Ca and Phosphate

Question 1

Ca fxn

Answer 1

99% structural in bone, 1% biochem w/EC coupling, etc

Must be maintained 8-10 mg/dl

Question 2

Phosphate fxn

Answer 2

Structural: bone
Biochem: buffer, phosphorylation rxns
Must be maintained 3-4 mg/dl

Question 3

FGF23

Answer 3

GF in kidney

Decreases serum level of P and inhibits Vit D

Question 4

Parathyroid H

Answer 4

increase plasma Ca (Gs) & decrease Phosphate
short term regulator
Bone: rapid effect of Ca from labile bone and slow release from remodeling, but low dose pusatile dose = formation

Question 5

PTH in Kidney and GI

Answer 5

Kidney: increased Ca resorption in distal tubule, decreased P resorb, increased active vit D
GI: indirect more Ca absorb through vit D (vit dep in duodenum)

Question 6

PTH secretion regulation

Answer 6

Normal/high Ca: Ca binds Gq = no signaling

Low Ca: not bound = signaling through receptor = secretion

Question 7

Calcitonin

Answer 7

Released by parafollicular C cells if high Ca or gastrin, CCK, secretin, or glucagon
Decreased efflux labile bone
Increase Ca acute storage

Question 8

Vit D

Answer 8

long term reg Ca and P stores - more synth Ca BP, RANK-L, down Ca & P excretion

Question 9

Vit D synth

Answer 9

1. 7-dehydrocholesterol in skin to Vit D3 by sunlight
2. in liver to 25-OH Vitamin D3
3. in kidney to 1,25 (OH)2 Vitamin D3 (active, aka calcitrol) by 1-hydroxylase
   Active broken down by 24-hydroxylase

Question 10

Ca absorb increased by

Answer 10

pregnancy, adolescence, lactose, gastric acid, dietary protein (more excreted though so net zero)

Question 11

Ca absorb decreased by

Answer 11

Vit D def, steatorrhea, oxalic acid, phytates, gastric alkalinity, increased Na intake

Question 12

RANK-L

Answer 12

expressed on osteoblasts & binds receptor on osteoclasts stimulating them

Question 13

OPG

Answer 13

Opposes RANK-L to inhibit osteoclasts

Question 14

Primary Hyperparathyroidism

Answer 14

85% adenoma, 15% hyperplasia
Familial AD
MEN 1 - mutation in menin
MEN 2A - ret gene
> 50% are asymptomatic
 “Bone, Stones, Groans, and
Moans”skeletal, kidney, GI, &
psychiatric, ban keratopathy
High Ca, PTH, Cl. Low P

Question 15

Hypercalcemia of Malignancy

Answer 15

Lung (esp squamous), breast, etc
Tumors release PTH related peptide
Decreased serum PTH
 Increased serum PTH-RP
 Low chloride/phosphate
ratio

Question 16

Secondary Hyperparathyroidism

Answer 16

Caused by low Ca, high P, or low Vit D

Question 17

Hypoproteinemia Ca

Answer 17

Correct Ca by adding .8 mg/dl for every 1g/L albumin

Question 18

Hypocalcemia Sx

Answer 18

Paresthesias
 Muscle cramps and weakness  Chvostek’s sign (facial nerve
spasm when tap facial nerve)
 Trousseau’s sign (hand spasm
with blood pressure cuff)

Question 19

Pseudohypoparathyroidism

Answer 19

Mutation of G subunit of PTH
Low Ca, high P, high PTH
Short 4/5th metacarpals
Tx: Ca, calcitriol, thiuzide diuretic

Question 20

Rickets & Osteomalacia

Answer 20

kids vs adults
Impaired bone mineralization = soft weak bones
Osteomalacia: pain (long bones) 
deformities, fractures
 Rickets: pain (long bones), bowing, muscle weakness, short statures, delayed epiphyseal calcification

Question 21

Osteoporosis

Answer 21

Fragility fracture is diagnostic
Less than -2.5 bone mineral density score
urine NTX/CTX (bone resorption marker), high serum alk phos (bone formation marker)

Question 22

Paget’s Disease

Answer 22

Idiopathic, excessive bone resorption/formation
Combo genetic (SQSTM1/P62 mut) & env (chronic paramyxovirus infection)
Pain, hypervascularity
Most in pelivis, skull, vertebrae, femur, tibia
Also Deafness, CN, Cv sx
‘blade of grass’ sign

Question 23

Paget Phases

Answer 23

1. Osteoclastic (high urine NTX/CTX -resorption marker)
2. High both (same + high alk phos)
3. Osteoblastic (low NTX/CTX & varible alk phos)