Endocrinology - Lecture 2 Flashcards

1
Q

What are the 2 different tissues of the pituitary gland?

A

adenohypophysis and neurohypophysis

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2
Q

What is the adenohypophysis tissue also known as?

A

anterior pituitary

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3
Q

What is the neurohypophysis tissue also known as?

A

posterior pituitary

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4
Q

What kind of tissue is the anterior pituitary?

A

endocrine tissue

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5
Q

What kind of tissue is the posterior pituitary?

A

neural tissue

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6
Q

What 2 hormones does the posterior pituitary produce?

A

vasopressin and oxytocin

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7
Q

What 6 hormones does the anterior pituitary produce?

A
  1. TRH
  2. GnRH
  3. somatostatin
  4. GRH
  5. PIH
  6. CRH
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8
Q

What 2 nuclei synthesize oxytocin and vasopressin?

A

supraoptic nucleus and paraventricular nucleus

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9
Q

Where do the supraoptic and paraventricular nuclei run and terminate?

A

run: down the pituitary stalk
terminate: in the posterior pituitary close to capillary blood vessels

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10
Q

What are processed in secretory granules during axonal transport of supraoptic and paraventricular nuclei?

A

prohormones

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11
Q

What is the name of the mature hormones liberated from the carrier molecules produced in the posterior pituitary?

A

neurophysins

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12
Q

What are the circulating half lives of the neurophysins produced by the posterior pituitary?

A

1-3 minutes

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13
Q

What are the 3 functions of oxytocin in females?

A
  1. parturition
  2. milk ejection
  3. behavioural effects
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14
Q

How is oxytocin important in parturition?

A

dilation of uterine cervix by fetal head causes release of oxytocin -> uterine contraction, which assists the expulsion of fetus and then placenta.

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15
Q

How is oxytocin important in milk ejection?

A

it causes milk filled ducts to contract and squeeze milk out

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16
Q

What are the behavioural effects of oxytocin in females and males?

A

it reduces anxiety and enhances bonding, pro-social behaviour

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17
Q

What are the 2 functions of oxytocin in males?

A
  1. ejaculation
  2. behavioural effects
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18
Q

How is oxytocin important in ejaculation?

A

there is a surge of oxytocin during sexual activity which assists in epididimal passage of sperm and ejaculation

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19
Q

What is the major component of the thyroid gland?

A

thyroglobulin

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20
Q

What hormones are present in the thyroid gland?

A

T4 and T3

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21
Q

What controls the synthesis of thyroglobulin?

A

TSH of pituitary gland

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22
Q

What does thyroglobulin provide for T4 and T3 prior to release?

A

storage

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23
Q

What is the mass of the thyroid gland and what does its size vary with?

A

15 to 20g, varies size with sex, age, diet, reproductive state

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24
Q

The thyroid gland is larger in ___ than in ___.

A

females, males

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25
Q

How many grams of healthy thyroid are needed to maintain euthyroid state?

A

3 g

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26
Q

What element do thyroid hormones contain?

A

iodine

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27
Q

Which kinds of cells are able to trap iodide and transport it across the cell against a chemical gradient?

A

thyroid follicular cells

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28
Q

What is iodine used for?

A

iodination of tyrosine residues of thyroglobulin

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29
Q

What does thyroglobulin produce after it becomes iodinized?

A

monoiodotyrosine and diiodotyrosine

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30
Q

Oxidative coupling of how many DIT forms T4?

A

2

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31
Q

Oxidative coupling of how many MIT and DIT forms T3?

A

1 of each

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32
Q

What is the synthesis of thyroid hormones stimulated by?

A

TSH

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33
Q

Without ___, thyroid has very low turnover of thyroid hormones.

A

TSH

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34
Q

What is the synthesis and release of TSH controlled by?

A

hypothalamic thyrotropin releasing hormone TRH

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35
Q

What happens to the release of TRH and TSH when T4 and T3 in blood increases?

A

it decreases

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36
Q

What happens to the synthesis of thyroid hormones when the supply of iodide is deficient?

A

it decreases

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37
Q

What happens to TSH when there is an iodine deficiency?

A

it increases and the thyroid follicular cells are constantly stimulated

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38
Q

What happens to the thyroid gland when there is iodine deficiency?

A

it enlarges and may form a visible lump (goiter)

39
Q

What happens to cardiac output, oxygenation of blood and rate of breathing when thyroid hormones stimulate the calorigenesis in most cells?

A

cardiac output: increases
oxygenation of blood: increases
rate of breating: increases

40
Q

How can thyroid hormones effect carbohydrate metabolism?

A

Increased lipid synthesis; Increased lipid mobilization; Increased lipid oxidation

41
Q

How can thyroid hormones effect protein metabolism?

A

it stimulates protein synthesis

42
Q

How can thyroid hormones promote normal growth?

A

they promote neural branching and myelination of nerves, maturation of nervous sytem, stimulate bone growth

43
Q

What do thyroid hormones T3 and T4 increase?

A

BMR

44
Q

What does absence of thyroid hormones at early stages of development lead to?

A

irreversible mental retardation

45
Q

What growth factor do thyroid hormones stimulate?

A

nerve growth factor NGF

46
Q

What does NGF induce?

A

dendritogenesis and regeneration of sympathetic neurons

47
Q

How are thyroid hormones analogous to the mechanism of action of steroid hormones?

A

T3 and T4 enter target cell nucleus, bind to their cognate nuclear receptor. Alters the transcription of specific genes, and thus levels of encoded proteins.

48
Q

What do thyroid hormones interact with to induce some effects?

A

plasma membrane and mitochondria

49
Q

Where is a specific receptor for T4/T3 located in the mitochondria?

A

in the inner mitochondrial membrane

50
Q

What can T4/T3 hormones increase the uptake of?

A

amino acids

51
Q

What are the 4 kinds of hypothyroidism?

A

primary, secondary, tertiary and infantile

52
Q

What is primary hypothyroidism at the level of?

A

the thyroid gland

53
Q

What is primary hypothyroidism?

A

inability to synthesize active thyroid hormones

54
Q

What sex is primary hypothyroidism more common in?

A

females

55
Q

What are the 3 main causes of primary hypothyroidism?

A
  1. Atrophy of the thyroid .
  2. Autoimmune Thyroiditis
    A.K.A. autoimmune thyroiditis or Hashimoto’s disease. More common in women.
  3. Goitrous Hypothyroidism or Non-Toxic Goitre
56
Q

What is autoimmune thyroiditis?

A

destruction by antibodies against cellular components of thyroid

57
Q

What is goitrous hypothyroidism or non-toxic goitre?

A

blockage in a step of T4/T3 synthesis.

58
Q

What is secondary hypothyroidism at the level of?

A

pituitary

59
Q

What is secondary hypothyroidism?

A

synthesis of little or no thyroid stimulating hormone TSH

60
Q

What is tertiary hypothyroidism at the level of?

A

hypothalamus

61
Q

What is tertiary hypothyroidism?

A

synthesis of little or no thyrotropin releasing hormone TRH

62
Q

What is infantile hypothyroidism?

A

absence of thyroid gland or incomplete development of thyroid gland at birth

63
Q

Why is early treatment of infantile hypothyroidism important?

A

because otherwise the child will have dwarfism and mental retardation will be associated with cretinism

64
Q

How can all types of hypothyroidism be effectively treated?

A

with thyroid hormones

65
Q

What are the 3 kinds of hyperthyroidism?

A

primary, secondary and tertiary

66
Q

What are the 2 kinds of primary hyperthyroidism?

A
  1. toxic diffuse goiter (graves disease)
  2. thyroid adenoma or thyroid cancer
67
Q

What is primary hyperthyroidism at the level of?

A

the thyroid gland

68
Q

What is Graves Disease?

A

presence of LATS that are constantly stimulated which increases mass of thyroid leading to the formation of goitre synthesizes biologically active T4/T3; known as toxic goitre.

69
Q

What is LATS?

A

long acting thyroid stimulator, an antibody that mimics the action of TSH and stimulating release of T3 and T4

70
Q

What is thyroid adenoma?

A

synthesis of thyroid hormones is independent of TSH stimulation

71
Q

What is secondary hyperthyroidism at the level of?

A

anterior pituitary gland

72
Q

What is secondary hyperthyroidism?

A

no negative feedback from increased levels of T3/T4 and synthesize autonomously thyroid stimulating hormone (TSH).

73
Q

What often causes secondary hyperthyroidism?

A

pituitary tumour

74
Q

What is tertiary hyperthyroidism at the level of?

A

hypothalamus

75
Q

What is tertiary hyperthyroidism?

A

no negative feedback of high T3/T4 to decrease synthesis of thyrotropin releasing hormone (TRH)

76
Q

What often causes tertiary hyperthyroidism?

A

hypothalamic tumour

77
Q

What are the 3 treatments for hyperthyroidism?

A
  1. surgery plus replacement therapy
  2. administration of radioactive iodide
  3. administration of antithyroid drugs like propylthiouracil
78
Q

What is radioactive iodide administered to those with hyperthyroidism?

A

because the radioactive iodide concentrates in the cells of the thyroid follicles and destroys them

79
Q

What is the function of propylthiouracil to treat hyperthyroidism?

A

it blocks the addition of iodine to thyroglobulin

80
Q

What is the function of calcium?

A

-essential structural component of the skeleton.
- important in normal blood clotting.
- with Na+ and K+ helps maintain transmembrane potential of cells.
-important in excitability of nervous tissue
-important in contraction of muscles
-important in release of hormones and neurotransmitters.

81
Q

What is the concentration of calcium in cellular and ECF?

A

10mg/100 mL

82
Q

How is calcium in the circulation?

A

50% free 50% bound to albumin

83
Q

About 99% of the body’s calcium is in ___.

A

bone

84
Q

How do hormones control calcium?

A
  • maintenance of plasma calcium is achieved mainly by exchange between bone and plasma under influence of hormones.
  • hormones also affect intestinal absorption of calcium and excretion of by kidneys.
85
Q

What 3 hormones are important in controlling calcium levels?

A
  1. parathyroid hormone PTH
  2. calcitonin
  3. vitamin D
86
Q

Does PTH increase or decrease calcium levels?

A

increases

87
Q

Does calcitonin increase or decrease calcium levels?

A

decreases

88
Q

Does vitamin D increase or decrease calcium levels?

A

increases

89
Q

Where is calcium absorbed in the digestive tract?

A

the duodenum and upper jejunum

90
Q

What is calcium absorption increased by?

A

vitamin D and PTH

91
Q

What increases calcium deposition in bone?

A

calcitonin

92
Q

Where can calcium go?

A
  1. through the kidney and into the urin
  2. deposited in bone
93
Q

What does PTH stimulate the reabsorption and removal of when plasma concentration of calcium is below 10mg/100 mL?

A

reabsorption: of calcium from the kidney
removal: of calcium from the bone