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Endo > Ca-Po4 > Flashcards

Ca-Po4 Flashcards

1
Q

the journey of Vit D that’s absorbed

A

A) skin 80% - makes it colecalciferol (D3)
B) dietary <20% (D2, ergocalciferol)
- both go to liver - stores it as 25-OH (=calcidiol) via 25 hydroxylase!
- kidney hydrolyses 25-OH > 1,25-OH (=cantriol) via ONE alpha hydroxylase!

Action on 1,25-OH:
1) bones: resorption
2) kidneys: less Ca/PO4 excretion
3) intestines: absorb Ca

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2
Q

when to use 25-OH vs 1,25-OH Vit D tests

A

25-OH reflection of stores
1,25-OH = active Vit D, tests renal disease

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3
Q

Ca regulation in body e.g. low Ca

A

low Ca > inc PTH:
1) bones: resoprtion in MINUTES
2) kidneys: inc Ca abs, decr PO4 abs, inc 1,25-OH creation in DAYS
3) gut: inc Ca and PO4 abs in MINUTES

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4
Q

what does pH do to Ca?

A

alkalosis increases anionic binding sites, so inc Ca binding, reducing ionised Ca

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5
Q

Ca vs PO4 absorption by gut

A

Ca poorly absorbed by GIT - only 20-30%

PO4 easily absorbed

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6
Q

Stimuli for increased vs decreased PTH release

A

Inc PTH: dec CALCIUM, and INC phos
Dec PTH: inc Calcium, and calcitriol

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7
Q

overall action of the following on Ca and PO4:
1. PTH
2. Vit D
3. Calcitonin

A
  1. PTH: inc Ca, reduces PO4
  2. Vit D: inc Ca, INC PO4
  3. calcitonin: reduces Ca, reduces PO4
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8
Q

PTH action in kidneys: where??

A

inc Ca abs from DCT!
INHIBITS PO4 abs PCT!

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9
Q

how do glucocorticoids cause osteoporosis?

A
  1. bones: increase resorption, inhibit osteoblasts
  2. gut: less Ca absorption
  3. kidney: decreased Ca absorption
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10
Q

what are some clinical exam signs for spasm with hypoCa?

A
  1. Trousseau’s sign = carpal spasm from inflated BP cuff for 3-5mins >15mmHg above SBP
  2. Chovstek’s sign = facial spasm from tapping facial nerve in front of ear
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11
Q

why do we correct calcium?

A

for albumin, as Ca binds to it
= Ca total + (40-alb) x 0.02

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12
Q

neonatal hypocalcaemia - causes

A

early hypoCa (D2-3):
- prematurity
- FGR
- GDM
- hypoPTH or maternal hyPERPTH
- hypoMg (–> less and resistance to PTH)

late hypoCa (D7):
- hypoPTH
- PTH resistance
- high PO4 intake (cow’s milk)
- hypoMg
- mat Vit D deficiency
- DiGeorge

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13
Q

familial hypocalcaemia - key features

A
  • AD (gain of function) mutation of CaSR > change in set point for PTH release
  • low Ca
  • normal/low PTH
  • high Ca urinary excretion (rather than expected low excretion!)
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14
Q

APECED - key features

A
  • AR mutation in AIRE
  • candidiasis, hypoPTH, addison’s (late)
  • and alopecia, malabsorption, vitiligo, T1DM etc
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15
Q

causes of high PTH

A
  1. vit D deficiency (diet/skin/malabs)
  2. abnormal Vit D metabolism (liver, kidneys, or genetic)
  3. pseudohypoparathyroidism
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16
Q

types of genetic Vit D abnormal metabolism

A

1-alpha hydroxylase deficiency = VDDR type 1. Can’t produce 1,25-OH Vit D

Hereditary resistance to vitamin D (HRVD) = VDDR type 2. Vit D receptor sucks, so 1,25-OH is actually high.

17
Q

pseudohypoparathyroidism - key features

A

end organ resistance to PTH:
1. hypocalcaemia
2. hyperphosphataemia
3. elevated PTH

18
Q

what is the most common type of pseudohypoparathyroidism? key features.

A

type 1a = albright hereditary osteodystrophy:
- AD GNAS1 MATERNAL mutation > Gs protein cannot signal > PTH receptor cannot couple cAMP
- short stature, short 4th 5th digits, obese and round face, and other hypoCa signs
- also get other end organ resistance: PTH > TSH > LH/FSH, GHRH

19
Q

what is pseudo-pseudohypoparathyroidism?!

A

subtype of albright osteodystrophy
gene is PATERNAL
no PTH resistance - normal PTH and Ca

20
Q

Mg and Ca relationship

A

hypoMg causes:
1) PTH resistance
2) reduced PTH
3) less 1,25 vit D

all of which > hypoCa
hypoMg could be congenital absorption problem (will respond to Mg supps), but if acquired/renal, then won’t work

21
Q

FRACP: syndrome for hyper vs hypoCa

A

hyperCa = Williams
hypoCa = DiGeorge

22
Q

hypercalcaemia symptoms / signs

A

stones, bones, groans, abdo groans (n,v, pancreatitis), and psychic moans
… and short QT

23
Q

how to treat hypercalcaemia

A

if really bad >3.5: HYDRATE +/0 diuretics

long term: low Ca diet, steroids and bisphosphonates (peak in a week)

24
Q

neonatal hypercalcaemia - what could be causing it?

A
  1. neonatal hyperPTH 13q13
  2. transient hyperPTH
  3. Williams
  4. fat necrosis! esp after delivery trauma
  5. familial hypocalciuric hypercalcaemia (FHH)
25
Q

outside of neonatal period, causes of hypercalciuria (think pathophys)

A
  1. inc vit D - Vit D toxicity (granulomatous disease!!), Williams
  2. inc PTH - hyperPTH, adenoma, MEN
  3. inc bone turnover - immbolisation
  4. malignancy
26
Q

hyperPTH - MEN1 or 2?

A

MEN1 90%, less common in MEN2 which is more malignant driven

27
Q

what is the problem in familial hypocalciuric hypercalcaemia?

A

AD INACTIVATVING mutation in Ca sensing receptor > change in set point: high Ca, normal PTH

28
Q

biggest risk factor for neonatal vit d deficiency?

A

maternal vit D def! foetal levels come from placenta, and last for 3mo. premmies bad bc less time to accumulate levels

29
Q

ways you can get low Vit D

A
  1. not enough in e.g. diet, prem, BF, skin type, sun
  2. can’t get it in e.g. malabs, CF
  3. can’t make it right - genetic disorders
  4. can’t recognise it
  5. meds - steroids!
30
Q

normal vit D minimum level?

A

50nmol/L

31
Q

when to give vit D in asymptomatic neonate?

A

exclusively breastfed + one other risk factor (no sun, skin, medical conditions) > 400IU daily until 12mo

32
Q

rickets vs osteomalacia

A

Rickets = deficient mineralisation at the growth plate i.e. only in growing bones!

Osteomalacia = impaired mineralisation of the bone matrix

33
Q

signs/symptoms of rickets

A
  • head: delayed fontanelle clousre, frontal bossing, craniotabes
  • delayed dentition
  • rachitic rosary
  • initially manifest bone pain: distal forearm, knee > #
  • radiologcal fraying, cupping, widening of growth plate
  • genu varum (bowed legs in toddler)
  • If hypocalcaemic > Sx
  • if phosphopenic > dental abscess
34
Q

best biochem marker of rickets

A

ALP

35
Q

Ca, PO4 and PTH levels in hypoCa vs hypoPO4 rickets

A
  • PO4 = ↓ calcipenic ↓ phosphopenic
  • Ca = ↓ or N in calcipenic, usually N in phosphopenic
  • PTH = usually ↑ calcipenic rickets, N or mildly ↑in phosphopenic
36
Q

most common pathophys of phosphopenia?

A

renal wasting - thinkg e.g. fanconi, distal RTA

37
Q

where will you find the calcium sensing receptors?

A

parathyroid chief cells, renal tubular cells, c-cells of thyroid

Endo (8 decks)

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