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Block 1 > Thyroid Physiology > Flashcards

Thyroid Physiology Flashcards

1
Q

Describe the anatomy of the thyroid gland

A

-Located superior to 3rd tracheal ring -2 lateral lobes + isthmus -Enlargement is obvious

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2
Q

Describe the histology of the thyroid gland

A

-Follicular cells surrounding a colloid containing thyroid hormone bound to glycoprotein -Surrounded by capillaries - Some parafollicular cells

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3
Q

Describe the blood supply of the thyroid

A

1) Superior thyroid artery (from common carotid) 2)Inferior thyroid artery (from thyrocervical trunk).. Close to recurrent laryngeal nerve 3) Thyroid ima artery

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4
Q

Describe the drainage of the Thyroid

A

1) Superior thyroid vein –> Internal jugula
2) Middle thyroid vein –> Internal jugula
3) Inferior thyroid vein –> Left braciocephalic vein

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5
Q

Describe how thyroid hormones are regulated?

A

1) Neuron in PVN releases TRH into the portal vein
2) Thyrotrope cells in AP release TSH into systemic circulation
3) TSH acts on thyroif to release T3 & T4.

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6
Q

Where in the hypothalamus is TRH released from?

A

Paraventricular Nucleus

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7
Q

Briefly describe TRH

A
  • Consists of 3 peptides
  • released into hypophyseal portal circulation (AP)
  • short-lived, lasts only 2ish mins before being broken down
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8
Q

Briefly describe TSH

A
  • Glycoprotein
  • Similar to LH & FSH (Same alpha chain, different Beta chain)
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9
Q

Which is more prevalentand weaker? T3 or T4?

A

T4

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10
Q

Why does the thyroid trap iodine?

A
  • Needs a good supply in order to keep synthesising thyroid hormones, to avoid deficiency which could lead to hypothyroidism
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11
Q

How is iodide taken into the follicle cell of the thyroid?

A

Via the Sodium/Iodide NIS symporter

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12
Q

How is Iodide released from the follicular cell of the thyroid?

A

Via PENDRIN transporter

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13
Q

What converts Iodide into Iodine? Where does this occur?

A

TPO - Thyroperoxidase

Occurs on the luminal membrane of follicular cells

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14
Q

How is thyroglobulin released from the follicular cells?

A

Exocytosis

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15
Q

Briefly explain the structure of thyroglobulin and how it combines with iodine?

A

Thyroglobulin has tyrosine residues, iodine binds to either one or two positions on the tyrosine ring side chin to form either

MIT - monoiodotyrosine

or

DIT - Diiodotyrosine

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16
Q

How are thyroid hormones released into circulation?

A
  • Microvilli extend from the cell surface and engulf the tyrosine residues
  • This becomes a vesicle, fuses with a lysosome where proteases hydrolyse tyrosine residues to release T3 & T4 into the blood and Thyroglobulin back into the follicular cell.
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17
Q

Explain how thyroid hormones are produced?

A

1) Follicle cells produce thyroglobulin which is secreted into the lumen by exocytosis.
2) Iodide is brought into the cell via the NIS symporter. It is brought out of the cell via the Pendrin transporter
3) Iodide is converted to Iodine by TPO on the luminal membrane of the follicular cell
4) Iodine attches to tyrosine ring side chain Thyroglobulin in either one or two places to form MIT or DIT
5) MIT + DIT = T3, DIT + DIT = T4
6) Microvilli come out of the cell membrane, engluf the tyrosine residue to form a vesicle. Fuse with lysosome, proteases are released which hydrolyse tyrosine residue. T3 & T4 exit into blood stream, Thyroglobulin enters follicular cells to be recycled.

18
Q

How does TSH increase production of thyroid hormones?

A
  • Increases every step of thyroid hormone synthesis
  • TSHR is a GPCR
  • cAMP –> Activates Protein Kinases –> Phosphorylations
19
Q

How do Thyroid hormones reach target cells?

A
  • They are lipophilic do cannot travel readily in blood
  • They travel bound to proteins
  • ~70% attached to TBG, ~30% Albumin

(TBG has a higher affinity to T4)

  • Hormone bound to protein is inactive
20
Q

How do thyroid hormones affect target cells?

A

Thyroid hormones enter cells via diffusion and MCT8 (10) transporter.

Only T3 is active - T4-T3 conversion occurs via deiodinases

T3 binds to cell. Hormone/Receptor complex travels to the nucleus, binds to DNA where is alters mRNA , protein synthesis and the thyroid hormone response occurs.

21
Q

What is the main function of thyroid hormones?

A
  • Affects all metabolic pathways
  • Increase metabolic rate
22
Q

How do thyroid hormones increase metabolic rate?

A
  • Increase number and size of mitochondria
  • Stimulate synthesis of enzymes in the respiratory chain
  • Increase conc. of Na+/K+ -ATPase in the cell membrane to maintain EC gradient across the membrane
23
Q

How do thyroid hormones affect the heart?

A
  • Increas HR
  • Increase FOC
  • Increases expression of Ca2+ channels in SR = increase Ca 2+ release during systole = Increase contractile activity (Hyperthyr.)
24
Q

If thyroid hormones increase MR, this means oxygen requirements increase, how is this need met?

A
  • Incr resp & vent rate
  • Inc HR, BF & CO = Incr delivery to CVS
  • Incr. protein/lipid/carb metabolism to provide substrate for oxidation
25
Q

What are the consequences of greater oxygen consumption?

A
  • Incr Ventilation
  • Incr CO

More substrates needed so:

  • incr food intake
  • Incr mobilisation of fats, protein and carbs
26
Q

What are the consequences of increased metabolic rate?

A
  • Incr CO2
  • Incr vent.
  • Incr urea prod.
  • Incr renal function (waste excretion)
  • decr muscle mass
  • decr adipose tissue
  • increased thermogenesis
27
Q

How do thyroid hormones affect neurological functions?

A
  • Incr synapse formation
  • Incr myelinogenesis
  • Incr neuronal growth
28
Q

Why are iodine and thyroid hormones important in development?

A
  • Vital for growth and development of CNS
  • Deficiencies = defects
  • ~12 wks gestation, thyroid secreted T3/4 under control of foetal hyp/pit.

E.g CRETINISM - delayed physical and neurological development due to iodine deficiency in foetal/postnatal development.

29
Q

Hyperthyroidism would show what on a blood test ?

why?

A
  • Low TSH
  • High T4

Decreased TSH levels because excess hormones are feeding back negatively to stop production in the pituitary.

If high TSH = problem in or above pituitary

30
Q

Briefly explain primary and secondary hyperthyroidism?

A

Primary = Thyroid gland problem

Secondary = Pituitary adenoma secreting excess TSH (rare)

31
Q

List some symptoms of Hyperthyroidism:

A
  • Warm, sweating
  • Weight loss despite incr appetite
  • Diarrhoea
  • Palpitations/Rapid pulse
  • Tiredness, weak muscles
  • Nervousness/irritability
  • Thirst, polyuria
  • Itchiness
  • Goitre
32
Q

What are the treatments for Hyperthyroidism?

A
  • CARBIMAZOLE
  • PROPYLTHIOURACIL
  • RADIOACTIVE IODINE (destroys gland)
  • SURGERY (Risk of damaging vocal cord nerves)
33
Q

What would you expect to see on blood results for a hypothyroid patient?

A

HIGH TSH, LOW T4

34
Q

What are the symptoms of hypothyroidism?

A
  • Fatigue,
  • Sensitivity to cold
  • Constipation
  • Dry skin, alopecia
  • Low mood, mental slowness
  • Goitre
  • Overweight/Obese
  • Heavy periods/fertility problems
35
Q

Name 2 causes of hypothyroidism?

A
  • Hashimoto’s (Autoimmune destruction)
  • Iodine deficiency
36
Q

What are the treatments for hypothyroidism?

A

-Hormone replacement:

LEVOTHYROXINE - synthetic T4

LIOTHYRONINE - limited use

37
Q

What are 3 causes of Goitre?

A
  • IODINE DEFICIENCY, reduced T4 induces TSH secretion
  • GRAVES DISEASE (Incr T4)
  • TUMOURS
38
Q

How can both High and low T4 induce Goitre?

A
  • Continual stimulation of the gland by thyroid hormones causes increase in cell activity and number = hypertrophy & growth = goitre
    1) Iodine def. = low T3/4. Feeds back to pituitary to produce more TSH = Incr TSH, Low T4
    2) GRAVES - TSI mimics TSH. decr TSH but TSI still causes T4 release.
39
Q

What is Graves disease?

A
  • an autoimmune condition
  • Auto-Antibody produced = TSI (Thyroid Stimulating Immunoglobulin) which mimics TSH.
  • Causes incr release of T4. This negatively feeds back onto pituitary but TSI causes continual release of T4.
  • Cont-nual stimulation of thyroid gland = incr cell activity and number, Hypertrophy & growth = Goitre.
  • Bulging eyes
40
Q
A

Block 1 (11 decks)

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