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Bloc D - Renal > Jan11 M1-Divalent Cations > Flashcards

Jan11 M1-Divalent Cations Flashcards

1
Q

% body Ca in bone and % in ECF

A

99% in bone

0.1% in ECF

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2
Q

% phosphate in bone , in ICF and in ECF

A

85% bone, 15% ICF 1% ECF

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3
Q

Ca and PO4 in bone exist as ________

A

hydroxyapatite

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4
Q

2 factors in Ca homeostasis

A
  1. body Ca amount depends on balance of GI abso and kidney excretion
  2. distribution of Ca between bone and ECF (largely by PTH)
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5
Q

diff types of Ca in the body and % and which is sense by CaSR

A
  • protein bound 40%
  • ultrafilterable complexed to anions 10%
  • ultrafilterable ionized Ca 50% (sensed by CaSR)
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6
Q

stimulus for PTH secretion

A

low plasma ionized Ca sensed by CaSR

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7
Q

3 ways PTH raises Ca levels

A
  • Ca resorption from bone (PO4 resorption at the same time)
  • increased 1-alpha hydroxylase in the kidney leading to formation of calcitriol so more GI abso of Ca
  • more renal Ca reabso (acts on luminal Ca channel in DCT)
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8
Q

PTH effect on phosphate

A

resorption from bone with Ca resorption BUT promotes PO4 excretion in the kidney so overall lowers PO4 levels

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9
Q

primary hyperPTH def + Ca, PO4 and calcitriol levels

A

adenoma of one of 4 PT glands. hyperCa. hypoPO4. high calcitriol

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10
Q

secondary hyperPTH def + Ca, PO4 and calcitriol levels

A

renal failure led to hyperplasia of the 4 PT glands (bc of constant hyperPO4 and low calcitriol)
low Ca, high PO4, low calcitriol

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11
Q

tertiary hyperPTH def

A

dialysis over years led to prolonged secondary hyperPTH. PTH now released at all times

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12
Q

tertiary hyperPTH Ca, PO4 and calcitriol levels

A

Ca high, PO4 high, calcitriol low

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13
Q

what happens if you remove hyperPO4 and hypocalcitriol stimuli in secondary and tertiary hyperPTH

A

secondary: stop producing PTH
tertiary: keep producing PTH bc now autonomous

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14
Q

steps to produce active vit D (calcitriol)

A

diet or 7-dehydrocholesterol + UV light = vit D. 25-hydroxylation in liver. 1alpha hydroxylation in the kidney. get 1,25 vit D

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15
Q

main action of calcitriol

A

keep Ca and PO4 available for bone formation (and prevent hypoCa and hypoPO4)

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16
Q

2 stimuli to calcitriol production

A

high PTH

low phosphate

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17
Q

3 stimuli to PTH prod and which one is indirect and how

A
  • low Ca
  • high PO4 (indirect effect. no receptor for it but when high PO4, binds Ca so less Ca for the CaSRs)
  • low calcitriol
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18
Q

calcitriol sites of action (how does it increase Ca and PO4) and which thing does PTH not do

A
  1. Ca and PO4 abso in the intestine (PTH can’t do that)
  2. resorption from bone (with PTH)
  3. reabso at distal tubule (with PTH)
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19
Q

2 receptors on PT gland and consequence on PTH prod

A

CaSR: low Ca = more PTH

calcitriol receptor: high calcitriol = less PTH prod

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20
Q

how hyperPO4 causes increased PTH

A

PO4 binds Ca so less Ca for CaSRs

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21
Q

if low PO4 stimulates calcitriol,

how hyperPO4 acts to inhibit it

A

hyperPO4 impairs 1 alpha hydroxylation

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22
Q

calcitonin exact site of prod + type of molecule

A

peptide hormone. C cells of the thyroid gland

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23
Q

calcitonin: stimulus for its release and what it does

A

high Ca.

calcitonin inhibits Ca resorption form bone (opposite of PTH)

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24
Q

Ca in the nephron in %

A

65% PCT
25% loop (TAL)
8% DCT
less 1% excrtion

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25
Q

Ca in PCT

A

passive reabsorption with favorable electrochem gradient

26
Q

Ca in the loop of Henle

A

moves down electrochem gradient in tight junctions. favorable gradient bc lumen is positive bc K+ keeps being pumped out by ROMK even though Na-K-2Cl is pumping K in

27
Q

where CaSR found other than PTH + fct

A

cells of TAL. if senses high Ca (in the blood), inhibits ROMK, Na-K-2Cl and impairs paracellular (tight junctions) reabso of Ca

28
Q

condition where CaSR not working where + pathophgy

A

familial hypocalciuric hypercalcemia. CaSR not working so always reabso of Ca in TAL + need higher Ca to suppress PTH

29
Q

where is Ca reabso hormonally regulated and how

A

in DCT. decreases Ca excretion. (PTH and calcitriol)

30
Q

only part of the nephron where Na and Ca are not coupled

A

DCT

31
Q

why can become hyperCa when on thiazides

A

cause volume contraction so more Na and Ca reabso ‘‘together’’ proximally

32
Q

how acid base balance influences Ca levels

A

acidosis increases Ca excretion (bc mobilizes it from bone. bone buffers H+)
alkalosis decreases Ca excretion

33
Q

common causes of hyperK

A
  • primary hyperPTH
  • excess 1,25 D prod
  • excess Ca ingestion (or vit D)
  • malignancy
  • thiazides
  • familial hypocalciuric hypercalcemia
34
Q

if see lab of high Ca, low PO4 and normal Cr, what’s the likely dx

A

primary hyperPTH

35
Q

if see lab of high Ca, Cr of 200, high PO4, normal PTH, + history of weight loss*** what’s the likely dx

A

malignancy involving bones

36
Q

4 symptoms of hypercalcemia

A
  • confusion, lethargy
  • bone pain
  • kidney stones
  • poor appetite, nausea, vomiting, abdominal pain
37
Q

normal response to hyperCa (4)

A
  • less PTH
  • less calcitriol (via less PTH)
  • CaSR stimulation in kidney so less Ca reabso
  • more calcitonin
38
Q

causes of hypoCa

A
  • hypoPT
  • vit D deficiency
  • low Mg (Mg important for PTH release)
  • CKD (high phosphate and low calcitriol)
39
Q

symptoms of hypoCa

A
  • neuromuscular irritability
  • seizures
  • arrhythmias
40
Q

normal response to hypoCa (3)

A
  • more PTH
  • more calcitriol (via more PTH)
  • less CaSR stim in TAL so more paracellular reabso of Ca
41
Q

what % of phosphate is protein bound

A

10%

42
Q

2 factors in phosphate homeostasis and hormones acting on that

A
  1. balance of PO4 abso (GI) and excretion by kidneys (PTH)

2. distribution between ECF and ICF (PTH and calcitriol)

43
Q

PO4 in PCT (% and mechanism) and what % in what parts of PCT

A

85% reabso in PCT (15% in more distal part of PCT/in TDL)

Na-PO4 cotransporter

44
Q

3 factors regulating PO4 transport in the kidney

A
  • plasma PO4
  • PTH
  • FGF-23
45
Q

how plasma PO4 regulates PO4 reabso

A

more PO4 filtered = less Na-PO4 cotransporter activity

46
Q

how PTH regulates PO4 reabso

A

high PO4 leads to low Ca and low calcitriol. PTH is produced and PTH reduces the Na-PO4 cotransporter activity

47
Q

Ca, PO4, calcitriol and PTH in CKD

A

high PO4, low calcitriol, high PTH, low Ca

48
Q

causes of hyperPO4 with main one

A

renal failure**, rhabdomyolysis or lysis after chemo, hypoPTH

49
Q

normal response to hyperPO4

A
  • more PTH (so more excretion in PCT) (direct downregulation of Na-PO4 cotransporteR)
  • less calcitriol (less GI abso and bone resoprtion)
50
Q

causes of hypoPO4 and main one

A

primary hyperPTH, Fanconi syndrome, GI loss** (typically), beta adrenergic stimulus causing ECF to ICF shift

51
Q

Fanconi syndrome 2 types and def

A

congenital or acquired. patient has PCT dysfct (a.a, glucose, PO4, etc. waisted in urine)

52
Q

normal response to hypoPO4

A

more calcitriol (more GI abso and bone resorption), less PTH (so more reabso).

53
Q

Mg distribution in the body

A

60% bone
35% ICF and muscles
1% ECF

54
Q

% Mg protein bound vs free

A

30% protein bound 70% free

55
Q

renal handling of Mg (%)

A

30% PCT 60% TAL 5% DCT

56
Q

main determinant of renal Mg excretion

A

plasma Mg concentration

57
Q

Mg in the TAL

A

(same as Ca). favorable electrochem gradient bc positive lumen bc K keeps going back in lumen so Ca moves in in tight junction

58
Q

in what condition can Mg bind to CaSR and how would that be useful

A

in hyperMg. would stop the electrochem gradient (same as in hyperCa) so Mg would stay in tubule

59
Q

Mg in the distal tubule (% and mechanism: give exact channel name)

A

5% reabso in DCT. active transport via the TRPM6 channel. (meds can act on that)

60
Q

causes of low plasma Mg

A

GI losses, renal losses (diuretics, diabetes, drugs that block Mg reabso in TAL or DT)

61
Q

why diabetes associated with hypoMg (1/3 diabetes have it)

A

we don’t know

62
Q

what more important condition (electrolytes) associated with hypoMg

A

hypoCa (bc often cause of hypoMg will also cause hypoCa)

Bloc D - Renal (32 decks)

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