Thyroid gland Flashcards

1
Q

What does hypo release which acts on pituitary

A

TRH

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2
Q

What does pituitary release which acts on THG

A

TSH

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3
Q

Thyroid glands

A

C cells release calcitonin which regulates Ca2+ homeostasis

THG releases thyroid hormones

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4
Q

Thyroid hormones

A
Thyroxine (T4)
Tri iodothyronine (T3)
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5
Q

What’s required for action of THG

A

Dietary iodine

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6
Q

Thyroid hormones action

A

Act on nuclear receptors to regulate gene transcription (TRE’s- thyroid response element) in target genes

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7
Q

Effect on metabolism

A

protein (lipid, carbohydrates) metabolism
Leading to growth

Body weight effects

Regulated BMR

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8
Q

THG structure

A

L and R lobes
Well vascularised

Has thyroid follicles which store thyroglobulin (tyrosine residues). This is stored in the centre of follicles, and the follicle cavities are surrounded by epithelial cells , where synthesis of hormones takes place.
Core contains protein rich element: colloid
C cells adjacent to follicles
Blood vessel capillaries directly associated with follicle cells, allowing direct release of hormones into the blood

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9
Q

TH synthesis

A

Iodination of tyrosine occurs at 2 sites either to form MIT (mono-iodotyrosine) or DIT (di-iodotyrosine)

Then there is coupling of MIT and DIT to make T4/T3

Tyrosine residues bolted together to form Thyrogobulin

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10
Q

T4

A

thyroxine

DIT +DIT

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11
Q

T3

A

Triiodothyronine

DIT +MIT

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12
Q

What happens after formation of T3 and T4

A

Iodinated thyroglobulin enters lumen (colloid) by exocytosis, from epi follicle cells where it is synthesised
Stored thyroglobulin re-enters follicle cells by endocytosis
Lysosomal enzymes release T3 and T4
MOst are bound by binding proteins in plasma
‘Free’ fraction of T3 and T4 can enter target tissues

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13
Q

Inside the follicle cells

A

Tyrosine residues form thyroglobulin
Iodine taken up by iodide transporters into cells- cotransported with NA ions
Peroxidases iodinate tyrosine residues under influence of thyroid peroxidase
When you need thyroid hormone it is endocytosed back into the cell where T3 and T4 are liberated by lysosomal digestion (from thyroglobulin) and released into the blood
Remaining tyrosine residues recycled (ie make throglobulin again)
Whole process requires TSH to be released fro pituitary- lysosomal digestion occurs under influence of TSH

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14
Q

TRH (Hypo) under influence of

A

GH (-ve)
Cold (+ve)
Sympathetic activation (+ve)
Cortisol (-ve)

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15
Q

TSH (anterior pituitary) under influence of

A

TRH (+ve)

Somatostatin (-ve)

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16
Q

Incr TSH causes

A

Incr I uptake, incr T3 and T4 synthesis in thyroid gland- released into blood

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17
Q

T3 and T4 feedback

A

+ve onto Somatostatin

-ve onto TRH release and TSH

18
Q

TSH

A

TH production requires TSH
+ iodine uptake from blood by pump
+ TH synthesis by iodinase
+ thyroglobulin breakdown by lysosomal proteases

19
Q

TH’s involved in

A

Growth and development
Stimulate protein, carbohydrate and lipid metabolism
Regulate energy metabolism
Body temp
Regulation of nervous system, CV, musculo-skeletal and reproduction

20
Q

Actions of TH’s

A

Most is released as T4
Most of both T3/T4 are bound by thyroid binding globulin rest by thyroid binding prealbuin
Only unbound T3 and T4 can enter target tissues
Most physiological effects of TH’s are due to T3

21
Q

TH receptors

A

regulate gene transcription

22
Q

Actions of TH’s on mitochondria

A

receptors incr in size and number
Incr ATP production due to binding to receptor
Nuclear receptor increases transcription and translation via TRE’s
Incr in enzyme synthesis

23
Q

Effect of TH’s on BMR

A

BMR= amount of calories body needs at rest

Stimulates BMR to incr over days

24
Q

How does TH incr BMR

A

TH’s enter cell, bind to TH receptors, stimulating synthesis of NA+/K+ ATPase
Leads to incr heat production, so incr BMR

Also, TH binding leads to incr size, number and SA of mitochondria- incr rate of ATP production (same affect on heat –> incr BMR)

25
Q

How does TH stimulate protein metabolism

A

TH binding to TH receptor triggers incr protease synthesis, incr protein breakdown, more energy expenditure, so incr BMR

Also stimulates incr protein synthesis, so tissue growth

catabolic/anabolic balance as TH is dose dependent

26
Q

Low TH

A

anabolic

27
Q

High TH

A

catabolic

28
Q

How does TH stimulate carbohydrate metabolism

A

T3/T4 binding to TH receptor
Leads to general incr in enzyme synthesis:
- incr release of insulin, leads to incr glycogenesis
- Incr glucose uptake by GI tract, liver and muscle
- Incr gluconeogenesis
-Incr glycogenolysis

Balance of gluconeogenesis/glycogenolysis is TH dose-dependent

29
Q

How does TH stimulate fat metabolism

ADD

A

TH binding to receptors stimulates incr lipoprotein receptors on liver cells, so incr cholesterol secretion, and decr plasma cholesterol

Also incr lipase synthesis, so incr lipid metabolism, so incr plasma free fatty acids

30
Q

Physiological effects of TH

A

Body weight:decreased, incr appetite
CV: incr CO, positive inotropic vasodilation, incr BV, incr pulse pressure
Respiration: incr depth, incr rate
Muscle: incr tension, incr force of contraction
CNS: incr excitability, incr speed of thought
GI tract: incr secretions, incr motility

31
Q

Underactive TG

A

high colloid levels
incr TSH- lose negative feedback onto it
flattened cells
Storing more thyroglobuln

32
Q

HIghly active TG

A

low colloid levels

columnar cells

33
Q

Hypothyroidism

A
incr TSH due to incr TRH
decr T4/T3
Caused by autoimmune disease, iodine deficiency, altered H-P activity
Swelling of TG (not always)
fatigue
lose thyroid hormone negative feedback
34
Q

Hypo factors

A

Bodyweight: incr, decr appetite
GI: constipation
CNS: sluggish mentally, fatigue, somnolence
Muscle: weakness, stiffness, swelling
Trophic effects: decr hair growth, loss of hair, scaly skin, brittle nails
CV: decr CO, decr force of contraction, decr rate “, decr BV, heart enlargement and arteriosclerosis
Other: husky voice, myxedema, decr fertility incr menstruation, cold intolerance

35
Q

Hyperthyroidism

A

Gland incr in size and incr rate of secretion
Largely autoimmune disease- graves disease- antibodies bind to TSH receptors and continually activate them
May also be caused by thyroid adenoma secreting lots of TH

36
Q

Hyperthyroidism factors

A

Bodyweight: decr, incr appetite, incr food intake
CV: CO, incr contraction force and rate, incr BV, vasodilation, atrial arrthymias , congestive heart failure
Trophic effects: excess hair growth, separation of fingernails, hair loss
GI tract: incr bowel movements
CNS: nervousness, irritability, emotional instability, sleeplessness
Other: fatigue, myedema, expothalmus,amennorhea, heat intolerance, sweating

37
Q

T4 conversion into T3

A

by deiodonases (enzymes) in target cells

38
Q

Major thyroid hormone

A

T3

39
Q

thyrosine peroxidase

A

oxidises iodides and attaches them to tyrosines on thyroglobin

40
Q

Goiter

A

enlarged THG

41
Q

Where in the cell are receptors for TH present

A

nucleus