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Block 1 > Thyroid Physiology and Intro to Endocrinology > Flashcards

Thyroid Physiology and Intro to Endocrinology Flashcards

1
Q

Where does the thyroid sit?

A

Anterior to the third tracheal ring

Between C5- T1

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2
Q

What are the three main arteries supplying the thyroid and their origins?

A

Superior thyroid artery (first branch of external carotid)

Inferior thyroid artery (thyrocervical trunk)

(10%) Thyroid ima (brachiocephalic trunk, arch of aorta)

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3
Q

What are the three main veins draining the thyroid and where do they drain into?

A

Superior thyroid vein (internal jugular vein)

Middle thyroid vein (internal jugular vein)

Inferior thyroid vein (brachiocephalic vein)

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4
Q

Why is it possible to remove part of the thyroid?

A

Because it has numerous blood supplies that can take over if arteries/veins are removed

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5
Q

Which parts of the thyroid does the superior thyroid artery supply?

A

Superior and anterior parts

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6
Q

Which parts of the thyroid does the inferior thyroid artery supply?

A

Posterior and inferior parts

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7
Q

What three hormones does the thyroid make and secrete?

A

Thyroxine (T4)

Tri-iodothyronine (T3)

Calcitonin (calcium homeostasis)

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8
Q

What are T4 and T3 derivatives of?

A

Tyrosine

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9
Q

T4 has 4 molecules of ___

A

Iodine

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10
Q

T3 has 3 molecules of ___

A

Iodine

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11
Q

Which cells make calcitonin?

A

Parafollicular (C) cells in the thyroid

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12
Q

Where are thyroid hormones made and stored?

A

Inside the follicular cells of the thyroid

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13
Q

What are the six steps of thyroid hormone synthesis?

A

Thyroglobulin synthesis

Uptake and concentration of iodide

Oxidation of iodide to iodine

Iodination of thyroglobulin

Coupling of 2 iodinated tyrosine molecules

Secretion

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14
Q

Are T3 and T4 fat soluble?

A

Yes

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15
Q

How is T3 and T4 transported in the blood?

A

By plasma proteins -

Thyronine Binding Globulin (70%)
Albumin (30%)

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16
Q

How does iodide enter the thyroid cell?

Iodide trapping

Draw the diagram (slide 11)

A

By a Na Iodide symporter (NIS) (both move in together)

Can move into the cell against a concentration gradient.

Uses energy provided by Na/K ATPase pump that moves Na+ out of cell and K+ in

Allows the thyroid to concentrate iodide.

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17
Q

What are some dietary sources of iodine?

Why do we need to trap iodide?

A 
Milk and dairy 
Seafood
Sea salt
Fruit and vegetables 
Sauerkraut 
Supplemented salts

Need to trap iodide because it is rare in our diet

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18
Q

Which transporter is used to get iodine from the follicle cell into the follicular lumen?

A

Pendrin

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19
Q

Which transporter is used to get iodine from the blood into the follicle cell?

A

Na Iodide symporter (NIS)

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20
Q

What converts iodide to iodine?

dirty to clean

A

An enzyme called thyroid peroxidase (TPO)

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21
Q

Where does thyroglobulin synthesis take place?

A

Follicle cell

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22
Q

What does iodine join with?

A

Tyrosine on the thyroglobulin chain

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23
Q

What is MIT?

A

Mono-iodotyrosine

1 iodine joined to a thyroglobulin chain

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24
Q

What is DIT?

A

Di-iodotyrosine

2 iodine molecules joined to thyroglobulin chain

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25
Q

What makes T3?

A

MIT + DIT = T3

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26
Q

What makes T4?

A

DIT + DIT = T4

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27
Q

How is the thyroglobulin backbone with MIT, DIT, T3 and T4 taken into the follicular cell from the colloid?

A

Engulfed by microvilli on follicular cell and make vesicles out of colloid

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28
Q

What attaches to the vesicles of TG chain when it is in the follicular cell?

A

Lysosomes

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29
Q

What do lysosomes release when they attach to vesicles?

A

Protease

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30
Q

What does protease do in the follicular cell?

A

Breaks down molecules:

Releases thyroglobulin + MIT & DIT that did not attach properly back into the colloid via pendrin

Releases T3 and T4 into the blood

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31
Q

Where is thyroid peroxidase (TPO) found?

A

On the luminal membrane of the follicular cell

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32
Q

WHITE BOARD:

Draw out T3 and T4 synthesis on a whiteboard and use PowerPoint slide/hand drawing to mark

A

See slide/drawing

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33
Q

Where is TSH released from?

A

Anterior pituitary gland

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34
Q

WHITE BOARD:

Regulation of secretion of T3 and T4
negative feedback loop, endocrine glands

A

Hypothalamus - TRH

TRH —> Anterior pituitary

Anterior pituitary - TSH

TSH —> Thyroid

Thyroid - T4, T3

Increase in T4 and T3 decreases production of TRH from hypothalamus and TSH from anterior pituitary

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35
Q

Where is TRH released from?

A

Hypothalamus

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36
Q

Out of TRH, TSH, T4, and T3, which are tropic and which are trophic?

A

Tropic - TRH, TSH

Trophic - T3, T4

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37
Q

What is the relationship between TSH, LH and FSH?

A

All are glycoproteins with alpha and beta chains

Alpha chains are identical to each other

Beta chains are protein specific (individual to each hormone)

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38
Q

How does TSH increase production of thyroid hormones?

A

Increases every step of production and secretion of T3 and T4

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39
Q

Why can’t thyroid hormones dissolve in blood?

A

They are lipophilic (fatty)

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40
Q

Which of the thyroid hormones is active and which is inactive?

Which one is produced more?

A

T3 - active, body produces less

T4 - inactive, body produces more

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41
Q

Thyroxin binding globulin (TBG) has a higher affinity for ____

A

T4

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42
Q

Why can diseases of the liver affect thyroid hormone circulation?

A

30% of thyroid hormones in the blood are bound to albumin which is made in the liver

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43
Q

What does T3/T4 have to do to enter the target cell?

A

Be unbound from plasma proteins

T4 has to change to T3 to bind to the receptor

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44
Q

What is the name given to the enzymes that convert T4 to T3?

A

Deiodinases

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45
Q

How many types of deiodinases are there?

A

3 types

They are tissue specific

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46
Q

Why can different tissues produce different responses to circulating thyroid hormones?

A

There are tissue specific enzymes called deiodinases that either activate or deactivate thyroid hormones

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47
Q

What is the name of the transporter that allows thyroid hormones into a target cell?

A

MCT8(10)

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48
Q

How do thyroid hormones have an effect on target cells?

A

They bind to receptors inside the target cell.

Receptor-hormone complex moves to the nucleus where it binds to DNA and alters protein synthesis

This will then produce a thyroid hormone response.

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49
Q

What 4 broad effects to thyroid hormones have?

A

Metabolism - affects basal metabolic rate (BMR)

Maturation and differentiation

Neurological function

Growth

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50
Q

By which week of gestation does a fetus make and secrete its own thyroid hormones?

A

Week 12

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51
Q

Define Cretinism

A

Impaired physical and neurological development due to iodine deficiency during foetal or postnatal development

52
Q

How do we screen newborns for TSH?

A

Heel prick test

53
Q

Explain why an excess of T3 will increase ventilation rate

A

T3 increases the amount of mitochondria respiratory enzymes and basal metabolic rate.

More O2 is needed to meet the demand.

Hyperventilation occurs, alongside increased HR and blood flow to supply the O2 to tissues

54
Q

Why does hyperthyroidism increase the patient’s temperature?

A

Because their metabolic rate has increased due to excess T3

55
Q

Why does hyperthyroidism increase the patient’s appetite?

A

Because the patient is ingesting substrates for O2 consumption as a result of the increased metabolic rate caused by excess T3
e.g. proteins/lipids/carbohydrates

56
Q

What can cause clinical problems of the thyroid (2 broad categories)

A

Thyroid gland function

  • gland formation/function
  • iodine supply
  • signalling pathways
  • congenital or acquired

Response to T3/T4
-thyroid hormone resistance (T3R defect)

57
Q

What does a thyroid function test (TFT) measure?

A

TSH
T4 (free)

T3 (sometimes, free)

58
Q

What blood results would you expect to see in hypothyroidism?

A

TSH - high

T4 - low

59
Q

What blood results would you expect to see in hyperthyroidism?

A

TSH - low

T4 - high

60
Q

List some common symptoms of hyperthyroidism

A 
Palpitations/rapid pulse
Diarrhoea 
Heat intolerance 
Tiredness
Weak muscles 
Nervousness
Thirst 
Polyuria 
Goitre
61
Q

What is the name for a sever form of hyperthyroidism?

A

Grave’s disease

Exophthalmos

62
Q

List some common symptoms of hypothyroidism

A 
Fatigue
Tiredness
Sensitivity to cold
Constipation
Dry skin and hair 
Alopecia (outer 1/3 of eyebrow)
Low mood 
Goitre
63
Q

What is the name of the autoimmune disease that can cause hypothyroidism?

A

Hasimotos thyroiditis

64
Q

How does hypothyroidism cause a goitre?

A

Low levels of iodine decrease the amount of T4 produced

Decrease in T4 signals anterior pituitary gland to secrete more TSH.

The thyroid is still unable to make T4 because of the iodine deficiency

The thyroid hypertrophies because the number of cells increases in an effort to increase levels of T4 in response to an increase in TSH

65
Q

How does Grave’s disease (hyperthyroidism) cause a goitre?

A

The autoimmune disease produces thyroid stimulating immunoglobulin (TSI) which mimics TSH

TSI will increase the amount of T4 produced by the thyroid

Increase T4 will decrease TSH production from anterior pituitary.

However decreased TSH will not decrease T4 because there is still TSI working to increase T4.

This causes hypertrophy of the gland, causing a goitre

66
Q

What are the 3 treatments for hyperthyroidism?

A

Drugs (inhibit production)

Radioactive iodine (destroy gland)

Surgery

67
Q

What are the treatments for hypothyroidism?

A

Levothyroxine (synthetic T4) - aim for normal TSH in response to treatment

Liothyronine (synthetic T3)

68
Q

What type of gland is the thyroid gland?

A

An endocrine gland

69
Q

Define endocrinology

A

The study of the endocrine glands and the substances they secrete

70
Q

Define endocrine gland

A

A gland that makes and secretes hormones into the BLOODSTREAM, through which they travel to affect DISTANT targets

71
Q

Define hormone

A

A chemical substance produced by cells and released especially into the blood and having a specific effect on cells or organs usually at a distance from the place of origin

72
Q

Define exocrine gland

A

A gland that secretes its products through DUCTS opening into an epithelium rather than the blood

73
Q

Define paracrine

A

Acts on adjacent cells

74
Q

Define autocrine

A

Acting on surface receptors of the same cell it is secreted from

75
Q

What type of signalling to neurotransmitters display?

A

Paracrine (adjacent cell)

76
Q

What type of input does the endocrine system receive?

A

Chemical and physical stimuli

77
Q

What type of response does the endocrine system display?

A

Chemical response

78
Q

Name some endocrine organs

A 
Hypothalamus
Pituitary 
Thyroid
Thymus
Adrenal glands
Pancreas
Kidneys
Ovary
Uterus
Testes
79
Q

List the main endocrine hormones

A

Glucocorticoids

Insulin, glucagon

Thyroid hormones

Gastric hormones (CSK, gastrin)

Enteric hormones

ADH, RAAS hormones

80
Q

What are the three major molecular types of hormones?

A

Polypeptides (chains of amino acids)

Modified amino acids (proteins)

Steroids

81
Q

Name some hormones derived from amino acids

A

Serotonin (single)

Thyroid hormones (dipeptides)

Insulin
FSH, TSH, LH (complex polypeptides)

82
Q

Name some hormones derived from lipid precursors

A

Cholesterol (sex steroids, vitamin D)

Fatty acids (prostaglandins)

83
Q

Where on the cell do amino acid-derived hormones have their receptors?

A

Cell membranes

84
Q

Where on the cell do lipid-derived hormones have the receptors?

A

Intracellular

sex hormones

85
Q

Why do lipid hormones have intracellular receptors?

A

Because they are usually hydrophobic

86
Q

How are protein and peptide (amino acid) hormones released from cells?

A

Exocytosis in secretory vesicles

87
Q

How are steroid hormones released from cells?

A

Diffusion

88
Q

Define primary endocrine dysfunction

A

Too much of the effector hormone (trophic) from endocrine organ

89
Q

Define secondary endocrine dysfunction

A

Overstimulation of the effector endocrine organ by excessive tropic hormone

90
Q

What is Cushing’s Syndrome?

A

Excess of glucocorticoid

91
Q

List the 6 steps of protein and peptide hormone synthesis:

A

A. Gene transcription

B. mRNA to rER

C. Translation on rER

D. Post-translational processing

E. Packaging into secretory vesicles

F. Exocytosis

92
Q

List the 4 steps of steroid hormone synthesis:

A
  1. Hydrolysis of esters and release of cholesterol/Ch. uptake
  2. Cholesterol to pregnenolone
  3. Processing
  4. Diffusion
93
Q

List some key differences between protein/peptide and steroid hormone synthesis:

A

Protein + peptide
1. Involves gene transcription

  1. Translation on the rER
  2. Undergoes exocytosis in secretory vesicles

Steroid hormones
1. No gene activation/ transcription

  1. Cholesterol is changed to pregnenolone in the mitochondrion
  2. Processing happens on the sER
  3. Hormones diffuse through the plasma membrane
  4. Type and activity of enzymes determines type and amount of hormones
  5. Indirect genetic control of production of steroid hormones - enzymes that help with the process are controlled by genes
94
Q

What subunits can a G-protein coupled receptor have?

A

Alpha
Beta
Gamma

95
Q

What do protein kinases do?

A

Add phosphate groups

96
Q

Draw the pathway from activation of a G-protein to release of Ca2+ from the endoplasmic reticulum

A

Binding to G-protein coupled receptor

Activated G protein stimulates activity of phospholipase C

Stimulates IP3

Release of Ca2+ from endoplasmic reticulum

97
Q

Draw the pathway from activation of a G-protein to release of protein kinases

A

Binding to G-protein coupled receptor

Activated G protein stimulates activity of adenylate cyclase

Adenylate cyclase takes ATP and cyclizes it to cAMP (removes 2 phosphates, energy gain)

This produces a second messenger which stimulates protein kinases (+ phosphate groups to things, usually activating them)

98
Q

Describe the tyrosine kinase receptor system

A

Signalling molecule binds to receptor which brings the 2 halves of the receptor together

The receptor uses energy from ATP –> ADP and the spare phosphate groups to phosphorylate the receptor into an active form (Dimer)

Proteins recognise the phosphorylated form and they become active (phosphorylate)

Active proteins bring about cellular changes

99
Q

List some major features of water soluble hormones

A

Are large and hydrophilic

Cannot pass through membranes

Bind to cell surface receptors (GPCR/tyrosine kinase)

100
Q

List some major features of fat soluble hormones

A

Steroids and thyroid hormones

Large and hydrophobic (lipid soluble)

Bind to intracellular and cell surface receptors

101
Q

What is a tropic hormone?

A

A chemical signal released from an endocrine gland that tells another endocrine gland to increase or inhibit secretion

102
Q

What is an effector hormone?

A

A hormone released from a gland that has an effect on a target cell

103
Q

What is a trophic hormone?

A

A hormone that affects growth and development directly

104
Q

Use the words tropic and trophic to describe negative feedback

A

Endocrine organ releases a tropic hormone

Has an effect on another endocrine organ

2nd endocrine organ releases a trophic hormone which stimulates growth and development

Release of trophic hormone inhibits the action or tropic hormones upstream which inhibits the release of the trophic hormone

105
Q

Give an example of hormones producing a positive feedback cycle

A

Oestrogen causing increase in luteinising hormone (release of ovum)

106
Q

What can cause an excess of a hormone?

A

Neoplasm (CA)

Hyperplasia

Ectopic production

107
Q

What can cause a hormone deficit?

A

Gland destruction (trauma, disease, autoimmune)

Undeveloped gland

108
Q

What can cause hormone resistance (failure to respond)?

A

Receptor problems

Intracellular signalling defects

109
Q

Where are glucocorticoids made?

A

Adrenal glands

110
Q

What is the plasma half life of a peptide (amino acid) hormone compared to a steroid/thyroid (lipid) hormone?

A

Amino acid half life is seconds - minutes

Steroid half life is minutes - days

111
Q

Draw hormone synthesis for protein and peptide hormones, and steroid hormones.

Where on the rER does mRNA bind to to undergo translation?

A

Slide 18 of intro to endo lecture

Ribosomes on the rER

112
Q

List some features of a hydrophobic hormone

A

Transported bound to plasma proteins - binding affinity is important

The hormone when it is bound is considered inactive, is protected from degredation and acts as a reservoir

113
Q

What type of receptor is the insulin receptor?

A

Tyrosine-kinase receptor system

114
Q

What type of receptors do water soluble hormones bind to. Give examples

A

Cell surface receptors

G-protein coupled receptors
Tyrosine kinase receptors

115
Q

Outline the typical pathway that a steroid hormone takes to produce new proteins.

A

Typically transfuses through the cell (although can bind to receptors on cell surface)

Binds to cytoplasmic or nuclear receptor to produce an activated transcription factor

Transcription produces mRMA

Translation on ribosomes of rER

New protein made

116
Q

Where are ‘releasing hormones’ released from?

Where do they normally go to?

A

The hypothalamus

Anterior pituitary gland

117
Q

What is Addison’s disease?

List some symptoms

A

Hypo-adrenalism

Reduced glucocorticoids (CORTISOL) and mineralcorticoids

Weight loss, anorexia
Weakness
Fever
Depression
N + V
Diarrhoea/constipation
Confusion
Abdo/back pain
118
Q

What is Cushing’s syndrome?

List some symptoms

A

Glucocorticoid (CORTISOL) excess

Weight gain
Moon face 
Depression, psychosis
Insomnia
Thin skin, bruising
Back pain 
Polyuria
119
Q

What, that is attached to thyroglobulin, eventually makes thyroid hormones?

A

Tyrosines attached to thyroglobulins eventually make thyroid hormones

120
Q

Where is the majority of iodine found?

Why is this useful?

A

In the colloid of the follicles

The follicles accumulate iodine from the blood and secrete it into colloid

Useful for imaging - inject radioactive iodine

121
Q

Describe a type 1 deiodinase

A

Cell surface of most cells (especially liver, kidney, thyroid, brain)

Inner and outer ring deiodination

ACTIVATING T4 –> T3

122
Q

Describe a type 2 deiodinase

A

Intracellular - CNS, brown fat, placenta, skeletal and cardiac muscle

Outer ring deiodination

ACTIVATING T4 –> T3

123
Q

Describe a type 3 deiodinase

A

Placenta + CNS

Removes iodine from T4 to make reverse T3.

Inner ring deiodination

INACTIVATING T4 –> rT3 –> T2

124
Q

Where is T4 converted to T3?

A

Inside a target cell by deiodinases

125
Q

What autoantibody does Grave’s disease produce?

A

Thyroid stimulating immunoglobulin

Acts like TSH

Low TSH
High T4

126
Q

What is Hasimotos thyroiditis?

A

Autoimmune destruction of the thyroid gland that leads to hypothyroidism

High TSH
Low T4

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