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physiology 2 > thyroid physiology > Flashcards

thyroid physiology Flashcards

1
Q

thyroid is located

A 
wraps around the trachea 
larger in females 
increases in size with pregnancy 
two large lateral lobes connected by a thin isthmus 
contains 4x parathyroid glands 
receives very high blood flow 
abundant nerve supply
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2
Q

thyroid gland structure

A

follicles - hollow vissicles

THs are synthesised in epithelial cells lining the follicle

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3
Q

follicle interior is filled with

A

thyroglobulin (glycoprotein)

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4
Q

each follicle is surrounded by

A

dense capillary network

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5
Q

thyroid hormones are derived from

A

tyrosine amino acid

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6
Q

2 thyroid hormones

A

thyroxine - T4

triiodothyronine - T3

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7
Q

thyroxine

A

major secretory product
low biological activity
usually transformed to T3 within target cells

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8
Q

need for iodine to produce thyroid hormone

A

thyroid hormones need large amounts of iodoine

- low levels are absorbed int the body and absorbed as iodide and need to be oxidised to iodine (thyroid peroxidase)

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9
Q

iodide oxidation to iodine

A

by thyroid peroxidase

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10
Q

how does the thyroid gland concentrate iodine

A

powerful iodide pumps

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11
Q

thyroglobulin precursor TGB

A

large protein
has lots of tyrosine residues
stores thyroid hormones as a colloid (holds 4 or 5 hormone molecules)

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12
Q

thyroglobulin precursor molecule is made in

A

follicular cells and exocytosed into the follicle lumen

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13
Q

steps in thyroid hormone production

A
  1. iodide trapping
  2. synthesis of thyroglobulin
  3. oxidation of iodide and iodination of tyrosine residues
  4. coupling of tyrosine residues
  5. endocytosis and digestion of colloid
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14
Q

iodide trapping

A

sodium iodide symporter
pumps 2x Na and 1x I- from plasma into the follicle cells
concentration of iodide in the follicle is 30x plasma concentration

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15
Q

synthesis of TGB

A

made on rough endoplasmic reticulum

exocytosed into the colloid where it waits for iodine

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16
Q

pendrin

A

passive transporter

iodide transported into the follicular lumen where thyroid peroxidase can oxidise the iodide

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17
Q

once the iodide is oxidised

A

once it is oxidise it can be added to the tyrosine residues present on the thyroglobulin

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18
Q

iodination of tyrosine molecules forms

A

DIT - diiodotyrosine

MIT - monoiodotyrosine

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19
Q

coupling of tyrosine

A

forms either T4 or T3
mature hormone is still attached to TGB storage molecules in the follicle lumen
DIT + DIT = T4
MIT + DIT = T3

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20
Q

iodine availability

A

TGB allows storage of large amounts of Th precursor so the body becomes independent on day to day iodine availability

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21
Q

secretion of thyroid hormone

A

when stimulated thyroglobulin is exocytossed
endocytotic vesicles fuse with lysosomes
proteases release T3 and T4 released from TGB storage molecule
thyroid hormones migrate to the basal membrane
actively transported into the circulation via monocarboxylate transporter8

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22
Q

thyroid hormones are transported into the circulation by

A

monocarboxylate transporter 8

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23
Q

thyroid hormone is mosty released as

A

T4

24
Q

dominant plasma proteins binding thyroid hormones

A

TBG = thyroid binding globulin (main one)
transthyretin
albumin

needs to be unbound to work

25
Q

to work, thyroid hormone must be

A

unbound

26
Q

T3 half life

A

much shorter half life than T4

3.5 days

27
Q

T4 half life

A

6.5 days - longer

28
Q

thyroid hormones enter cells via

A

iodothyronine transporters
organic anion transporters
(passive, but probably involved ion exchange) OR monocarboxylate transporter (active transport - powerful scavenging)

29
Q

TH receptors

A

10x more affinity for T3

are ubiquitous

30
Q

T4 conversion to T3

A

deiodinase enzymes convert T4 to T3

31
Q

thyroid hormone functon

A

thyroid hormones bind intracellular nuclear receptors, and act to regulate the activity of specific genes

32
Q

control of thyroid function

A

hypothalamus releases thyrotropin releasing hormone TRH
acts on anterior pituitary to release thyroid stimulating hormone TSH
acts on the thyroid gland to release thyroid hormone T3 and T4

33
Q

hypothalamus stops anterior pituitary production of TRH with

A

somatostatin

34
Q

stimuli to increase thyroid function axis

A

cold

35
Q

thyrotropin releasing hormone stimulates production of

A

thyroid stimulating hormone / thyrotropin / TSH

36
Q

TSH binds

A

TSHR to increase cAMP

37
Q

TSHR

A

TSH receptor
increases cAMP
increases thyroid activity in 3 ways
- increases hormone synthesis (increases activity of sodium iodide symporter pump and thyroglobulin production)
- increases thyroid hormone secretion (vesicular reuptake and active transport)
- increases blood flow to the thyroid

38
Q

TH is main determinant of

A

basal metabolic rate

  • influences synthesis and degradation of CHOs, fats, and proteins
  • increases the sensitivity to sympathetic NS signal (increases receptors and receptor signal)
39
Q

why doesn’t ATP production cause negative feedback

A
  1. (burn it off) ion gradients are expensive
    TH increases the activity of pumps involved in Na/K across the plasma membrane and Ca2+ gradients between cytoplasm
  2. uncouple ADP phosphorylation in mitochondria - TH induces uncoupling protein expression which means protons are pumped but leak back out, burning fuel but not creating ATP

both these processes produce lots of heat

40
Q

CHO metabolism

A

T3 accelerates CHO utilisation by

  • increasing glucose absorption by the GIT
  • increasing glucose oxidation in liver, fat and muscle cells
  • amplifies signals from other signalling hormones (e.g. insulin)

T3 acts by increasing the synthesis of specific metabolic enzymes

41
Q

TH effects on lipid metabolism

A

optimal TH levels determine rates of lipolysis and lipogenesis in the liver
stimulates mobilisation from fat cells (increase n free fatty acids and decrease in plasma TG and cholesterol)

42
Q

TH effects on nitrogen metabolism

A

rate of protein synthesis and degradation is Th-dependant

43
Q

Th effect on temperature

A
  • energy utilisation
  • TH increases BAT theromegenesis
  • THs also act indirectly by stimulating the sympathetic nervous system to mobilise Cho and fat needed to fuel the shivering response and increase circulation to skeletal muscle and adjust blood flow to skin
44
Q

Th effect on cardiovascularr regulation

A

increase tissue blood flow

increase cardiac output (increase heart rate and contractility

45
Q

Th effects on skeletal system

A

T3 acts synergistically with growth hormone, IGF and other growth factors to signal increased bone formation
bone maturation ie. closing of epiphysis (cartilaginous growth plates of bones)

46
Q

TH effects of CNS

A

Th is essential for normal brain development

47
Q

primary hypothyroidism

A

hashimotos disease

  • lack of energy, problem with fatty acid mobilisation causing increase in body weight
  • decreased sensory capacity, impaired memory and psychosis may occur
  • poor tolerance of cold
  • oedema due to accumulation of water-retaining hyaluronic acid and condition sulphate
48
Q

TH deficiency in children

A
  • short stature, bone retardation, malformed facial bone structure
  • severe, irreversible mental and physical retardation (cretinism)
49
Q

treatment for goitre

A

thyroxine tablets

50
Q

most common cause of hypothyroidism

A

decreased dietary iodine

51
Q

deiodinase deficiency

A

cells can’t convert T4 to T3
hypothyroidism
goitre because negative feedback loop isn’t triggered

52
Q

severe selenium deificiency

A

deiodinases are selenoproteins - same as deiodinase deficiency

53
Q

allan-herndon-dudley syndrome

A

MCT8 mutations - cells can’t actively take up TH

  • particularly effects CNS - moderate to severe intellectual impairment, plus aphasia and ataxia
  • highly limited IQ, patients may never talk or walk, may need feeding tube
54
Q

hyperthyroidism

A

Graves’ disease
elevated metabolic rate and heat production - poor heat tolerance
increase protein degradation, severe catabolism of muscle, increase fatty acid mobilisation
exaggerated autonomic responses
goitre, high bone age, exophthalmos - oedematous fluid retention behind the eyes

55
Q

autoimmune hyperthyroidism

A

production of thyroid stimulating immunoglobulins that bind to the TSH receptor and activate increase in TH

56
Q

thyroid tumours

A

TH-secreting tumours are most common
treated with antithyroid drugs to decrease TH production by blocking coupling of iodine
or beta blockers
or radioiodine which concentrated in the thyroid and kill of thyroid cells

physiology 2 (21 decks)

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