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Physiology Block III > Thyroid & Parathyroid > Flashcards

Thyroid & Parathyroid Flashcards

1
Q

How does increased TH effect Oxygen consumption and heat production in everywhere except the brain?

A

INCREASE

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2
Q

The lumen of the thyroid cells are filled with:

A

Colloid (thyroid hormones attached thyroglobulins)

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3
Q

Where is the increased heat coming from in response to thyroid hormone?

A

Since it’s controlling rate of the Na/K pumps, the heat is coming from the ATP burning

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4
Q

Where is the site of synthesis of thyroid hormone within the thyroid cell?

A

The colloid - the home of thyroglobulin

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5
Q

Thyroid follicle has a basal membrane which is exposed to ______ and the apical membrane exposed to the _____.

A

blood, lumen

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6
Q

What is the most RELEASED form of TH?

A

T4

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7
Q

What is the most ACTIVE form of TH?

A

T3

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8
Q

What is the 3 or 4 after T in reference to?

A

The number of iodines attached

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9
Q

Is tyrosine an ESSENTIAL AA?

A

No, body can synthesize it

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10
Q

What is the LIMITING AGENT for thyroid synthesis?

A

Iodide (need it from diet)

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11
Q

What is the enzyme that removes a Iodide, creating an active T3 form?

A

5’ - iodinase

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12
Q

If a patient is HYPERTHYROID, what could be do to the enzyme creating T3 to treat?

A

INHIBIT it, keep more in T4 form (decreasing active T3)

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13
Q

How do we bring TYROSINE into the epithelium from the BL membrane?

A

via Na-symporter (is an AA)

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14
Q

How do we bring IODIDE into the epithelium from the BL membrane?

A

via Na-symptorter

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15
Q

In order to move the IODIDE into the colloid, what is necessary to do to it?

A

Needs to be converted to ioDINE (I2) form via peroxidase and will diffuse out into the colloid lumen

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16
Q

How many tyrosine’s get added to the THYROGLOBULIN molecule?

A

2 = creates the SCAFFOLDING for TH

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17
Q

What is the compound called when 1 iodine binds to tyrosine?

A

MIT = monoiodotyrosine

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18
Q

What is the compound called when 2 iodine binds to tyrosine?

A

DIT = diiodotyrosine

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19
Q

DIT + DIT + Thyroglobulin =

A

T4

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20
Q

MIT + DIT + Thyroglobulin =

A

T3

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21
Q

How does thyroid hormone get back out to the blood circulation?

A

Endocytosed back into epithelium and fuses with LYSOSOME and releases T3 & T4 off and then exits out to blood because lipid soluble

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22
Q

Once T4 reaches target cells and gets deiodinated to T3, and acts on cell nucleus to do what intracellularly?

A 
INCREASE:
mitochondria,
Na/K ATPase pumps,
Enzymes,
O2 consumption,
Metabolic rate
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23
Q

Since TH is the PRENATAL controller of growth, what do we see in a child born in the absence of TH?

A

Cretinism

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24
Q

What effect does TH on beta-receptors?

A

INCREASES them

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25
Q

How do epinephrine and TH work together?

A

Since TH increases the beta receptors it increases the effect of epinephrine – increase CO, etc

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26
Q

How does TH increase the kidney function?

A

Due to increased metabolism, have more nitrogen waste and needs to rev the kidneys up to excrete it

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27
Q

TSH stimulates the thyroid gland to secrete TH, where does TSH come from?

A

Anterior Pituitary

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28
Q

TRH stimulates the Anterior Pituitary to secrete TSH, where does TRH come from?

A

Hypothalamus

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29
Q

What 2 locations do high levels of TH can FEEDBACK on to decrease TH production?

A

Anterior Pituitary,

Hypothalamus

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30
Q

If the body needs TH, then what will it do to the individual follicular cells in the thyroid gland?

A

Increase their size and replication - can see growth of thyroid gland

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31
Q

How are TH levels affected with PREGNANCY?

A

Make more thyroglobulin when pregnant and will stimulate T3 and T4 production because lowering the levels in the blood (because it’s bound up!)

32
Q

How are TH levels affected with LIVER DISEASE?

A

Make LESS thyroglobulin and less bound (more free), so will INHIBIT TH production

33
Q

How are TH levels affected by the IMMUNE SYSTEM?

A

immune system can create a substance that looks just like TSH to the thyroid gland, and will STIMULATE TH production.

34
Q

What is the effect of TOO MUCH Iodine?

A

Will down-regulate TH production

35
Q

T/F. A hyperthyroid individual has symptoms similar to a person with an adrenal medullary tumor.

A

True (increased epinephrine production - they work in permissibly)

36
Q

Most of the increased TEMP in HYPERthyroidism is produced where?

A

LIVER

37
Q

What is an uncontrolled growth of a thyroid gland called?

A

GOITER

38
Q

Goiter results from:
A. Hyperthyroid
B. Hypothyroid
C. Both

A

BOTH

39
Q

What is the mechanism of HASHIMOTO’s Disease, and do we expect to feel thyroid gland on palpation?

A

AUTOIMMUNE destruction of thyroid gland itself/

Yes, will be firm

40
Q

What effect does Low T3,4 have on TSH production?

A

Less negative feedback, so TSH increased by anterior pituitary

41
Q

What do we expect hormone levels to be if we have IODINE Deficiency?

A

LOW T3, T4

HIGH TSH

42
Q

What is the mechanism of GRAVES disease? and what do we expect hormone levels to be?

A

Autoimmune mimicking immunoglobulin stimulates the thyroid:
HIGH T3, 4 (so high negative feedback)
LOW TSH

43
Q

T/F. Graves disease is not influenced by negative feedback, from high thyroxine levels.

A

TRUE - is non functional feedback

44
Q

What physical exam finding do you find on the face in HYPERTHYROIDISM?

A

Exopthalmos

45
Q

Hyper or Hypo:

  • weight loss
  • goiter
  • sweating
  • more urea in urine
A

HYPER

46
Q

Hyper or Hypo:

  • weight gain
  • drooping eyelids
  • goiter
  • brittle nails
  • cold sensitivity
A

HYPO

47
Q

Who are the “keepers of calcium”?

A

Parathyroid glands

48
Q

Beside regulation of calcium, what else does parathyroid regulate?

A

Phosphate

49
Q

Parathyroid glands secrete _____, the calcium regulating hormone.

A

PTH - parathyroid hormone

50
Q

How much of total calcium is protein-bound, which protein?

A

40% to Albumin

51
Q

Since Albumin in negatively charged, in addition to binding calcium, it also binds what?

A

Protons

52
Q

What is the result of ACIDOSIS on Free Calcium?

A

Protons will outcompete Ca, and Albumin will release Ca and INCREASE levels = HYPERcalcemia

53
Q

Consequence of HYPOcalcemia?

A

INCREASED excitability of plasma membranes

54
Q

Consequence of HYPERcalcemia?

A

Cardiac ARRTHYMIAS and DECREASED excitability of membranes

55
Q

In response to LOW calcium, the parathyroid gland INCREASES PTH secretion, which targets which 3 tissue types?

A
  1. BONE
  2. KIDNEYS
  3. INTESTINE
56
Q

What effect does PTH have on BONE?

A

Increase RESORPTION

57
Q

What effect does PTH have on KIDNEYS?

A

Increase Ca REABSORPTION

Increase Vit D PRODUCTION

58
Q

What effect does PTH have on INTESTINES?

A

Increase Ca ABSORPTION from diet

59
Q

What cells in the bone DISSOLVE aka resorb bone?

A

osteoCLASTS

60
Q

What are the bone FORMING cells?

A

OsteoBLASTS

61
Q

2/3 of bone mass is crystals of calcium and phosphate, called:

A

Hydroxyapatite

62
Q

Hormones that favor bone FORMATION: (decrease Ca levels)

A 
Insulin
GH
IGF-1
Estrogen & Testosterone
Calcitonin
63
Q

Hormones that favor bone RESORPTION: (decrease Ca levels)

A

PTH
Cortisol
TH (T3,4)

64
Q

Which bone cells have the receptors for PTH?

A

OsteoBLASTS (formation cells)

65
Q

T/F. Most of the calcium you eat is Absorbed.

A

False - is under hormonal control, ca absorption is vitamin D dependent

66
Q

Plasma Vitamin D comes from which 2 sources?

A
  1. Diet

2. Sunlight

67
Q

Plasma Vit D needs to be hydroxylated TWICE in order to be active. Where does this happen?

A

First in LIVER

Second in KIDNEYS (increased with PTH)

68
Q

What is the mechanism for which Vit D INCREASES Ca absorption?

A

D generates MORE Calbindin, which binds up intracellular Ca and keep the concentration gradient up for more Ca to come in!

69
Q

What is the RATE-LIMITING step in Activating Vit D?

A

The 2nd hydroxylation at the KIDNEYS, this enzyme is stimulated by PTH

70
Q

What happens to bone REFORMATION as we age?

A

DECREASES - increased risk of fractures from osteoporosis

71
Q

When bone is broken down to increase Ca levels, what other levels rise in the plasma?

A

Phosphate

72
Q

How does PTH and the kidneys manage this increased rise in Phosphate after bone resorption?

A

PTH inhibit reabsorption of P and you pee it out!

73
Q

What hormone is an ANTAGONIST of PTH at bone? What is it’s effect?

A

Calcitonin - inhibits osteoclasts, therefore bone resorption

74
Q

A tumor in the parathyroid gland can secrete unregulated PTH levels, and not suppressed by high Ca levels, so become HYPERCALCEMIC but the excess PTH will do what?

A

INCREASE bone resorption + kidney absorption + vitamin D

75
Q

Other causes of HYPERcalcemia?

A

Autoimmune - PTHrp mimicks PTH

Excessive ingestion of Vit D

76
Q

What is the effect of pseudohypoparathyroidism?

A

in presence of normal PTH in blood (similar to insulin in type 2 diabetes) problem is in the receptors! resistance to them on bone or on blasts or proximal tubule of kidney = HYPOCALCEMIA

Physiology Block III (8 decks)

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