Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SGUL - Physiology 1 > Thyroid Gland > Flashcards

Thyroid Gland Flashcards

1
Q

Give a brief overview of thyroid function.

A
  • essential for normal development, especially the CNS and bone
  • essential for normal metabolism of many body tissues
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the functions of the different cells in the thyroid?

A
  • Follicular cells synthesise and secrete thyroid hormone.
  • Colloid is where TH is stored.
  • C-cells secrete calcitonin - to reduce plasma Ca2+
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Thyroid hormones are derived from two iodinated tyrosine molecules.
Describe two thyroid hormones learnt.

A

T4: major form released to blood, less active (prohormone)
T3: active form, converted in target cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the steps to TH synthesis? PART 1

A
  • Active uptake of I- across the basolateral membrane, against the concentration gradient. Done by the Na/I symporter, and stimulated by TSH.
  • Iodide efflux (by diffusion) then occurs across the apical membrane via pendrin exchanger
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the steps to TH synthesis? PART 2

A
  • At the extracellular apical membrane, iodide is oxidised to iodine and covalently bind to tyrosine residues within thyroglobulin (TG) macromolecules.
  • Requires TPO and H2O2.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the steps to TH synthesis? PART 3

A
  • Tyrosine residues may be iodinated in one (mono-iodotyrosine, MIT) or two (DIT) positions.
  • Coupling of iodotyrosine residues produces T4 (DIT-DIT) and a smaller amount of T3 (DIT-MIT). Catalysed by TPO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the steps to TH release? PART 1

A
  • Under influence of TSH, colloid droplets consisting of thyroid hormones within TG molecules are taken back up into the follicular cells by pinocytosis.
  • Fusion of the colloid droplets with the lysosomes causes hydrolysis of TG and release of T3 and T4.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do thyroid hormones circulate?

A
  • Bound to plasma proteins.
  • Mainly TBG (~70%), transthyretin (10-20%) and albumin (10-20%).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How do thyroid hormones act on target tissues? PART 1

A
  • TH receptors (TRs).
  • Belong to the nuclear receptor superfamily - high affinity for T3
  • Ligand-activated transcription factors.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How do thyroid hormones act on target tissues? PART 2

A
  • Activation requires dimerisation with another TR or a retinoid X receptor (RXR).
  • TRs are encoded by two genes: TR α and TR β.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the metabolic regulation of THs.

A
  • Done by selenodeiodinases, abbreviated to D1-3.
  • Used selenium as their trace element, so it is essential in the diet.
  • Regulate the amount of T3 available to bind with the receptor.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Outline the functions of the selenodeiodinases.

A
  • Activate by converting T4 to T3 (D2)
  • Inactivate by converting T3 to T2 (D3)
  • Inactivate by converting T4 to rT3 (D3).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are some ways TH increases metabolic rate?

A
  • affects number and size of mitochondria, enzymes, Na/K ATPase activity, etc.
  • positive inotropic and chronotropic effects on the heart
  • synergises with the sympathetic nervous system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some ways TH is involved in energy metabolism?

A
  • antagonises insulin signalling
  • gluconeogenesis, lipolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe how TH moves across the membrane.

A
  • HYPOTHESIS: TH diffused across the cell membrane to work.
  • TRUTH: TH transporters are required to allow TH across membrane e.g MCT8.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What genetic mutation is MCT8 linked to?

A

Allan-Herndon-Dudley Syndrome

17
Q

Describe the role of the hypothalamic-pituitary-thyroid axis.

A
  • Negative feedback control of thyroid hormone synthesis and secretion
  • Hypothalamic neurosecretory cells release TRH into the portal capillaries.
  • TRH stimulates thyrotrophs of the anterior pituitary to secrete TSH.
18
Q

What happens with high levels of T4 and T3?

A
  • Release of TSH and TRH are turned down.
19
Q

Describe congenital hypothyroidism.

A
  • Inadequate thyroid hormone production in neonates.
  • Occur because of anatomic defects in gland, an inborn error of thyroid metabolism, or iodine deficiency.
20
Q

How is congenital hypothyroidism investigated and treated in neonates?

A
  • Preventable with a simple neonatal heel prick before testing for TSH levels.
  • Possible congenital hypothyroidism if the levels of TSH are high.
21
Q

Describe the TSH receptor and its actions.

A
  • G-protein coupled receptor
  • Done through Adenylate Cyclase (αGs and the cAMP-PKA cascade).
  • Leads to iodide uptake, the transcription of NIS (Na+/I- symporter), TG and TPO, etc.
22
Q

What are the actions of TSH?

A
  • increases iodine uptake
  • stimulates other reactions involved in TH synthesis (eg. TPO)
  • stimulates uptake of colloid
  • induces growth of the thyroid gland (which can lead to goitre)
23
Q

Define hyperthyroidism.

A
  • Occurs when there is TH excess.
  • Primary - problem with the thyroid gland
  • Secondary - problem with pituitary regulation
24
Q

Define hypothyroidism.

A

TH deficiency

25
Q

Describe Grave’s Disease.

A
  • Common cause of primary hyperthyroidism.
  • Autoimmune disease characterised by high levels of circulating TH/ low levels of TSH.
  • Antibodies are directed to the TSH receptor - work as pharmacological agonists, so we end up with unregulated overproduction of TH.
26
Q

What are the symptoms of Grave’s Disease?

A
  • Weight loss (due to the increased metabolism)
  • Tachycardia
  • Fatigue
  • Diffuse goitre (due to TSH receptor stimulation)
  • Ophthalmopathy (an inflammatory disorder of the orbit and periorbital tissues).
27
Q

Describe Hashimoto’s Disease.

A
  • Cause of hypothyroidism.
  • Autoimmune disease characterised by low levels of circulating TH/high levels of TSH.
  • Antibodies cause thyroid destruction and dysfunction.
28
Q

What are the symptoms of Hashimoto’s Disease?

A
  • Lethargy
  • Weight gain
  • Lack of growth and development
  • Diffuse goitre.
29
Q

What are the 2 main branches that supply the thyroid?

A
  • Inferior thyroid artery - subclavian
  • Superior thyroid artery - carotid
30
Q

What is reverse T3?

A
  • Iodinated on a different side
  • Inactive
31
Q

What 2 factors stimulate the hypothalamus to produce TH?

A
  • Stress
  • Cold
32
Q

Why is high TSH and high TRH indicative of HYPOthyroidism?

A

→ If thyroid isn’t producing T3 or T4
→ There is no negative feedback
→ TRH and TSH concentration are high

33
Q

What is the diagnosis for low TRH and low TSH but high T4 and T3?

A

Primary hyperthyroidism

34
Q

What is the diagnosis for high TRH & TSH but low T4 and T3?

A

Primary hypothyroidism

35
Q

What is the diagnosis for low TRH, high TSH and high T4 and T3?

A

Secondary hyperthyroidism

SGUL - Physiology 1 (68 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions