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Physiology > Hypothalamic-Pituitary-Thyroid and GI Hormone Physiology > Flashcards

Hypothalamic-Pituitary-Thyroid and GI Hormone Physiology Flashcards

1
Q

what stimulates the thyroid gland?

A

cold temps of low concentration of hormones

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2
Q

what hormone does the hypothalamus release to stimulate the anterior pituitary gland?

A

thyroid releasing hormone

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3
Q

what hormone does the AP release to stimulate the thyroid gland?

A

Thyroid stimulating hormone (TSH)

aka thyrotropin

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4
Q

what are the two major thyroid hormones?

A

T4 and T3

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5
Q

what gland is known as the master gland of metabolism?

A

thyroid gland,

largest gland in the body

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6
Q

what things increase the size of the thyroid gland?

A

bigger in men
as you age it gets bigger
increase in body weight

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7
Q

what deceases the size of the thyroid gland?

A

iodine intake

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8
Q

what are the 3 characteristics of an inactive thyroid gland?

A

colloid (thyroglobulin)
follicles are large
cells lining follicle are flat

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9
Q

what are the 3 characteristics of an active thyroid gland?

A
  • small follicles
  • cuboidal follicle lining cells
  • edges are scalloped with many small resorption gaps resulting from the uptake of colloid
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10
Q

what are the two primary functions of the thyroid?

A
  • secretion of the two biologically active thyroid hormones T4 and T3
  • secretion of calcitonin by parafollicular cells (C cells)
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11
Q

what two things increase when thyroid hormones are released?

A

basal metabolic rate

heat production

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12
Q

what happens when blood calcium levels are high?

A

parafollicular cells release calcitonin, which inhibit the resorption of bone by osteoclasts

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13
Q

what are the three key hormones that regulate calcium levels?

A
  • 1,25 dihydroxycholecalciferol (vitamin D steroid hormone)
  • Parathyroid hormone (chief cells in parathyroid glands in response to low blood calcium)**stimulates osteoclasts
  • calcitonin (parafollicular cells in response to high calcium) **inhibits osteoclasts
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14
Q

T4 and T3 are synthesized from what?

A

iodine and tyrosine

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15
Q

where is T4 produced?

A

exclusively in the thyroid gland

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16
Q

where is T3 produced?

A

extrathyroidally from T4
60% liver
20% intestines
20% converted to inactive form of T3 (rT3)

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17
Q

which is more potent T3 or T4

A

T3 is 4x more potent than T4, because the vast majority of T4 produced gets quickly converted to T3 peripherally once hormones are released from thyroglobulin stores

18
Q

what enzyme makes the active form of T3 from T4?

A

5’ de-iodinase enzyme
**note the prime
made mostly in the liver

19
Q

what enzyme makes the inactive form of T3 (rT3) from T4?

A

5-de-iodinase enzyme
**note there is no prime
made mostly in the liver

20
Q

feedback inhibition at the level of the anterior pituitary most efficiently inhibits what?

A

thyroid releasing hormone

21
Q

which hormone can act independently of HPT Axis regulation?

A

T3, because it is made extrathyroidally

22
Q

without sufficient iodine, thyroid hormones are not released. What builds up and what happens to the thyroid?

A

TSH builds up leading to oxidative stress leading to hyperplasia and dysplasia of epithelial cells lining the follicles (goiter)

23
Q

what is the thyroid hormone mechanism of action?

A

binds to nuclear receptors that act as hormone activated transcription factors
-thyroid hormones act by modulating gene expression to direct protein synthesis

24
Q

what is the name of the protein in which T3 and T4 are stored?

A

thyroglobulin (TGB)

25
Q

what are the only cells in the body that can absorb iodine?

A

thyroid cells

26
Q

what is goiter?

A

the result of excess growth when thyroid cells are exposed chronically to too much TSH or HCG
-may also occur from iodine deficiency, pregnancy or Hashimoto’s disease

27
Q

common goitrogens?

A
  • medications that may promote goiter often by interfering with iodine uptake in the thyroid gland
    eg: anti-thyroid meds, sulfonamide antimicrobials, amiodarone, lithium, salofalk
  • Environmental compounds eg: mercury, arsenic, nitrates
28
Q

Iodine deficiency disorder (IDD)

A

patients commonly present with goiter or diffuse thyroid enlargement
-if goiter gets large enough, patients may complain of compressive symptoms, such as: hoarseness, shortness of breath, couch, dysphagia

29
Q

Congenital hypothyroidism (Cretinism)

A

most extreme IDD
due to deficiency of iodine in the mother’s diet during pregnancy resulting in fetal and/or neonatal hypothyroidism from birth

30
Q

signs and symptoms of cretinism

A 
growth retardation
reduced BMR
large tongue
coarseness of skin 
dry brittle hair
premature tooth loss
infertility
31
Q

how can both too much and too little thyroid hormone lead to goiter?

A
  • Hashimoto’s disease: autoimmune hypothyroidism which results in damage and under production of thyroid hormone production. Causes AP to release too much TSH
  • Grave’s disease a autoimmune hyperthyroidism with exopthalmos(bulging eyes). Abs attack thyroid, thyroid defensively overproduces thyroid hormones leading to goiter
32
Q

the regulation of GI function involves what types of communications?

A

endocrine
paracrine
neurocrine

33
Q

what hormone can act in endo, para, and neurocrine function?

A

cholecystokin (CCK)

34
Q

what essential to normal GI functions?

A

balance of + and - hormonal regulation

35
Q

the brain in your gut is known as what?

A

enteric nervous system

36
Q

where are there no nerves of the enteric nervous system?

A

lumen of the gut

37
Q

what is the source, stimuli for release and action of gastrin hormone?

A
  • source: G cells of stomach
  • stimuli for release: stomach distention, peptides in gastric lumen
  • action: stimulates parietal cells to release acid and proliferation of gastric mucosa
38
Q

what is the source, stimuli for release and action of cholecystokinin (CCK)?

A
  • source: I cells in mucosa of duodenum and jejunum
  • stimuli for release: digestive products of fats, fatty acids, monoglycerides
  • action: contracts gall bladder to expel bile to sm. intes.
39
Q

what is the source, stimuli for release and action of secretin hormone?

A
  • source: S cells of duodenum mucosa
  • stimuli for release: acidic pH in lumen of sm. intes.
  • action: stimulates pancreas to release bicarb
40
Q

what is the source, stimuli for release and action of gastric inhibitory peptide?

A
  • source: mucosa of upper sm. intes
  • stimuli for release: fatty acids>AAs>carbs
  • action: inhibits gastric secretions and motility. increases insulin release when duodenum is overloaded with food and when BG is elevated
41
Q

what are the three major pancreatic hormones?

A

glucagon
insulin
somatostatin

42
Q

what does somatostatin do?

A
  • slows production of insulin, glucagon, gastrin and other hormones
  • basically puts the brakes on digestion
  • excess leads to diabetes

Physiology (14 decks)

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