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Physiology > ENDO III- Thyroid and Parathyroid hormones > Flashcards

ENDO III- Thyroid and Parathyroid hormones Flashcards

1
Q

what are the percentages of active hormones secreted by the thyroid gland

A

93% T4 and 7% T3

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2
Q

what are the names for T4 and T3

A

T4: thyroxine
T3: triidothyronine

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3
Q

which is more potent T3 or T4

A

T3

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4
Q

what do thyroid hormones do

A

impact metabolism and growth/development
- permissive action on catecholamines

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5
Q

what is thyroglobulin stored in

A

colloid follicle

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6
Q

what do parafollicular cells secrete

A

calcitonin

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7
Q

what does calcitonin do

A

decreases plasma calcium

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8
Q

what molecule is required for thyroid hormone synthesis

A

iodine

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9
Q

what is on the blood side of the follicular cell

A

sodium/ iodide symporter

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10
Q

what gets iodine into colloid

A

pendrin

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11
Q

what does peroxidase do

A

makes thyroid hormones

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12
Q

what is located on the apical membrane of the follicular cell

A

Cl-/I- exchanger AKA pendrin

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13
Q

where are T3 and T4 produced and what are they complexed with

A

produced in the colloid complexed with thyroglobulin

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14
Q

what is the precursor for T3 and T4

A

tyrosine

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15
Q

how is T3 and T4 secreted into the blood

A

-colloid is internalized by endocytosis
-the vesicles fuse with lysosomes in the cell
-proteases cleave T3 and T4 from TG
-T3 and T4 diffuse out of the cell and into capillaries

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16
Q

what do T3 and T4 bind with for transport

A

plasma proteins: TBG,TTR, and albumin

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17
Q

which has a longer half life T3 or T4

A

T4

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18
Q

what dictates half life

A

the strength of binding to the transport protein

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19
Q

is T3 or T4 secreted more

A

T4

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20
Q

how do target cells make active T3

A

by using enzymes called deiodinases that remove and iodine from T4

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21
Q

what do the 3 different deiodinases contain

A

rare AA called selenocysteine with selenium in place of sulfur

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22
Q

what conditions inhibit deiodinases

A

selenium deficiency, burns, trauma, advanced cancer, cirrhosis, chronic kidney disease, MI, febrile states, fasting, stress

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23
Q

what could the inhibition of deiodinases lead to

A

hypothyroidism

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24
Q

which actions occur sooner and when is max activity

A

T3, at 2-3 days

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25
Q

which has a longer duration of action

A

T4

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26
Q

where is T4 converted into T3

A

anterior pituitary and hypothalamus

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27
Q

what effect does thyroid hormones have on the cardiovascular system

A

-increased CO
-increased blood flow
- increase HR
- Increased heart strength
-increased respiration
-increased beta receptor expression

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28
Q

what effect does thyroid hormones have on metabolism

A

-increased glucose absorption
-increased gluconeogenesis
-increased fat metabolism (lipolysis)
-increased protein catabolism and synthesis
-increased BMR!!!
-increased mitochondria
-increased sodium potassium ATPase
-increased O2 consumption

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29
Q

what is the control of thyroid hormone secretion

A

negative feedback mainly at the level of the anterior pituitary gland

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30
Q

what hormone is responsible for most of the negative feedback of thyroid hormones

A

T4

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31
Q

what is the main circulating form of the thyroid hormones

A

T4

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32
Q

when does TSH secretion peak

A

midnight

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33
Q

describe TSH secretion

A

pulsatile and tonic

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34
Q

how do thyroid hormones stimulate carbohydrate metabolism

A

-causes uptake of glucose by cells
- enhances glycolysis and gluconeogenesis
- increases rate of CHO absorption from GI tract

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35
Q

how do thyroid hormones stimulate fat metabolism

A

-increases lipid mobilization and oxidation of fatty acids by cells
- required to convert beta carotene to vitamin A
-decreases circulating cholesterol levels

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36
Q

what thyroid disorder is hyperlipidemia associated with

A

hypothyroidism

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37
Q

how do thyroid hormones effect the nervous system

A

-normal development of NS
- impacts reflex time
-muscle tremors due to increased reactivity of neuronal synapses
-feeling of tiredness but difficulty sleeping
-anxiety, worry, paranoia

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38
Q

how do thyroid hormones effect the endocrine system

A

-increased glucose consumption results in increased insulin secretion to maintain blood glucose levels
-activation of bone formation causes a need for increased PTH secretion
- causes increased inactivation of glucocorticoids which leads to more ACTH release

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39
Q

how do thyroid hormones affect the cardiovascular systrm

A

-increased expression of beta adrenergic receptors
-increased blood flow, heart rate, and heart contractility

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40
Q

how do thyroid hormones affect the GI system

A

-increased appetite and food intake
- increased rate of secretion and motility of GI tract

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41
Q

what is goiter

A

enlarged thyroid that does not indicate functional status

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42
Q

what is euthyroidism

A

normal thyroid

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43
Q

what can goiter be caused by

A

excessive amounts of TSH secretion,, high TSH stimulates thyroid to secrete large amounts of thyroglobulin colloid into follicles resulting in gland enlargment

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44
Q

what is the most common form of hyperthyroidism

A

graves disease

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45
Q

besides graves disease how else can hyperthyroidism occur

A

a thyroid adenoma

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46
Q

what is graves disease

A

antibodies to TSH receptor called thyroid stimulating immunoglobulins (TSIs) stimulate the thyroid gland to excess

47
Q

how do TSI antibodies affect the thyroid gland compared to TSH

A

TSI antibodies have prolonged stimulating effect on thyroid gland lasting longer

48
Q

what do high levels of thyroid hormone secretion caused by TSI do

A

suppress anterior pituitary TSH secretion

49
Q

what type of endocrine disorder is graves disease

A

primary

50
Q

what are symptoms of hyperthyroidism

A

-exopthalmos
-fine hair
-nervousness
-restlessness
-emotional instability
-insomnia
-increased apatite
-fine tremor
- pretibial myxedma

51
Q

how is hyperthyroid treated

A

radioactive iodine thyroid ablation or antithyroid drugs. rarely surgery

52
Q

what medication is given in hyperthyroidism while awaiting resolution

A

propanolol- beta blocker

53
Q

what is L-thyroxine used for in hyperthyroidism

A

to prevent hypothyroidism in patients who have undergone ablation or surgery

54
Q

what are the oral symptoms of hyperthyroidism

A

-burning mouth syndrome
-gum disease
-excessive salivation
- weakening of mandible
- increased caries risk

55
Q

what is a thyroid storm

A

elevated thyroid hormone with stressful events or serious illness

56
Q

what are the symptoms of a thyroid storm

A

fever, tachycardia, elevated BP, nausea, vomiting, diarrhea, breathing problems

57
Q

what is contraindicated in patients with hyperthyroidism

A

administration of epinephrine

58
Q

what is hashimotos thyroiditis

A

autoimmune reaction against thyroid gland destroys gland

59
Q

what is the most common cause of hypothyroidism

A

hashimotos thyroiditis

60
Q

what is the first symptom of hashimotos

A

thyroiditis or thyroid inflammation

61
Q

what does thyroid inflammation lead to in hashimotos

A

fibrosis of thyroid resulting in decreased secretion of thyroid hormone

62
Q

what does goiter vs no goiter mean in hypothyroid states

A

goiter: iodine deficiency
no goiter: TSH deficiency

63
Q

is hypothyroidism due to iodine deficiency a primary or secondary endocrine disorder

A

primary

64
Q

is hypothyroidism due to TSH deficiency a primary or secondary endocrine disorder

A

secondary

65
Q

is goiter a primary or secondary endocrine disorder

A

primary

66
Q

what are the symptoms of hypothyroidism

A

-coarse, dry brittle hair
-loss of lateral eyebrows
-lethargy and impaired memory
- cold intolerance
-constipation
-weight gain

67
Q

when is myxedema seen

A

in severely hypothyroid patients

68
Q

what causes myxedema

A

increased quantities of hyaluronic acid and chondroitin sulfate bound with protein plus water accumulate in skin

69
Q

what are other characteristics of hypothyrodism

A

-low BMR
-low mental capacity
-low body temp
-low appetite
-low HR
-low RR
-low BP
-weight gain
-increased cholesterol and blood lipids

70
Q

what does the face look like with myxedema

A

dull,expressionless face with puffiness of eyelids. skin appears swollen, cool, waxy, dry, coarse

71
Q

what is cretinism

A

physical and mental retardation due to either congenital absence of thyroid gland or iodine deficient diet

72
Q

what is more inibited in cretinism: skeletal growth or soft tissue

A

skeletal growth

73
Q

what are the oral manifestations of hypothyroidism

A

-macroglossia
-dysgeusia
-delayed tooth eruption
-poor wound healing and increased risk of infection due to decreased activity of fibroblasts
-increased periodontal disease
-salivary gland enlargement

74
Q

where the bodys phosphate stored

A

85% in bones, 14-15% in cells, less than 1% in EC fluid

75
Q

where is calcium stored

A

-0.1% in EC fluid
-1% in cells
and rest in bones

76
Q

what does too low of calcium result in

A

neuronal hyperexcitability like carpal spasm

77
Q

what does too high of calcium result in

A

neuronal depression

78
Q

what are the control points for calcium and phosphate

A

-absorption- via intestines
- excretion- via urine and feces
- temporary storage- via bones as hydroxyapatite

79
Q

what hormones regulate plasma calcium

A

-PTH
-calcitriol
-calcitonin

80
Q

what does PTH do

A

-increases calcium
-decreases phosphate
-mobilizes calcium from bone
-increases renal absorption of calcium
-increases intestinal absorption of calcium

81
Q

what does calcitriol do

A

increase plasma calcium and increase phosphate

82
Q

what is the primary hormone that enhances intenstinal absorption of calcium

A

calcitriol

83
Q

what does calcitonin do

A

-decreases calcium
-decreases phosphate

84
Q

what is bone formation stimulated by

A

calcitonin, insulin, GH, IGF1, estrogen and testosterone

85
Q

what effect does vitamin D and PTH have on bone matrix

A

stimulates bone matrix resorption

86
Q

how do vitamin D and PTH stimulate bone matrix resorption

A

stimulates osteoclasts through RANKL

87
Q

what effect does calcitonin have on bone matrix

A

stimulates deposition

88
Q

how does calcitonin stimulate deposition

A

uses more OPG and inhibits osteoclast

89
Q

what are the risk factors for osteoporosis

A

vitamin D deficiency, secondary hyperparaythyroidism, inadequate calcium intake, glucocorticoid medications, reduced physical activity, estrogen deficiency

90
Q

what are the treatments for osteoporosis

A

-exercise
-PT
-estrogen
- calcium
-vitamin D

91
Q

what is PTH secreted by

A

chief cells

92
Q

what does PTH do

A

-increases plasma calcium by increasing intestinal absorption, decreasing renal excretion and increasing bone resorption
- decreased plasma phosphates by increased renal excretion

93
Q

what does decreased ECF Ca2+ concentration cause

A

increased rate of PTH secretion hypertrophy of parathyroid gland seen in pregnancy and rickets

94
Q

what does increased ECF Ca2+ cause

A

-decreased activity of Parathyroid gland
-decreased size of parathyroid gland caused by increased vitamin D intake

95
Q

how does PTH increase plasma calcium

A

-bone resorption
-reabsorption of calcium by renal tubules which reduced excretion
-converts to vitamin D to cause intestinal absorption

96
Q

how does PTH decrease plasma phosphate

A

decreased reabsorption by renal tubules leading to increased urinary excretion

97
Q

what organs are targets of PTH

A

kidneys, bone, intestine

98
Q

what is a precursor for calcitriol

A

vitamin D

99
Q

where and how long is vitamin D3 stored

A

in the liver for months

100
Q

how is calcitriol synthesized

A

stored in liver, activated in kidney by PTH where it results in intestinal absorption of calcium

101
Q

what is the main effect of calcitriol

A

absoprtion of calcium and phosphate

102
Q

how does calcitonin lower plasma calcium

A

by decreasing activity of osteoclasts, thus decreasing bone resorption

103
Q

does calcitonin have major control over calcium

A

NO

104
Q

what is primary hyperparathyroidism due to

A

parathyroid gland tumor

105
Q

what does extreme osteoclastic activity in primary hyperparathyroidism cause

A

cystic bone disease called osteitis fibrosa cystica

106
Q

what happens in osteitis fibrosa cystica

A

-hypercalcemia leads to polyuria and calcuria
- low phosphate due to increased renal excretion
- muscle weakness and easy fatigability
- osteoblastic activity also increased leading to high secretion of alkaline phosphatase

107
Q

what are the primary signs and symptoms of primary hyperparathyroidism

A
  • kidney stones and polyuria
    -psychic moans
    -abdominal groans
  • osteitis fibrosa in bones
108
Q

what is secondary hyperparathyroidism

A

High PTH levels occur as compensation for hypocalcemia not due to primary abnormality of parathyroid glands

109
Q

what are the causes of hypocalcemi

A

-vitamin D deficiency
- chronic renal disease - cannot make vitamin D3

110
Q

what does vitamin D deficiency cause

A

rickets in childre, osteomalacia in adults, and high PTH which causes bone resorption

111
Q

what is primary hypoparathyroidism caused mainly by

A

accidental surgical parathyroid gland removal

112
Q

what does parathyroid gland removal do to calcium levels

A

decreases plasma Ca levels from 10 mg/dl to 6-7 mg/dl

113
Q

what does hypocalcemia lead to

A

increases membrane Na+ permeability leading to neuromuscular excitability and muscle spasms and tetany

Physiology (41 decks)

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