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Endocrine Pathophysiology > Pathophysiology of the Parathyroid Glands > Flashcards

Pathophysiology of the Parathyroid Glands Flashcards

1
Q

what cells secrete calcitonin?

A

parafollicular cells (C cells) in thyroid gland

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2
Q

calcitonin acts to ____________ calcium concentration

A

decrease

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3
Q

what hormone does calcitonin oppose?

A

parathyroid hormone

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4
Q

what are the general effects of parathyroid hormone?

A

increase calcium
decrease phosphorous

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5
Q

what hormone is the major regulator of calcium?

A

parathyroid hormone

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6
Q

who are parathyroid/Kursteiner’s cysts common in?

A

dogs
incidental finding

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7
Q

how common is primary hypoparathyroidism?

A

uncommon

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8
Q

what are the etiologies of primary hypoparathyroidism?

A

lymphocytic parathyroiditis
bilateral thyroidectomy
metastatic neoplasia
sepsis
idiopathic

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9
Q

what cytokines inhibit parathyroid hormone secretion?

A

IL-1
IL-6

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10
Q

is there a breed disposition to primary hypoparathyroidism?

A

no apparent

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11
Q

what are the clinical signs of primary hypoparathyroidism due to?

A

low extracellular (blood) calcium concentration

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12
Q

why does lack of calcium have neuromuscular effects?

A

calcium makes nerves less permeable to sodium
calcium is needed for release of acetylcholine

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13
Q

what are the laboratory findings for primary hypoparathyroidism?

A

low to undetectable iPTH
decreased total calcium and iCa: hypocalcemia
increased phosphorous: hyperphosphatemia

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14
Q

what is primary hyperparathyroidism caused by?

A

parathyroid tumor

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15
Q

what is the most common cause of primary hyperparathyroidism in dogs, cats, and horses?

A

parathyroid (chief cell) adenoma

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16
Q

what laboratory findings are associated with primary hyperparathyroidism?

A

within normal limits or increased iPTH
increased calcium and iCa
low to lower-end of RI phosphorous

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17
Q

true/false: the mass is usually not palpable with primary hyperparathyroidism

A

true

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18
Q

what do primary hyperparathyroidism patients get in the urinary tract?

A

calcium-containing uroliths: 30%
secondary urinary tract infections: 24%

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19
Q

when can we see nephrocalcinosis with primary hyperparathyroidism?

A

Ca>16 mg/dL

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20
Q

when can skeletal changes be seen with primary hyperparathyroidism?

A

chronic cases

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21
Q

what skeletal changes can be seen with chronic cases of primary hyperparathyroidism?

A

diffuse skeletal demineralization
pathologic fractures
changes can be most notable in skull

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22
Q

what is secondary hyperparathyroidism commonly due to?

A

dietary problem

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23
Q

what dietary problems can lead to secondary hyperparathyroidism?

A

improper calcium:phosphorous ratio in diet
low vitamin D

24
Q

who is secondary hyperparathyroidism most common in?

A

growing animals or exotic species

25
Q

what are the laboratory findings with secondary hyperparathyroidism?

A

low-end of reference interval to decreased total calcium and iCa
low, within normal, or occasionally high phosphorous
increased iPTH

26
Q

what are the clinical signs of secondary hyperparathyroidism usually due to?

A

hypocalcemia

27
Q

what skeletal changes can chronic secondary hyperparathyroidism lead to?

A

pain on movement
limb deformities
generalized skeletal demineralization and fibrous oseodystrophy
thinning of long bone cortices

28
Q

what is reptile metabolic bone disease due to?

A

secondary hyperparathyroidism

29
Q

what is seen in reptile metabolic bone disease?

A

pathologic fractures
swelling of long bones
decalcification and shortening/bowing of mandible
soft, deformed shells of eggs

30
Q

what animals are at a higher risk for reptile metabolic bone disease?

A

insectivores may need fortified food
herbivores with limited exposure to UV light should get vitamin D3 supplementation

31
Q

which animals are not at increased risk of reptile metabolic bone disease?

A

those housed outside
reptiles that eat whole mammalian prey

32
Q

who is more likely to have secondary hyperparathyroidism due to renal?

A

adult mammals

33
Q

what is secondary hyperthyroidism due to renal triggered by?

A

decreased calcium and rising serum phosphorous

34
Q

GFR determines filtration of _____________ and ____________

A

calcium
phosphorous

35
Q

what are calcium levels like in dogs with chronic renal failure?

A

10% have low total Ca
40% have low ionized Ca

36
Q

what are the clinical signs in renal secondary hyperparathyroidism due to?

A

renal failure

37
Q

what clinical signs are associated with renal secondary hyperparathyroidism?

A

vomiting, dehydration, PU/PD
mild hypocalcemia

38
Q

what happens to the parathyroid glands in chronic renal failure?

A

hypertrophy

39
Q

how often do we see skeletal changes with renal secondary hyperparathyroidism?

A

occasionally

40
Q

what is the most common cause of persistent hypercalcemia in dogs?

A

humoral hypercalcemia of malignancy

41
Q

what tumors have the highest incidence of humoral hypercalcemia of malignancy?

A

lymphoma
apocrine gland anal sac adenocarcinoma
multiple myeloma
squamous cell carcinoma

42
Q

what does humoral hypercalcemia of malignancy produce?

A

parathyroid hormone related protein

43
Q

what are the laboratory findings associated with humoral hypercalcemia of malignancy?

A

increased calcium and iCa
low to within normal phosphorous
decreased iPTH
increased PTHrp

44
Q

what are the causes of reptile metabolic bone disease?

A

diet problems
lack of exposure to UVA and UVB
cool temperatures

45
Q

what hormones regulate calcium homeostasis?

A

parathyroid hormone
calcitriol/active vitamin D
calcitonin
parathyroid hormone-related peptide
fibroblast growth factor-23

46
Q

what inhibits parathyroid hormone secretion through the Ca-sensing receptor?

A

high calcium
high calcitriol

47
Q

what does cacitriol binding to a receptor that modulates DNA expression do?

A

control expression for calcium absorption and transport in the gastrointestinal tract
increases calcium, phosphorous, and magnesium absorption
inhibits parathyroid hormone secretion

48
Q

do skeletal changes occur with primary hypoparathyroidism?

49
Q

what are the clinical signs of primary hyperparathyroidism?

A

usually mild
pu/pd
anorexia/GI signs
generalized muscle weakness
occasional, mild CNS signs

50
Q

low phosphorous in primary hyperparathyroidism makes mineralization _______________

A

less likely

51
Q

what is the ideal ratio of Calcium:Phosphorous in a diet?

A

2:1
bad: low calcium, excess phosphorous

52
Q

what are the neuromuscular signs associated with nutritional secondary hyperparathyroidism?

A

nervous, ataxic, weak
rub muzzle, eyes, ears
intermittent muscle tremors
generalized tetany
convulsive seizures

53
Q

what triggers renal secondary hyperparathyroidism?

A

decreased GFR and rising serum phosphorous
hyperphosphatemia

54
Q

what happens in the kidneys that contributes to secondary hyperparathyroidism?

A

decreased filtration: increased phosphorous
decreased absorption: decreased calcium
decreased activation of vitamin D: decreased calcium

55
Q

does the hypocalcemia in renal secondary hyperparathyroidism cause clinical signs?

A

not usually

56
Q

what skeletal changes might you see with renal secondary hyperparathyroidism?

A

demineralization
fibrous osteodystrophy

Endocrine Pathophysiology (6 decks)

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