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VET 410: Endocrinology > Parathyroid Physiology > Flashcards

Parathyroid Physiology Flashcards

1
Q

what form is the majority of body calcium in

A

stored in bone as Ca-P complexes

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2
Q

what the measurable form of calcium

A

extracellular

50% ionized, 50% protein or mineral bound

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3
Q

functions of calcium

A
  1. structural: stored in bone to provide integrity to skeleton and teeth, protect organs, house hematopoietic cells, and Ca reservoir
  2. functional: cell signaling, muscle contraction, nerve conduction, hormone secretion, coagulation
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4
Q

what form is the majority of body phosphorus in

A

bone

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5
Q

functions of phosphorus

A
  1. structural: skeletal integrity, nucleic acids, phospholipids/membranes
  2. functional: enzyme cofactor, energy transfer (ATP to ADP), intracellular processes
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6
Q

what hormones are responsible for Ca and P maintenance in the body

A

protein/peptides: PTH, calcitonin, FGF-23

steroids: vitamin D3

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7
Q

what secretes PTH

A

chief cells in the parathyroid gland

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8
Q

what stimulates PTH secretion

A

low ionized Ca

NOT under pituitary control

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9
Q

effect of magnesium on PTH

A

cofactor - if Mg is low, PTH will not function as well leading to low Ca

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10
Q

what inhibits PTH secretion

A
  • high Ca
  • high FGF-23
  • high calcitriol
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11
Q

how do chief cells detect Ca concentration

A

CaSR (Ca sensing receptor)

Ca binding to receptor will inhibit PTH secretion

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12
Q

is the half life of PTH short or long

A

short

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13
Q

net effects of PTH

A

increase Ca
decrease P

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14
Q

direct effects of PTH

A

kidney: stimulate Ca reabsorption and P excretion in tubules

bone: stimulate Ca and P reabsorption from bone

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15
Q

indirect effects of PTH

A

indirect effect on the gut

stimulates 1-a-hydroxylase in the kidneys to convert inactive vitamin D3 –> calcitriol to increase gut absorption of Ca and P

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16
Q

effect of calcitriol

A

stimulates dietary Ca and P absorption from the GI lumen

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17
Q

how is calcitriol produced in carnivores

A

dietary vitamin D3 (required in carnivores, do not produce in skin) –> liver –> gets converted to calcidiol –> kidneys –> gets converted to calcitriol

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18
Q

what secretes calcitonin

A

parafollicular / C cells located between the follicles in the thyroid

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19
Q

what stimulates calcitonin secretion

A

high ionized Ca

20
Q

effects of calcitonin

A

decreases Ca

bone: decreases osteoclast activity (dec. Ca/P reabsorption from bone)

kidneys: minor increase in Ca excretion

21
Q

what secretes FGF-23

A

osteocytes in bone

22
Q

what stimulates FGF-23 secretion

A
  • high P
  • high calcitriol
  • high PTH
23
Q

effects of FGF-23

A

decrease phosphorus

kidneys: increases excretion of P
GI: inhibits 1-a-hydroxylase in the kidneys to decrease calcitriol –> dec. Ca/P absorption from gut

24
Q

what secretes PTHrp

A

certain neoplasms; leads to humoral hypercalcemia of malignancy (HHM)

25
Q

effects of PTHrp

A

increase Ca
decrease P

uses the same direct/indirect mechanisms as PTH

26
Q

ddx for hypercalcemia

A

H: hyperparathyroidism
O: osteolytic
G: granulomatous (fungal)
S: spurious - lab error
I: idiopathic
N: neoplastic & nutritional
Y: young
A: Addison’s disease
R: renal disease - increases total calcium NOT ionized
D: vitamin D toxicity

27
Q

ddx for hypocalcemia

A

P: primary hypoparathyroidism
E: eclampsia/“Milk Fever”
P: pancreatitis
E: ethylene glycol toxicity
R: renal disease - decreases ionized calcium NOT total
N: nutritional/GI malabsorption
I: iatrogenic - diuretics
S: spurious
H: hypoalbuminemia - decreases total calcium NOT ionized

28
Q

what species is primary hyperparathyroidism common in

A

older dogs

29
Q

what clinical signs are associated with primary hyperparathyroidism

A

often incidental

PU/PD, uroliths, lethargy, GI signs

30
Q

what is seen on lab work for primary hyperparathyroidism

A
  • high Ca
  • low/normal phosphorus
  • high/inappropriately normal PTH (should be 0)
31
Q

treatment for primary hyperparathyroidism

A

parathyroidectomy
heat albation

32
Q

what are the causes of hyperparathyroidism

A
  1. primary
  2. secondary nutritional
  3. secondary renal
  4. humoral hypercalcemia of malignancy
33
Q

primary hyperparathyroidism

A

functional parathyroid adenoma thats secretes excess PTH

34
Q

what lesion is associated with primary hyperparathyroidism

A

one enlarged PTG
rest atrophied PTGs

35
Q

secondary renal hyperparathyroidism

A

chronic kidney disease –> decreased P excretion and vitamin D3 activation –> high P and low calcitriol –> hypocalcemia –> stimulates PTH

PTH gets stimulated by low Ca levels, but renal failure prevents PTH from increasing calcium, so PTH continues to get secreted

36
Q

what lesion is associated with secondary renal hyperparathyroidism

A

all PTGs enlarged

37
Q

secondary nutritional hyperparathyroidism

A

low dietary Ca, vitamin D3, or high phosphorus leads to overstimulation of PTH

38
Q

what lesion is associated with secondary nutritional hyperparathyroidism

A

all PTGs enlarged

39
Q

primary hypoparathyroidism

A

low levels of PTH

40
Q

what species is primary hypoparathyroidism common in

A

middle aged dogs > cats

esp poodles

41
Q

what causes primary hypoparathyroidism

A

parathyroid atrophy

42
Q

clinical signs of primary hypoparathyroidism

A
  • muscle twitching (tetany, paresis)
  • weakness
  • facial pruritus
  • restlessness
43
Q

what labs are seen with primary hypoparathyroidism

A
  • severely low Ca
  • high/normal P
  • low PTH
44
Q

treatment for primary hypoparathyroidism

A

calcitriol
Ca supplementation

45
Q

metastatic mineralization

A

mineralization of the tissues (especially kidneys) when Ca/P is out of balance

46
Q

when does metastatic mineralization occur

A

when [Ca] x [P] > 60-80 mg/dL

47
Q

what parathyroid lesion spares tissue mineralization

A

primary hyperparathyroidism

decreases phosphorus despite increasing calcium

VET 410: Endocrinology (14 decks)

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