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Boards: AcidBase/Fluids/Electrolytes > Parathyroid/VitaminD/Calcium/P/Homeostasis > Flashcards

Parathyroid/VitaminD/Calcium/P/Homeostasis Flashcards

1
Q

How does calcium stabilize nerve cell membranes?

A

decreases membrane Na permeability

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2
Q

Name 5 things, calcium can complex with

A

Phosphate
Citrate
Bicarbonate
oxalate
lacvtate

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3
Q

Where is PTH synthesized and secreted?

A

Parathyroid gland
chief cells

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4
Q

What are the triggers for PTH synthesis?

A

low Ca
low calcitriol

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5
Q

What inhibits PTH synthesis?

A

Calcitriol
high Calcium

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6
Q

How does PTH increase calcium levels

A
  • Increases renal reabsorption
  • osteoclast activity bones
  • icreases active vitamin D levels - so indirectly increaes GI absorption
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7
Q

What type of vitamin D is ingested and where is it metabolized and activated (name the forms of VitD for each step)

A

Cholecalciferol
–> hydroxylated in the liver –> 25(OH)D3 (calcidiol)

–> hydroxylated in proximal tubular cells –> 1,25(OH)2D3 (calcitriol)

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8
Q

What is the enzyme activating vitamin D? What increases or decreases its activity?

A

1-alpha-hydroxylase

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9
Q

Where is calcitonin synthesized, how is the synthesis triggered, and what are its effects?

A

thyroid gland - parafollicular C cells

triggered by: hypercalcemia or calcium rich meal

main action: inhibits osteoclastic bone resorption
also: reduces renal tubular reabsorption of calcium

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10
Q

How does the pH of blood affect the calcium measurements?

A

iCa will be higher in acidemia and lower with alkalemia

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11
Q

How are hypercalcemia and hypocalcemia typically over/underestimated in dogs and cats if just using tCa?

A

Cats
* hypercalcemia underestimated
* hypocalcemia overestimate
* i.e., predicted lower than it is

Dogs
* opposite
* prediction higher than it is

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12
Q

List differentials for hypercalcemia

A

D Vitamin toxicity/ Drug related
Renal failure
Addison’s disease
Granulomateous disease
Osteolytic disease
Nutritional

Spurrious
Hyperparathyroidism
Idiopathic
Tumor

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13
Q

What are ECG findigns observed with hypercalcemia

A
  • QT shortening
  • PR prolongation
  • widened QRS
  • widened T wave
  • short of absent St segment
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14
Q

List 7 treatments for hypercalcemia and their mechanism of action

A
  • fluid administration, NaCl - calciuresis - Na competes for renal tubular calcium reabsorption
  • Furosemide - increases urinary calcium loss
  • glucocorticoids - reduced bone resorption, decreased intestinal absorption, increased renal excretion
  • Calcitonin - decreaes osteoclast activity and formation
  • Na-bicarbonate - crisis therapy - decreases iCa fraction
  • Dialsis - hemodialysis or peritoneal
  • Bisphosphate - decreased osteoclastic activity
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15
Q

Define the criteria for hypercalcemic crisis

A
  • elevated calcium iCa > 1.75 -1.88
  • acute encephalopathy
  • acute decline in renal function
  • cardiac arrhythmias
  • seizures
  • muscle twitching
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16
Q

What ECG changes are seen with hypocalcemia?

A
  • prolonged QT
  • prolonged ST segement
  • deep and wide T waves
  • AV block
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17
Q

What are the most likely causes for hypocalcemia if there is concurrent hyperphosphatemia

A
  • renal dysfunction
  • pancreatitis
  • excessive phosphate intake
  • primary hypoparathyroidism
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18
Q

List causes for hypocalcemia

A
  • AKI or CKD
  • EG toxicity
  • Phosphate enema or rapid IV phosphate infusion
  • Hypoalbuminemia
  • Pancreatitis
  • Soft tissue trauma, rhabdomyolysis, tumor lysis syndrome
  • Hypoparathyroidism
  • Bicarbonate administration
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19
Q

List 3 functions of calcium

A
  • skeletal and smooth muscle contraction
  • blood clotting
  • transmission of nerve impulses
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20
Q

What are the three forms of plasma calcium and how do their fractions compare?

A

iCa - 55%
Complexed (10%)
Bound with plasma proteins (35%)

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21
Q

Why does hypocalcemia cause nervous system hyperexcitatbility?

A

lowers threshold potential -> more negative and closer to resting membrane potential -> nerves and muscles more excitable

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22
Q

What complication occurs once total plasma Ca cc rises above 17 mg/dl?

A

Calcium-phosphate crystals are likely to precipitate

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23
Q

What percentage of the filtered Ca is normally reabsorbed by the kidneys?

A

99%

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24
Q

Where is the kidneys are what percentages of Ca reabsorbed. Which part is more important for Ca homeostasis?

A

90% - proximal tubules, loops of Henle, early distal tubules

10% - late distal tubules, early collecting ducts - more variable here, adjusted to needs

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25
Q

What is the most abundant form of Ca in the body, why is this molecule not encountered in other tissues than the bone?

A

Bone&raquo_space; hydroxyapatite

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26
Q

How does PTH cause bone resporption. What is the most important signaling molecule in this pathway?

A

PTH binds to osteoblast receptors –> stimulates RANKL synthesis (also called osteoprotegerin)

RANKL binds preosteoclasts –> differentiate into mature osteoclasts –> bone resorption

27
Q

What is 25-hydrocholecalciferol converted to when PTH levels are low?

A

24,25-dihydrocholecalciferol

28
Q

Where in the cell are vitamin D receptors?

A

within the nuclei of target cells

29
Q

How does Vitamin D increase intestinal Calcium absorption

A
  • increases formation of calbindin (Ca-binding protein) in intestinal epithelial cells –> transports Ca into the cytoplasm
  • Ca exits basolateral membrane through facilitated diffusion
  • Calbindin stays for weeks after VitD removed - long lasting effect
30
Q

How do Vitamin D effects on the bone compare between small quantities and large quantities?

A

high quantities&raquo_space; bone resorption
small quantities&raquo_space; bone calcifications

31
Q

What are the two direct effects of PTH on phosphate and which one overrides the other?

A
  • increased renal phosphate excretion
  • increased phosphate absorption (effect overriden by renal excretion)
32
Q

Describe and compare the rapid versus long-term phase of Ca/P mobilization from bone by PTH

A

Rapid
* activates already existing osteoclast cells
* activates the calcium pump - i.e., moves Ca from the bone fluid through the osteocytic membrane
* within minutes
* osteocyte osteoblast pump

Slow
* osteoclast activation through RANKL messanger via osteoblasts and osteocytes

33
Q

When PTH is increased, where in the nephron does it mostly affect Ca reabsorption

A
  • thick ascending loop of Henle (indirectly)
  • distal tubules (directly)
34
Q

Describe in detail how Ca suppressed further PTH synthesis/secretion

A

Ca –> bind to Calcium-sensing receptor (CSR) on parathyroid cell membranes
–> phospholipase C –> IP3 –> stimulates intracellular calcium release –> decreases PTH secretion

35
Q

Why is the effect of calcitonin short-lived?

A

decreased osteoclast activity will eventually cause lower osteoblast numbers

36
Q

What is the usual treatment for hypoparathyroidism?

A

Vitamin D administration
Calcium intake increase

37
Q

How does the calcium differ between primary and secondary hyperparathyroidism?

A

Primary - high Ca
Secondary - low Ca

38
Q

What are typical P levels (i.e., low, normal, or high) in primary hyperparathyroidism?

A

low

39
Q

What are the two main forms of P in the body and how are their ratios affects by the blood’s pH?

A

HPO4– (most)

H2PO4-

if plasma becomes more acidic –> more H2PO4-

40
Q

What triggers and what inhibits VitD activation/synthesis?

A

increases:
* decreased P or Ca
* decreased calcitriol
* PTH
* calcitonin

inhibits:
* increased P or Ca
* increased calcitriol
* FGF-23

41
Q

What are the effects of calcitriol?

A
  • increased intestinal Ca and P absorption
  • promotes bone formation and mineralization
  • osteoclast differentiation - bone resorption
42
Q

What are the effects of FGF-23?

A
  • phosphaturic
  • supresses calcitriol and PTH synthesis
43
Q

What are the long versus short negative feedback loops for PTH synthesis?

A

long feedback loop
* low Ca –> PTH secretion –> calcitriol increase –> GI absorption –> [Ca++] increases –> inhibits further PTH secretion
* takes long because VitD first needs to insert Calbindin in enterocytes

short feedback loop
* calcitriol can bind to VDR on Parathyroid gland -> inhibits PTH gene transcritption
* faster

note: hypercalcemia cannot suppress PTH secretion in the absence of VitD

44
Q

What is the major circulating Vitamin D?

A

calcidiol (25-hydroxyvitamin D3)

45
Q

How is calcitriol metabolize and excreted?

A

24-hydroxylase

–> 24,25-dihydroxyvitaminD - inactive form

excreted mostly via bile (4% in urine)

46
Q

Explain the pathophysiology of secondary hyperparathyroidism in renal disease

A
  • renal tubular cell dysfunction&raquo_space; less 1-alpha-hydroxylase activity&raquo_space; low calcitriol&raquo_space; lack of negative feedback on chief cell PTH synthesis and secretion&raquo_space; glandular parathyroid hyperplasia
  • impaired P excretion&raquo_space; high serum [P]&raquo_space; suppresses calcitriol synthesis and stimulates PTH secretion
  • very high serum [P]&raquo_space; reduces iCa by mass law effect
47
Q

How deos the iCa measurement between whole blood (e.g., heparinized blood gas sample) or serum/plasma differ?

A

whole blood sample underestimates iCa

48
Q

Which fraction of Calcium increases in CRF?

A

complexed Ca

more citrates, phosphates, lactates, bicarbonates, oxalates available

49
Q

How does granulomateous disease cause hypercalcemia?

A

macrophages can express 1-alpha-hydroxylase and will activate vitamin D/calcitriol

50
Q

What is the most common cause for hypercalcemia in dogs versus cat?

A

dogs - neoplasia

cats - idiopathic

51
Q

Which diuretic can actually worsen hypercalcemia?

A

thiazide diuretics - can inhibit calciuresis

52
Q

What are the functions of P?

A
  • production of ATP, ADP, cAMP, GTP, cGMP, phosphocreatine
  • normal bone and teeth matrix
  • 2,3-Diphosphoglycerate&raquo_space; regulation of oxygenation
  • cellular membrane structure (phospholipids)
  • buffer for acidosis
53
Q

Where in the body is most P?

A

80-85% bones - hydroxyapatite

  • 15% soft tissue
    only 1% in EC
54
Q

In what compartment (IC versus EC) is more organic versus inorganic P?

A
  • organic IC
    inorganic EC
55
Q

What are the different free, complexed, and protein phosphates and what are their proportions?

A
  • 85% free - either monohydrogen or dihydrogen phosphate (4:1)
  • 10% protein-bound
  • 5% complexed
56
Q

For dihydrogen and hydrogen phosphate, how do they act as buffers and how is their ratio affected by the body’s acid base status

A

dihydrogen phosphate - H+ donor

hydrogen phosphate - H+ acceptor&raquo_space; base

ratio of mono:dihydrogen 4:1
alkalosis&raquo_space; increaed ratio
acidosis&raquo_space; decreased ratio

57
Q

Where in the tubules is most P reabsorbed and how much of the filtered P is reabsorbed?

A

normally 60-90% reabsorbed

proximal convoluted tubules

58
Q

List hormones that increase or decrease P reabsorption in the kidneys

A

increase
* insulin
* growth hormone
* insulin-like growth factor 1

decrease
* PTH
* phosphatonins (e.g., FGF-23)

59
Q

What is considered severe hypophoshpatemia?

A

serum P < 1.0 mg/dL

60
Q

List differentials for hypophosphatemia from transcellular shift

A
  • alkalosis - increase in IC pH activates phosphofructokinase + glycolysis&raquo_space; P shifts into the cells
  • refeeding syndrome - stimulates insulin release&raquo_space; IC uptake of P in phase of total body depletion
  • insulin (+/- dextrose) adm in DKA, DM, HNS
  • cathecholamine release or administration
61
Q

List the clinical signs of hypophosphatemia

A

Related to ATP and 2,3-DPG depletion

  • RBC dysfunction and hemoylsis - spherocytes, red cell membrane rigidity
  • impaired Hb O2 release&raquo_space; tissue hypoxia
  • immunosuppression from leukocyte dysfunction
  • shortened PLT survival time
  • myocardial dysfunction
  • skeletal muscle weakenss, tremors, muscle pain, rhabdomyolysis
  • ataxia, seizures, coma
  • GI signs (nausea, vomiting, diarrhea, functional ileus)
62
Q

Why could a patient receiving parenteral P supplementation develop tetany?

A

hypocalcemia from complexes

63
Q

List differentials for hyperphosphatemia

A
  • Oversupplementation
  • tumor lysis syndrome, rhabdomyolysis, hemolysis
  • decreased renal excretion from AKI or CKD (most common cause)
  • Hypoparathyroidism
  • Hyperthyroidism
  • Vit D rodenticide
  • phosphate-containing enemas
  • young growing animal
  • urinary obstruction or uroabdomen
64
Q
A

Boards: AcidBase/Fluids/Electrolytes (13 decks)

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