Section 4 - Parathyroid Glands, Calcium & Vitamin D Flashcards

(46 cards)

1
Q

Describe the location of the parathyroid glands in the human body and identify key landmarks?

A

Typically four but range anywhere from 2 to 8. Adhere to the posterior surface of the thyroid gland. Vascularized and derive their blood supply from inferior thyroid arteries.

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2
Q

Histological and micro-anatomical features of parathyroid gland

A

1) principal (chief cells)

2) oxyphil cells - degenerated principal cells. number INCREASES with age

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3
Q

Summarize the distribution (throughout the body) and functions of both calcium and phosphorous (phosphate)

A

Calcium function - muscle contractions, exocytosis, blood clotting, formation of cardiac action potentials, enzyme activation, cell signaling, bone & teeth structure

Phosphate - essential for bone and teeth formation

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4
Q

what is the chemistry of hormone for the parathyroid hormone (PTH)?

A

peptide hormone

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5
Q

what stimulates PTH?

A

stimulation is hypocalcemia

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6
Q

when, where and how is PTH synthesized?

A

synthesized and secreted by chief cells based. Chief cells sense minute fluctuations of ECF Ca2+

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7
Q

what are the physiological effects of hormone?

A

stimulates osteoclast activity; reabsorption of Ca2+ in distal convoluted tubules; stimulates 1-hydroxylation of 25-hydroxycholecalciferol in kidneys, stimulates intestinal uptake of Ca2+ by “active” vitamin D; phosphaturia

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8
Q

what is the chemistry of hormone of calcitonin?

A

peptide hormone

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9
Q

what stimulates calcitonin?

A

hypercalcemia

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10
Q

when, where and how is calcitonin synthesized?

A

synthesized and secreted by parafollicular cells of the thyroid gland

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11
Q

what are the physiological effects of calcitonin?

A

it lowers the ECF Ca2+ by acting on bone.

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12
Q

what is the chemistry of hormone of vitamin D?

A

steroid hormone

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13
Q

what is the stimulation of vitamin D?

A

PTH stimulates secretion

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14
Q

when, where and how is vitamin D synthesized?

A

made into active version in kidneys when PTH is released

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15
Q

physiological effects of vitamin D

A

helps with calcium uptake in the intestines

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16
Q

hyperparathyroidism (all forms)

A

primary hyperparathyroidism

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17
Q

pathophysiology of primary hyperparathyroidism?

A

hypercalcemia

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18
Q

etiology of hyperparathyroidism?

A

adenomas

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19
Q

clinical manifestations of hyperparathyroidism?

A

stones (kidney, gallbladder)
thrones (frequent urination)
bones (pain in bone)
groans (constipation and muscle weakness)
psychiatric overtones (depressed mood, confusion)

20
Q

dental aspects of hyperparathyroidism?

A
gradual loosening
drifting and loss of teeth
spacing of teeth
"brown tumor" lesions raising the risk for fracture
malocclusion
dental pain
soft tissue calcification
sialothiasis (salivary duct stones)
21
Q

hypoparathyroidism (all forms)

A

primary hypoparathyroidism

22
Q

pathophysiology of primary hypoparathyroidism?

A

hypocalcemia and hyperphosphatemia

23
Q

what is the etiology of hypoparatyroidism?

24
Q

what are some clinical manifestations of hypoparathyroidism?

A

cardiac arrhythmias, trousseau’s sign, chovestek’s sign, parathesia

25
treatment of hypoparathyroidism includes
synthetic PTH, oral calcium carbonate tablets, and/or vitamin D
26
dental aspects of hypoparathyroidism includes
- enamel hypoplasia - delayed eruption or multiple unerupted teeth - poorly calcified dentin - microdontia - malformed roots - dental caries - parathesia
27
what is the pathophysiology of osteoporosis?
bone resorption is faster than bone formation
28
what is the etiology of osteoporosis?
lifestyle - low calcium intake, vitamin D deficiency, excess vitamin A intake, inadequate physical activity, smoking and alcohol abuse genetic factors - parental history of hip fracture medical conditions - hyperparathyroidism, Cushing syndrome medication - corticosteroids
29
Clinical manifestations of osteoporosis
fragility fracture, decreased bone mass
30
Treatment of osteoporosis
include calcium and vitamin D supplements (insufficient alone), bisphosphonates, selective estrogen receptor modulators, and calcitonin.
31
calcium supplements for osteoporosis
- calcium citrate: take with meals and can cause dyspepsia and constipation - calcium carbonate: best taken during fasting
32
Bisphosphonates
Bisphosphonates inhibits osteoclasts by imbibing itself into the osteoclasts to fall off and apoptosis. Can cause transient hypocalcemia, musculoskeletal pain, acute flu-like reaction (IV), and osteonecrosis of the jaw. Should not give with patients who have esophageal disorders (achalasia, esophageal varices, Barrett's esophagus) and patients with severe renal impairment.
33
What are the four types of bisphosphonates given?
alendronate risedronate ibandronate zoledronic acid
34
alendronate
oral and liquid
35
risedronate
oral
36
ibandronate
oral and IV
37
zoledronic acid
IV
38
How does estradiol prevent osteoclast maturation?
Estradiol increases production of OPG to inhibit RANKL preventing RANKL/RANK (receptor) interaction -> prevents osteoclast maturation. That's why we have selective estrogen receptor modulators/SERMs.
39
Type of estradiol that can cause increase risk of blood clots?
Raloxifine
40
Calcitonin
increases in cAMP levels -> decrease in resorptive ability. Can cause nausea, flushing, and runny nose. Can cause increase in cancer rates
41
Two types of calcitonin medications
miacalcin and fortical
42
denosumab
antibody against RANKL. Administered as SC injection. Adverse effects include musculoskeletal pain, hypercholesterolemia, and cysititis. Can cause ONJ but not as frequent as BP.
43
Dental aspects of osteoporosis
loss of bone mass in mandible | loosening of teeth or tooth loss and dentures to become ill-fitting; medication can cause osteonecrosis
44
Rickets and osteomalacia pathology?
soft bones
45
Etiology of rickets and osteomalacia?
calcium and vitamin D deficiency
46
Clinical manifestations of rickets and osteomalacia
weight - bearing bones bend and deform in children. increased amount of fractures in adults