
Q

Effect of PTH on the Kidney

A

□ Increases conversion of 25 vit D to 1,25 Vit D
□ Reabsorption of Ca2+ increased
□ Decreased Reabsorption of PO4

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8
Q

effect on PTH on bone

A

§ 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)

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9
Q

what is the most abundant anion in the body?

too much of this anion in the serum can lead to____

A

PO4

vascular calcification

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10
Q

how is phosphorous regulated in the body?

A

§ High Phosphorous –
□ Increased PTH —> Phosph excretion from the kidney

□ FGF23 (made in osteocytes) —> Causes phosph excretion from the kidney

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11
Q

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?

A

Primary Hyperparathyroidism –

□ 85% – single adenoma
□ 10% hyperplasia

Ca > 12 mg/dl

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12
Q

Signs and Symptoms of primary Hyperparathyroidism

A

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)
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13
Q

what are three inherited forms of Primary hyperPTH

A

Rare form: FHH (familial hypocalciuric hypercalcemia) – AD mutation to calcium sensing receptor

MEN1

MEN 2

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14
Q

three non PTH mediated forms of hypercalcemia

what is the most common form of inpatient hypercalcemia

A

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

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15
Q

3 REQUIREMENTS for the dx of primary HyperPTH

A

® Elevated Serum Calcium
® Elevated or Inappropriately Normal PTH
® Elevated or normal Urine Calcium

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16
Q

Treatment of HyperPTH

A

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

17
Q

Treatment of Hypercalcemia

A

Acute Treatment –
Saline, Loop Diuretics,
IV Bisphosphonates (stbilize bone)

Treat the underlying cause –
Surgery, chemorads, glucocorticoids

18
Q

what is secondary HyperPTH

Most common etiologies

Complications –

A

Parathyroid glands are reacting to something else such as low Calcium or Excess Phosphorous

etiologies –
CKD (most common); Hypercalcicuria, Vit D Deficiency

Bone Loss

19
Q

what is tertiary HyperPTH

A

§ 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

20
Q

main causes of hypoPTH

A

Post op (thyroidectomy, head and neck surgery)

Auto Immune

AD CASR Mutaiton which perceives high levels of calcium

Digeorge Syndrome

21
Q

requirements for dx of hypoPTH

A

□ Low PTH (Or inappropriately normal)

□ Low serum Ca

High Phosphorous

22
Q

Hallmark and other symptoms of Hypocalcemia

A

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

23
Q

Two bedside signs for hypocalcemia

A

Chvostek Sign – tap along facial nerve –> ipsilateral twitch

Trousseau Sign – BP cuff –carpal spasm

24
Q

what is Pseudo-Hypoparathyroidism

A

Rare resistance to PTH (eg at the level of the kidey)

aka Albright’s Hereditary Osteodystrophy

25
Q

pseudohypoparathyroid

labs
clinical features
genetics

A

® Low Serum Ca
® Elevated PO4
® Elevated PTH

® Short stature, short 4-5th metacarpals (seen also in Turner’s)
® Wide space nipples, mental retardation

Autosomal Dominant

26
Q

Etiologies of Vit D Deficiency

A

Low Sun
Fat Malabsorption (IBD pts)
Anticonvusalnts (increased Vit D metabolism)
Obesity – Vit D is sequestered in Fat

27
Q

manifestation of severe vit D deficinecy in adults vs children

A

Adults – bone pain, fractures

Childhood – Rickets,

28
Q

2 forms of Hereditary Vit D Resistance

A

HVDDR Type 1 – alpha 1 hydroxylase deficiency/mutation

HVDDR Type 2 – due to mutation in Vit D receptor

29
Q

name 2 monogenic Developmental bone disorders

what are the respective mutations?

A

Osteoporosis Pseudoganglioma Syndrome – LRP5 (Wnt Activator)

Osteogeneiss Imperfecta –
(Type 1 collagen)

30
Q

Risk factors for osteoporosis

A

older age, female, fam hx, whites and asians, low body weight, smoking, alcohol, hypogonadism, inactivity, low calcium

31
Q

A patient has is found to have a fragility fracture, but a T score WNL, does this patient has osteoporosis

describe how the dx of osteoporosis is made

A

yes – Diagnosis can be made by presence of fragility fracture (hip or spine compressure fracture)

vs DEXA scan 
T Scores (
32
Q

what drugs and therapies are used to treat osteoporosis

A

Bisphosphonates (staibilizes)

Denosumab (RANK Ligand Inhibitor)

SERM (Raloxifene) (estrogen agonist activity on bone)

Teriparatide PTH (activates osteoblasts in the breif, acute setting)

Calcium
Vit D
Exercise

33
Q

what is Paget’s Disease of the Bone –

genetics?
pathophys?
where does it most commonly occur?

Treatmnet?

A

AD

Increased rate of bone turnover
but in focal regions

axial skeleton

34
Q

Lab markers for increased bone foraiton and turnove

A

ALP and N telopeptide

35
Q

Pathognominc X ray finding for paget’s bone disease?

A

Picture frame sign of the vertebrae

36
Q

Symptoms of paget’s bone disease ?

Treatment?

Who is treated?

A

Symptoms – bone pain and neurologic symptoms; warmth over bone; neurologic features

ALL patients are treated; even if asymptomatic (bc its progressive)

Treatment – Bisphosphonates
symptomatic management

37
Q

what is renal oseotodystrophy; what is the classic radiological findng of the skull?

A

CKD –> poor response to PTH –> continual PTH secretion –> bone disease

Radiology: Salt and pepper of the skull