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physio fall midterm > Endocrinology Lecture 2 > Flashcards

Endocrinology Lecture 2 Flashcards

1
Q

is the thyroid gland vascular?

A

YES, HIGHLY vascular

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2
Q

the internal structure of the thyroid gland is a series of _______

A

hollow follicles formed by spheres of epithelial cells and filled with colloid

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3
Q

Epithelial cells are also called ________ and regulate ______

A

follicle cells; the production of two iodine-containing hormones

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4
Q

Thyroid hormones are ___________ and thus cannot __________

A

LIPOPHILIC; be stored in secretory vesicles

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5
Q

Thyroid hormones is synthesized

A

EXTRAcellularly in the colloid and CAN be stored in the colloid

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6
Q

Synthesis of thyroid hormones

A
  • Buckle in, it’s long
    1. Iodide is transported across basal side of follicle cells via Na/I transporter
    2. Iodide diffuses down concentration gradient across apical membrane into colloid of follicle (sequestered in colloid)
    3. Follicle cells synthesize large TYROSINE rich protein called thyroglobulin (TG) and enzyme thyroid peroxidase –> both exocytosed across apical membrane into colloid
    4. in colloid, Iodide oxidized by thyroid peroxidase and linked to TG –> this maintains conc. gradient needed by step 2 to sequester I in colloid
  • If 1 Iodide is added to tyrosine residue = monoiodotyrosine (MIT), if 2 added = diiodotyrosine (DIT)
    5. 2 DITs make thyroxine/tetra-iodothyronine/T4, 1 DIT plus 1 MIT makes Triiodothyronine/T3 phew that’s it, sorry for the length
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7
Q

secretion of thyroid hormones is stimulated by

A

thyroid stimulating hormone/TSH (shocker)

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8
Q

TSH is released from

A

anterior pituitary

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9
Q

TSH is released in response to

A

thyroid releasing hormone/TRH from the hypothalamus

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10
Q

TSH receptors are on

A

follicle cells

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11
Q

TSH acts to

A

increase synthetic activity of follicle cells and stimulate hyperplasia

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12
Q

Secretion of thyroid hormone

A
  • Another long one
    1. in response to TSH, droplets of colloid containing TG + T3/T4 are pinocytosed into follicle cells
    2. droplets fuse with lysosome containing enzymes that cleave T3 and T4 from the TG
    3. T3 and T4 released in cytoplasm by lysosomal hydrolysis
    4. T3 and T4 diffuse into capillaries –> AAs from degraded TG recycled into new TG
  • **TH has NEGATIVE FEEDBACK ACTION to regulate its secretion at hypothalamic and pituitary level
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13
Q

__________ of the thyroid hormone secreted from the thyroid gland is T3

A

10% –> it is 10x more biologically active than T4

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14
Q

__________ of the T4 secreted is converted into __________ in the _________ and __________

A

80%; T3; liver; kidney

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15
Q

Secreting mostly T4 then converting it into T3 in the circulation __________

A

maximizes the concentration gradient for free Iodide between blood (high) and colloid (low)

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16
Q

TH has __________ different receptor types

A

four; alpha type 1 & 2 and beta type 1 & 2

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17
Q

alpha type 2 receptor

A

does not bind T3 or T4; it is an inactive receptor

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18
Q

Receptors occupied by TH will

A

dimerize and form a DNA binding protein that regulates gene transcription

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19
Q

Unbound receptor dimers (aka absence of thyroid hormones) can

A

bind DNA and typically INHIBIT transcription

20
Q

The principle effect of TH is

A

to STIMULATE cellular metabolism:

  1. increase Na/K ATPase activity
  2. increase synthesis of respiratory enzymes
  3. increase substrate availability
  4. increase cellular heat production
  5. effects on mitochondria
21
Q

other effects of TH

A
  1. upregulation of Beta adrenergic receptors –> activation of the sympathetic nervous system
  2. increases sensitivities to catecholamines in both endocrine and nervous sytems
  3. regulates production of growth hormone: necessary esp. in bone
  4. important CNS development and function: growth cones and myelination of axons
22
Q

__________ is the most common of endocrine diseases: most conditions are due to __________

A

Thyroid disease; hypothyroidism

23
Q

True or False: thyroid disease affects women more than men

A

TRUE. sorry ladies

24
Q

An enlarged thyroid, hypo- and hyperthyroidism can lead to development of a

A

goiter

25
Q

Hypothyroidism is most often caused by

A

a primary defect in the thyroid gland; 95% of cases involve an iodine deficiency/damage to the gland

26
Q

without iodine, there is

A

insufficient production of TH –> lack of negative feedback increases TRH and TSH secretion –> growth of a goiter in response to TH stimulations (encourages growth of follicle cells)

27
Q

Consequences of iodine deficiency during prenatal development:

A

moderate deficiency (10-15 pt IQ reduction), cretinism, miscarriage or stillbirth

28
Q

cretinism

A

due to insufficient iodine by mother during pregnancy. cannot be reverse postnatally

29
Q

other PRIMARY defects leading to hypothyroidism

A
  • autoimmune thyroiditis (interferes with TH synthesis)
  • damage/destruction of the gland (radiation)
  • dysfunction associated with other illness (viral infection)
  • must be treated with exogenous TH bc gland cannot make TH
30
Q

secondary defects arise from

A

deficits in TRH/TSH synthesis and release or receptor deficits (basically, the gland is not receiving the proper stimulatory input)

31
Q

general symptoms of HYPOthyroidism

A
  • abnormal circulating concentration of TH and TSH
  • goiter develops if hypothyroidism is due to a PRIMARY defect
  • cretinism and mental retardation if condition existed during development
32
Q

symptoms of mild hypothyroidism

A

sensitivity to cold and slight weight gain

33
Q

symptoms of moderate hypothyroidism are due to

A

the effects of reduced BETA-adrenergic receptors and disruption of responses to catecholaminergic stimulation. Effects include fatigue, reduced bloodflow, changes in skin tone, sluggish GI motility and mental function

34
Q

what condition associated with severe hypothyroidism?

A

Myxedema: severe bloating due to accumulation of glycosaminoglycans in extracellular/interstitial fluid; most obvious in face

35
Q

HYPERthyroidism/thyrotoxicosis results from

A

having too much TH; much LESS COMMON than hypothyroidism

36
Q

hyperthyroidism can be caused by

A

primary defects such as thyroid tumors

37
Q

Graves disease

A

an autoimmune disease that is a common cause of hyperthyroidism; antibodies (abs) produced against TSH & these abs activate the TSH receptor –> leads to no feedback regulation of thyroid function

38
Q

True or False: TH concentrations are low in graves disease

A

FALSE: TH concentrations are HIGH even though TSH and TRH are low due to the feedback effects of increased TH

39
Q

thyrotoxicosis factitia

A

hyperthyroidism caused by consuming excess thyroid hormone in either medication or badly processed meat

40
Q

secondary defect causing hypertyroidism

A

tumors that secrete TSH without responding to feedback control by TH

41
Q

symptoms of hyperthyroidism

A
  • abnormal circulating concentrations of TH (high) and TSH (low)
  • goiter in Graves disease due to hyperstimulation of the TSH receptor (***TSH levels are low, abs are mimicking action of TSH)
  • heat intolerance, weight loss, increased appetite, sweating, and hypersensitivity of catecholaminergic responses –> general increase in activity of sympathetic nervous system; “thyroid storm”
  • ocular symptoms: exopthalmy, lid lag, decreased visual acuity (bc blood flow is regulated by beta adrenergic receptors)
42
Q

exopthalmy

A

symptom of hyperthroidism –> ab has effect on connective tissue behind eye and it bulges

43
Q

what are the treatments for hyperthyroidism?

A
  • surgical removal of gland
  • destruction using radioactive iodine
  • drugs that inhibit iodination of tyrosine, block release of TH, or lessen effects of TH in peripheral tissues
44
Q

in dental patients, cretinism can be associated with what?

A

retarded tooth development and maxillary prognathism

45
Q

in dental patients, symptoms of hypothyroidism include

A
  • exaggerated response to narcotics and barbiturates due to inadequate counteracting response from the sympathetic nervous system
  • myxedema leading to swelling of lips and tongue
  • diminished cardiac and respiratory function bc of lack of beta adrenergic receptors –> patients susceptible to hypothermia and hypotension

physio fall midterm (12 decks)

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