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

Parathyroid/VitaminD/Calcium/P/Homeostasis Flashcards

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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
What is the most abundant form of Ca in the body, why is this molecule not encountered in other tissues than the bone?
Bone >> hydroxyapatite
26
How does PTH cause bone resporption. What is the most important signaling molecule in this pathway?
PTH binds to osteoblast receptors --> stimulates RANKL synthesis (also called osteoprotegerin) RANKL binds preosteoclasts --> differentiate into mature osteoclasts --> bone resorption
27
What is 25-hydrocholecalciferol converted to when PTH levels are low?
24,25-dihydrocholecalciferol
28
Where in the cell are vitamin D receptors?
within the nuclei of target cells
29
How does Vitamin D increase intestinal Calcium absorption
* 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
How do Vitamin D effects on the bone compare between small quantities and large quantities?
high quantities >> bone resorption small quantities >> bone calcifications
31
What are the two direct effects of PTH on phosphate and which one overrides the other?
* increased renal phosphate excretion * increased phosphate absorption (effect overriden by renal excretion)
32
Describe and compare the rapid versus long-term phase of Ca/P mobilization from bone by PTH
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
When PTH is increased, where in the nephron does it mostly affect Ca reabsorption
* thick ascending loop of Henle (indirectly) * distal tubules (directly)
34
Describe in detail how Ca suppressed further PTH synthesis/secretion
Ca --> bind to Calcium-sensing receptor (CSR) on parathyroid cell membranes --> phospholipase C --> IP3 --> stimulates intracellular calcium release --> decreases PTH secretion
35
Why is the effect of calcitonin short-lived?
decreased osteoclast activity will eventually cause lower osteoblast numbers
36
What is the usual treatment for hypoparathyroidism?
Vitamin D administration Calcium intake increase
37
How does the calcium differ between primary and secondary hyperparathyroidism?
Primary - high Ca Secondary - low Ca
38
What are typical P levels (i.e., low, normal, or high) in primary hyperparathyroidism?
low
39
What are the two main forms of P in the body and how are their ratios affects by the blood's pH?
HPO4-- (most) H2PO4- if plasma becomes more acidic --> more H2PO4-
40
What triggers and what inhibits VitD activation/synthesis?
increases: * decreased P or Ca * decreased calcitriol * PTH * calcitonin inhibits: * increased P or Ca * increased calcitriol * FGF-23
41
What are the effects of calcitriol?
* increased intestinal Ca and P absorption * promotes bone formation and mineralization * osteoclast differentiation - bone resorption
42
What are the effects of FGF-23?
* phosphaturic * supresses calcitriol and PTH synthesis
43
What are the long versus short negative feedback loops for PTH synthesis?
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
What is the major circulating Vitamin D?
calcidiol (25-hydroxyvitamin D3)
45
How is calcitriol metabolize and excreted?
24-hydroxylase --> 24,25-dihydroxyvitaminD - inactive form excreted mostly via bile (4% in urine)
46
Explain the pathophysiology of secondary hyperparathyroidism in renal disease
* renal tubular cell dysfunction >> less 1-alpha-hydroxylase activity >> low calcitriol >> lack of negative feedback on chief cell PTH synthesis and secretion >> glandular parathyroid hyperplasia * impaired P excretion >> high serum [P] >> suppresses calcitriol synthesis and stimulates PTH secretion * very high serum [P] >> reduces iCa by mass law effect
47
How deos the iCa measurement between whole blood (e.g., heparinized blood gas sample) or serum/plasma differ?
whole blood sample underestimates iCa
48
Which fraction of Calcium increases in CRF?
complexed Ca more citrates, phosphates, lactates, bicarbonates, oxalates available
49
How does granulomateous disease cause hypercalcemia?
macrophages can express 1-alpha-hydroxylase and will activate vitamin D/calcitriol
50
What is the most common cause for hypercalcemia in dogs versus cat?
dogs - neoplasia cats - idiopathic
51
Which diuretic can actually worsen hypercalcemia?
thiazide diuretics - can inhibit calciuresis
52
What are the functions of P?
* production of ATP, ADP, cAMP, GTP, cGMP, phosphocreatine * normal bone and teeth matrix * 2,3-Diphosphoglycerate >> regulation of oxygenation * cellular membrane structure (phospholipids) * buffer for acidosis
53
Where in the body is most P?
80-85% bones - hydroxyapatite * 15% soft tissue only 1% in EC
54
In what compartment (IC versus EC) is more organic versus inorganic P?
* organic IC inorganic EC
55
What are the different free, complexed, and protein phosphates and what are their proportions?
* 85% free - either monohydrogen or dihydrogen phosphate (4:1) * 10% protein-bound * 5% complexed
56
For dihydrogen and hydrogen phosphate, how do they act as buffers and how is their ratio affected by the body's acid base status
dihydrogen phosphate - H+ donor hydrogen phosphate - H+ acceptor >> base ratio of mono:dihydrogen 4:1 alkalosis >> increaed ratio acidosis >> decreased ratio
57
Where in the tubules is most P reabsorbed and how much of the filtered P is reabsorbed?
normally 60-90% reabsorbed proximal convoluted tubules
58
List hormones that increase or decrease P reabsorption in the kidneys
increase * insulin * growth hormone * insulin-like growth factor 1 decrease * PTH * phosphatonins (e.g., FGF-23)
59
What is considered severe hypophoshpatemia?
serum P < 1.0 mg/dL
60
List differentials for hypophosphatemia from transcellular shift
* alkalosis - increase in IC pH activates phosphofructokinase + glycolysis >> P shifts into the cells * refeeding syndrome - stimulates insulin release >> IC uptake of P in phase of total body depletion * insulin (+/- dextrose) adm in DKA, DM, HNS * cathecholamine release or administration
61
List the clinical signs of hypophosphatemia
Related to ATP and 2,3-DPG depletion * RBC dysfunction and hemoylsis - spherocytes, red cell membrane rigidity * impaired Hb O2 release >> 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
Why could a patient receiving parenteral P supplementation develop tetany?
hypocalcemia from complexes
63
List differentials for hyperphosphatemia
* 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

Boards: AcidBase/Fluids/Electrolytes (13 decks)

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