Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrine > Section 4 - Parathyroid Glands, Calcium & Vitamin D > Flashcards

Section 4 - Parathyroid Glands, Calcium & Vitamin D Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

peptide hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what stimulates PTH?

A

stimulation is hypocalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the chemistry of hormone of calcitonin?

A

peptide hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what stimulates calcitonin?

A

hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

when, where and how is calcitonin synthesized?

A

synthesized and secreted by parafollicular cells of the thyroid gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the physiological effects of calcitonin?

A

it lowers the ECF Ca2+ by acting on bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the chemistry of hormone of vitamin D?

A

steroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is the stimulation of vitamin D?

A

PTH stimulates secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

when, where and how is vitamin D synthesized?

A

made into active version in kidneys when PTH is released

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

physiological effects of vitamin D

A

helps with calcium uptake in the intestines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

hyperparathyroidism (all forms)

A

primary hyperparathyroidism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

pathophysiology of primary hyperparathyroidism?

A

hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

etiology of hyperparathyroidism?

A

adenomas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

A

adenoma

24
Q

what are some clinical manifestations of hypoparathyroidism?

A

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

25
Q

treatment of hypoparathyroidism includes

A

synthetic PTH, oral calcium carbonate tablets, and/or vitamin D

26
Q

dental aspects of hypoparathyroidism includes

A
  • enamel hypoplasia
  • delayed eruption or multiple unerupted teeth
  • poorly calcified dentin
  • microdontia
  • malformed roots
  • dental caries
  • parathesia
27
Q

what is the pathophysiology of osteoporosis?

A

bone resorption is faster than bone formation

28
Q

what is the etiology of osteoporosis?

A

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
Q

Clinical manifestations of osteoporosis

A

fragility fracture, decreased bone mass

30
Q

Treatment of osteoporosis

A

include calcium and vitamin D supplements (insufficient alone), bisphosphonates, selective estrogen receptor modulators, and calcitonin.

31
Q

calcium supplements for osteoporosis

A
  • calcium citrate: take with meals and can cause dyspepsia and constipation
  • calcium carbonate: best taken during fasting
32
Q

Bisphosphonates

A

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
Q

What are the four types of bisphosphonates given?

A

alendronate
risedronate
ibandronate
zoledronic acid

34
Q

alendronate

A

oral and liquid

35
Q

risedronate

A

oral

36
Q

ibandronate

A

oral and IV

37
Q

zoledronic acid

A

IV

38
Q

How does estradiol prevent osteoclast maturation?

A

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
Q

Type of estradiol that can cause increase risk of blood clots?

A

Raloxifine

40
Q

Calcitonin

A

increases in cAMP levels -> decrease in resorptive ability. Can cause nausea, flushing, and runny nose. Can cause increase in cancer rates

41
Q

Two types of calcitonin medications

A

miacalcin and fortical

42
Q

denosumab

A

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
Q

Dental aspects of osteoporosis

A

loss of bone mass in mandible

loosening of teeth or tooth loss and dentures to become ill-fitting; medication can cause osteonecrosis

44
Q

Rickets and osteomalacia pathology?

A

soft bones

45
Q

Etiology of rickets and osteomalacia?

A

calcium and vitamin D deficiency

46
Q

Clinical manifestations of rickets and osteomalacia

A

weight - bearing bones bend and deform in children. increased amount of fractures in adults

Endocrine (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions