PARATHYROID HORMONE

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82 Terms

1
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THESE ARE FOUND NEAR THE POSTERIOR ASPECT OF THE THYROID GLAND

4 PARATHYROID GLANDS

2
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THESE ARE SMALL AND HAVE A BEAN-LIKE SHAPE

PARATHYROID GLANDS

3
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PARATHYROID GLAND HAS 2 CELLS WHICH ARE?

CHIEF CELLS AND OXYPHIL CELLS

4
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PARATHYROID HORMONE IS SYNTHESIZED BY WHAT CELLS?

CHIEF CELLS

5
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THIS TYPE OF CELL UNDER PARATHYROID GLAND HAS NO KNOWN FUNCTION

OXYPHIL CELLS

6
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TRUE OR FALSE. ALL PEOPLE HAVE 4 PARATHYROID GLANDS, NO MORE NO LESS.

FALSE

7
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THIS IS CONSIDERED TO BE THE SMALLEST ENDOCRINE GLAND IN THE BODY

PARATHYROID GLAND

8
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WHERE IS THE LOCATION OF THE PARATHYROID GLAND?

NEAR THE THYROID CAPSULE OR SOMETIMES WITHIN THE THYROID GLAND

9
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IF THE PARATHYROID GLAND IS NOT FOUN WITHIN THEIR NORMAL ANATOMIC SITE, WHERE COULD THEY BE FOUND?

BETWEEN THE HYOID BONE IN THE NECK AND MEDIASTINUM

10
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WHAT IS THE MAIN FUNCTION OF PARATHYROID HORMONE?

TO MAINTAIN THE BODY’S CALCIUM LEVEL

11
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WHO IS RESPONSIBLE FOR SECRETING THE PARATHYROID HORMONE?

CHIEF CELLS

12
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THIS HORMONE MOBILIZE CALCIUM AND PHOSPHATE FROM THE BONE

PARATHYROID HORMONE

13
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WHEN THERE IS LOW CALCIUM IN THE BLOOD, THERE IS AN INCREASED?

BONE RESORPTION

14
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INCREASED OR DECREASED. EFFECT OF PARATHYROID HORMONE IN PHOSPHATE EXCRETION

INCREASED

15
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INCREASED OR DECREASED. EFFECT OF PARATHYROID HORMONE IN RENAL H+ ION SECRETION

DECREASED

16
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INCREASED OR DECREASED. EFFECT OF PARATHYROID HORMONE IN CALCIUM EXCRETION

DECREASED

17
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THIS ENHANCES RENAL HYDROXYLATION D3 (CHOLECALCIFEROL)

PARATHYROID HORMONE

18
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THIS INCREASES CALCIUM ABSORPTION FROM GUT

PARATHYROID HORMONE

19
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IN ORDER FOR CALCIUM TO BE AVAILABLE IN THE BLOOD, CALCIUM MUST BE ABSORBED FROM THE?

SMALL INTESTINE

20
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TRUE OR FALSE. IN THE BONES, PTH STIMULATES OSTEOCLASTS TO INCREASE GROWTH AND METABOLIC ACTIVITY. PTH ALSO STIMULATES THE OSTEOCLASTS TO PROMOTE BONE RESORPTION TO RELEASE CALCIUM AND PHOSPHATE IN THE BLOODSTREAM

A. BOTH ARE TRUE

B. BOTH ARE FALSE

C. 1ST TRUE; 2ND FALSE

D. 1ST FALSE; 2ND TRUE

D

21
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CRYSTALLINE SALTS ALSO KNOWN AS HYDROXYAPATITE DEPOSITED IN THE ORGANIC MATRIX OF THE BONE WHICH IS COMPOSED PRINCIPALLY OF CALCIUM AND PHOSPHATE

BONE SALTS

22
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IN ORDER FOR BONE SALTS TO PRODUCE, WHAT MUST BE PRESENT?

HYPOCALCEMIA

23
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IN KIDNEYS, PTH INCREASES RENAL ABSORPTION OF CALCIUM BUT REDUCES REABSORPTION OF?

PHOSPHATE

24
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IN KIDNEYS, __ INCREASES THE CALCIUM AND REDUCES PHOSPHATE IN THE PLASMA

NET EFFECT

25
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IN THE INTESTINES VIA THE KIDNEY, PTH ENHANCES THE ABSORPTION OF CALCIUM IN THE INTESTINE BY INCREASING THE PRODUCTION OF?

ACTIVATED VITAMIN D

26
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IN THE INTESTINES VIA THE KIDNEY, THIS PROMOTES THE ABSORPTION OF EXOGENOUS CALCIUM (DIET-DERIVED CALCIUM)

ACTIVATED VITAMIN D

27
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THIS ACTIVATED FORM OF VITAMIN D INCREASES THE ABSORPTION OF CALCIUM BY THE INTESTINE VIA?

CALCITONIN

28
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PTH REDUCES THE REABSORPTION OF PHOSPHATE FROM THE ___ OF THE KIDNEY, WHICH MEANS MORE PHOSPHATE IS EXCRETED THROUGH THE URINE

PROXIMAL TUBULE

29
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PTH ENHANCES THE UPTAKE OF PHOSPHATE FROM THE __ AND __ INTO THE BLOOD

INTESTINES AND BONES

30
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IN THE ____, PHOSPHATE IS ABSORBED ALONG WITH CALCIUM. WHEN CALCIUM IS RELEASED THROUGH BONE RESORPTION, PHOSPHATE IS ALSO RELEASED

INTESTINE AND BONES

31
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IN THE ___, WHEN CALCIUM IS REABSORBED, PHOSPHATE WILL BE EXCRETED

KIDNEYS

32
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TRUE OR FALSE. IN THE INTESTINES, WHICH IS MEDIATED BY AN INCREASE IN ACTIVATED VITAMIN D, THE ABSORPTION OF PHOSPHATE IS NOT AS DEPENDENT ON VITAMIN D AS WITH THAT OF CALCIUM

TRUE

33
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VITAMIN D FOCUSES ON?

CALCIUM ABSORPTION

34
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IN THE REGULATION OF SERUM PHOSPHATE, THE END RESULT IS A:

A. SMALL NET DROP IN THE SERUM CONCENTRATION OF CALCIUM

B. LARGE NET DROP IN THE SERUM CONCENTRATION OF PHOSPHATE

C. SMALL NET DROP IN THE SERUM CONCENTRATION OF PHOSPHATE

D. LARGE NET DROP IN THE SERUM CONCENTRATION OF CALCIUM

C

35
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FOR VITAMIN D SYNTHESIS, PTH INCREASES THE ACTIVITY OF WHAT ENZYME

1-A-HYDROXYLASE ENZYME

36
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1-A-HYDROXYLASE, WHICH CONVERTS 25-HYDROXYCHOLECALCIFEROL TO ___ WHICH IS THE ACTIVE FORM OF VITAMIN D

1,25-DIHYDROXYCHOLECALCIFEROL

37
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DECREASED SERUM CA2+

A. STIMULATORS OF PTH

B. INHIBITORS OF PTH

A

38
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MILD DECREASE IN SERUM MG2+

A. STIMULATORS OF PTH

B. INHIBITORS OF PTH

A

39
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INCREASED SERUM CA2+

A. STIMULATORS OF PTH

B. INHIBITORS OF PTH

B

40
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SEVERE DECREASE IN SERUM MG2+

A. STIMULATORS OF PTH

B. INHIBITORS OF PTH

B

41
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PTH - BONE RESORPTION - CALCIUM IS REABSORBED IN THE KIDNEYS - WILL RISE TOWARDS NORMAL

A. HYPOCALCEMIA

B. HYPERCALCEMIA

A

42
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CALCITONIN - BONE MINERALIZATION - EXCESS CALCIUM IN THE BLOOD WILL BE ABSORBED BY THE BONE - WILL FALL TOWARDS NORMAL

A. HYPOCALCEMIA

B. HYPERCALCEMIA

B

43
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ACTIVATION SITE OF THE ACTIVE FORM OF VITAMIN D IS IN THE?

KIDNEYS

44
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THIS PROMOTES INCREASED ABSORPTION OF CALCIUM AND PHOSPHATE IN THE SMALL INTESTINE

ACTIVATED VITAMIN D

45
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DECREASED FUNCTION OF THE PARATHYROID GLANDS REDUCING ITS PRODUCTION OF PTH

HYPOPARATHYROIDISM

46
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THIS IS OFTEN DUE TO POSSIBLE REMOVAL OF THE PARATHYROID GLAND OR THE THYROID GLAND

HYPOPARATHYROIDISM

47
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SURGICAL REMOVAL OF THE GLAND IS DONE BECAUSE OF?

TRAUMA AND OTHER COMPLICATIONS

48
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THIS IS WHEN SERUM CALCIUM LEVEL DECREASES

HYPOPARATHYROIDISM

49
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THIS IS DUE TO ACCIDENTAL INJURY TO THE PT GLANDS DURING THYROID OR NECK SURGERY, REMOVAL OF THE GLANDS WITH THYROID GLANDS, OR IDIOPATHIC ATROPHY

HYPOPARATHYROIDISM

50
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A DISEASE WITH NO IDENTIFIABLE CAUSE

IDIOPATHIC

51
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WHAT IS/ARE THE OTHER CAUSES OF HYPOPARATHYROIDISM

AUTOIMMUNE PARATHYROID DESTRUCTION

52
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IMMUNE SYSTEM OF THE PATIENT ATTACKS THE PARATHYROID GLAND—IMMUNE SYSTEM PRODUCES ANTIBODIES TO ATTACK THE PTG. WHEN CHIEF CELLS ARE DESTROYED, THE PRODUCTION OF PTH DECREASES

AUTOIMMUNE PARATHYROID DESTRUCTION

53
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IN HYPOPARATHYROIDISM, INDIVIDUALS ARE UNABLE TO MAINTAIN CALCIUM CONCENTRATION IN BLOOD WITHOUT?

CALCIUM SUPPLEMENTATION

54
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A GENETIC CONDITION ASSOCIATED PRIMARILY WITH RESISTANCE TO PTH RESPONSE

PSEUDOHYPOPARATHYROIDISM

55
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PSEUDOHYPOPARATHYROIDISM IS DUE TO THE DEFECT ON THE PTH RECEPTOR WHICH IS THE __

ADENYLATE CYCLASE COMPLEX

56
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PSEUDOHYPOPARATHYROIDISM MAY ALSO BE RESISTANT TO?

TSH, GLUCAGON, GONADOTROPINS

57
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THIS IS PRODUCED BY THE APG

TSH AND GONADOTROPINS

58
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THIS IS PRODUCED BY THE ALPHA CELLS OF ISLET OF LANGERHANS OF THE PANCREAS

GLUCAGON

59
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THIS IS AN EXCESS OF PARATHYROID HORMONE IN THE BLOODSTREAM DUE TO OVERACTIVITY OF ONE OR MORE OF THE BODY’S FOUR PARATHYROID GLANDS

HYPERPARATHYROIDISM

60
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WHAT MAY BE THE CAUSE OF THE HYPERPARATHYROIDISM

TUMOR ON ONE OF THE PARATHYROID GLANDS

61
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TRUE OR FALSE. TUMOR MAY CAUSE HYPERACTIVITY OF THE PARATHYROID GLAND

TRUE

62
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WHAT ARE THE THREE TYPES OF HYPERPARATHYROIDISM

PRIMARY, SECONDARY, TERTIARY HYPERPARATHYROIDISM

63
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EXCESSIVE PTH SECRETION MAY BE DUE TO PROBLEMS IN THE GLANDS THEMSELVES, LEADING TO?

HYPERCALCEMIA

64
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THIS IS THE MOST COMMON CAUSE OF HYPERCALCEMIA

PRIMARY HYPERPARATHYROIDISM

65
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THIS IS DUE TO THE PRESENCE OF A FUNCTIONING PARATHYROID ADENOMA (TUMOR IN THE PTG)

PRIMARY HYPERPARATHYROIDISM

66
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PRIMARY HYPERPARATHYROIDISM ACCOMPANIES WITH ___ (INCREASED CALCIUM REABSORPTION, INCREASED PHOSPHATE EXCRETION IN THE URINE)

PHOSPHATURIA

67
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IF PRIMARY HYPERPARATHYROIDISM IF UNDETECTED, WHAT MAY OCCUR?

SEVERE DEMINERALIZATION

68
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TRUE OR FALSE. SEVERE DEMINERALIZATION MAY CAUSE THE BONE TO BECOME BRITTLE AND WEAK MAKING IT PRONE TO FRACTURE

TRUE

69
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THIS OCCURS IN RESPONSE TO LOW CALCIUM LEVELS

SECONDARY HYPERPARATHYROIDISM

70
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THIS IS ENCOUNTERED IN VARIOUS SITUATIONS SUCH AS VITAMIN D DEFICIENCY OR CHRONIC KIDNEY DISEASE

SECONDARY HYPERPARATHYROIDISM

71
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LOW CALCIUM ABSORPTION IN THE INTESTINE

VITAMIN D DEFICIENCY

72
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CANNOT SUPPORT THE BONES IN SUPPLYING CALCIUM RESULTING IN DECREASE OF CALCIUM IN THE PLASMA

CHRONIC KIDNEY DISEASE

73
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IF THE INTESTINE AND THE KIDNEYS CAN NOT PROVIDE SUFFICIENT CALCIUM, __ WILL BE THE SOURCE OF CALCIUM

BONES

74
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THIS DEVELOPS IN RESPONSE TO SERUM CALCIUM LEVEL IN THE PLASMA

SECONDARY HYPERPARATHYROIDISM

75
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THERE IS DIFFUSE HYPERPLASIA OF ALL 4 GLANDS

SECONDARY HYPERPARATHYROIDISM

76
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IN SECONDARY HYPERPARATHYROIDISM, THE PATIENT DEVELOPS WHAT DISEASE

SEVERE BONE DISEASE

77
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WHAT ARE THE CAUSES OF SECONDARY HYPERPARATHYROIDISM

VITAMIN D DEFICIENCY AND CHRONIC RENAL FAILURE

78
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THIS OCCURS WITH PATIENT WHO HAVE SECONDARY HYPERPARATHYROIDISM

TERTIARY HYPERPARATHYROIDISM

79
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THIS DEVELOP AUTONOMOUS FUNCTION OF THE HYPERPLASTIC PARATHYROID GLAND OR OF A PARATHYROID ADENOMA

TERTIARY HYPERPARATHYROIDISM

80
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EXCESSIVE PTH SECRETION DUE TO PROBLEMS IN PTG

PRIMARY HYPERPARATHYROIDISM

81
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IN RESPONSE TO SEVERELY LOW CALCIUM LEVELS IN THE BLOOD, VITAMIN D DEFICIENCY, AND CHRONIC KIDNEY DISEASE

SECONDARY HYPERPARATHYROIDISM

82
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PATIENT HAS SECONDARY HYPERPARATHYROIDISM AND THE PARATHYROID GLAND DEVELOPS AUTONOMOUS FUNCTION AND DEVELOPS INTO A TUMORE

TERTIARY HYPERPARATHYROIDISM