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Pharmacy Y3S1 > Thyroid > Flashcards

Thyroid Flashcards

1
Q

Where is the thyroid gland?

A

Infront of the trachea and cartilage

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2
Q

Which cells secrete T3 and T4? Describe these cells

A

Thyroid follicular cells

Thyroglobuilin filled follicular lumen - thyroglobulin contains iodide to supply thyroid hormones for 90 days

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3
Q

Which cells secrete calcitonin? Where are these?

A

Parafollicular C cells

Inbetween thyroid follicular cells

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4
Q

Describe the response to low temperature

A

Hypothalamus releases TRH
TRH stimulates anterior pituitary to produce TSH
TSH stimulates thyroid glands to secrete T3 and T4
T3 has actions on the body to increase metabolism and heat production

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5
Q

What effect does low T3 have on the pituitary thyrotropes?

A

Stimulates high TSH levels = thyroid enlargement and increased activity

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6
Q

What effect does high T3 have on the pituitary thyrotropes?

A

Stimulates low TSH levels = thyroid regression and reduced activity

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7
Q

How does TSH have an effect on the thyroid folicular cells?

A

Via TSH receptors
G-protein coupled (GPC) receptors
Activates adenylate cyclse to produce cAMP (intracellular messanger)

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8
Q

What roles does cAMP have in the thyroid cell?

A 
Activates:
Thyroglobulin synthesis
Iodine pumping
Iodination by throid peroxidase
Endocytosis, proteolysis and hormone release
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9
Q

How does iodid get into follicular cells?

A

Sodium/Iodide Symporter (NIS) - Na in against gradient brings I- basolateral membrane
Pendrin transports I- across apical membrane

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10
Q

What happens to I- once in the follicle lumen?

A

Oxidised to I by TPO

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11
Q

Which enzyme is responsible for iodination of thyroglobulin (Tg)?

A

Thyroid peroxidase (TPO) enzyme complex which spans the apical membrane

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12
Q

Which two complexes form when I is added to Tg?

A

Mono-iodotyrosine (MIT)

Di-iodotyrosine (DIT)

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13
Q

How do T3 and T4 form?

A

2 x DIT = T4

DIT + MIT = T3

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14
Q

Which method do the iodinated tyrosine residues get cleaved from the Tg by?

A

Proteolysis

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15
Q

How much of T3 and T4 is found in the blood?

A

90% T4

10% T3

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16
Q

How is T4 transported and why?

A

By specific binding proteins

Hydrophobic so is indoluble in serum

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17
Q

Why can liver disease affect T4 transport to peripheral tissues?

A

Binding proteins are synthesis in the liver

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18
Q

What are the three thyroid hormone binding proteins? How much T4 do they bind?

A

Albumin (5-10% T4)
Transthyretin (TTR) (30% T4 - CNS Delivery)
Thyroxine-binding globulin (70-75% T4 - prevents loss in urine)

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19
Q

Which of the throid hormone binding proteins bind T3 and T4?

A

TBG

Albumin

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20
Q

Which thyroxine hormones can enter cells and how?

A

Unbound T3 and T4 via specific transporters - MCT8, MCT10, OATP1c1

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21
Q

Are T3 and T4 biologically active?

A 
T3 = yes 
T4 = not really
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22
Q

How is T4 converted to T3?

A 
Iodothryonine deiodinases (DOI)
Selenium accepts iodide
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23
Q

Describe DIO1

A

Predominates liver, kidney, muscle (where highest blood supply)
Found in thyroid
Produces most circulating T3

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24
Q

Describe DIO2

A

Predominates CNSM pituitary thyrotropes
(skeletal muscle in some species)
Controls intracellular T3 conc
Important for feedback regulation

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25
Q

DIO3

A

Produces inactive rT3

Prevents thyroid hormone access to specific tissues e.g. during pregnancy

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26
Q

What happens to T3 once in the nucleus?

A

Binds to thyroid receptor
Binds to Thyroid response element (TRE)
Functions as a transcription factor
Increases/inhibits gene transcription

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27
Q

Describe the Thyroid hormone receptors

A

TRA and TRB
Found in the nucleus
Heterodimer with retinoid X receptor

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28
Q

The feedback of T3 on the anterior pituitary can cause:

A

Increased growth hormone
Reduced prolactin
Reduced alpha and beta subunits of TSH

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29
Q

What are the 5 biological actions of thyroid hormones?

A 
Control of metabolic rate
Growth
Foetal development
Cardiovascular effects
Musculoskeletal effects
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30
Q

How does the thyroid control basal metabolic rate?

A

Increase in metabolic proteins = Na+K+ATPase, mitochondrial and respiratory enzymes, other enzymes and proteins, proteins for tissue growth and maturation.
Need an increase in oxygen (input CO2 and substrates) which causes an increase in metabolic rate (output)

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31
Q

How do thyroid hormones have a role in growth regulation?

A

Synergise with other hormones
Deficiencies = abnormal growth, development, reproduction, behavior, metabolism
Effects on all organs and tissues throughout life

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32
Q

What is the role of thyroid hormones in foetal development?

A

Neural and skeletal systems

Loss of T4 supply to foetus = irreversible mental impairment and congenital iodine deficiency syndrome

33
Q

What are the effects of iodine deficiency on a foetus?

A 
Miscarriage
Stillbirth
Congenital abnormalities
Perinatal morbidity & mortality
Congenital iodine deficiency syndrome
34
Q

What are the effects of iodine deficiency on a neonate?

A

Neonatal goiter
Neonatal hypothyroidism
Impaired mental function

35
Q

What are the effects of iodine deficiency on a child and adolescent?

A

Goiter (subclinical) hypothyroidism
Impaired mental function
Impaired physical development

36
Q

What overall effect do the thyroid hormones have on the cardiovascular system?

A 
T3 increases:
cardiac contraction and output
heart rate
oxygen supply to tissues
CO2 removal from tissues
37
Q

What direct effects does T3 have on the cardiovascular system?

A

Increases myocardial Ca2+ uptake
Increases expression of a-myosin heavy chain and reduces beta
Increases expression of RYR in SR

38
Q

What indirect effects does T3 have on the cardiovascular system?

A

Increases metabolism = thermogenesis = vasodilation

Increases sensitivity to catecholamines

39
Q

What musculoskeletal effects does T3 have?

A

Potent stimulatory effect on bone turnover = increases formation and resorption
Increases linear bone growth after birth
Increases rate of muscle relaxation

40
Q

What causes hypothyroididm?

A

Autoimmune disease
Previous treatment for hyperthyroidism
Iodine imbalance
Congenital hypothyroidism

41
Q

What are the symptoms of hypothyroidism

A 
Lethargic
Weak
Dry scaly skin
Sensitive to cold
Depression
Hair loss
Memory loss
Weight gain
Constipation
Puffy face and gruff voice if untreated
42
Q

What is done to test thyroid function?

A

TFT’s
Thyroid peroxidase antibody used
Hypo = High TSH but Low unbound T4

43
Q

How is hypothyroidism managed in non-pregnant adults?

A

High TSH and low T4 = Levothyroxine

Low TSH and Low T4 = Look if symptoms
Yes = levothyroxine 6 months and see if it resolves
No = measure TPO antipody

44
Q

What is the initial hypothyroisism treatment for adults UNDER 50?

A

Initially 50-100mcg levothyroxine daily

Adjust by 25-50mcg every 3-4 weeks (to response)

45
Q

What is the initial hypothyroisism treatment for adults OVER 50 and in heart disease?

A

Initially 25mcg daily

Adjust by 25mcg

46
Q

What is the initial congenital hypothyroisism treatment?

A

Initially 10-15 mcg/kg for neonates (max 50mcg)

Adjust 5mcg/kg

47
Q

After initial treatment with levothyroxine, when should TSH be measured?

A

After 8-12 weeks

48
Q

What is the usual maintenance dose of levothyroxine?

A

Adults: 100-200mcg
Children: 50-200 mcg depending on age

49
Q

On maintenance of levothyroxine, how often should TSH be measured?

A

Adults: Yearly
Children: every 4-6 months

50
Q

What patient counselling should be given with levothyroxine?

A 
Lifelong treatment
Single daily dose
Do not take at the same time as calcium  or iron preparations or caffeine beverages
Three strengths
Monitoring 
Medical exemption certificate
51
Q

What causes hyperthyroidism?

A

Autoimmune disease (Grave’s)
Toxic nodules
Antibodies to TSH receptor stimulate the gland and increase the production of thyroid hormones

52
Q

What are the symptoms of hyperthyrodism?

A 
Anxious
Palpitations
Tremor
Weight loss
Tachycardia
Goitre
Heat intolerance
Warm moist skin
Difficulty sleeping
Diarrhoea
53
Q

What is the expected outcome of a thyroid function test for hyperthyroidism?

A

Low TSH and High free T4

54
Q

How does drug therapy stop hyperthyroidism?

A

Intereferes with thyroid hormone synthesis by inhibiting thyoperocidase activity in the follicular lumen

55
Q

What is the regime for Carbimazole?

A

15-40mg daily
Maintain until TFTs normal (1-8 weeks)
Maintain for 12-18 months - reduce by 25-30% monthly until 5-15mg

56
Q

What is a blocking-replacement regimen with carbamazole?

A

40-60mg for approx 4 weeks
THEN add thyroxine 50-100mg (treat up to 18 months)
Make temporarily hypothyroid

57
Q

Why should a blocking-replacement regimen not be used in pregnancy?

A

Only carbimazole can cross the placenta making foetus hypothyroid

58
Q

Can carbimazole be used in pregnancy?

A

Only consider after benefit-risk assessment at the lowest effective dose without any additional administration of thyroid hormones

59
Q

How much Propylthoiuracil should be given and when is it used?

A

Initially 200-400mg daily (3 doses)
Then 50mg TDS maintenance

Use in pregnancy or carbimazole intolerance

60
Q

How do carbimazole and Propylthoiuracil cause drug-induced agranulocytosis?

A

Cause bone marrow suppression

Reduce white cell count = infection

61
Q

What patient counselling should be given for carbimazole and Propylthoiuracil?

A

Carbimazole = OD
Propylthoiuracil = TDS
Duration and tapering to maintenance
Report agranulocytosis signs: sore throat, mouth ulcer, bruising
Report hepatic dysfunction (Propylthoiuracil): pruritis, jaundice, dark urine
Advise on contraception (contraception)
Need for regular reviews/tests
Hyper=NOT entitled to medical exemption certificate

62
Q

What is radioactive iodine preferred for?

A 
First-line treatment except for mild disease or if radioactivity unsuitable
If no response to drug treatment
If relapse after drugs
Comorbid cardiac disease
Toxic nodular goitre
63
Q

What is surgery preferred for?

A

Oesophageal obstruction
Intolerance to drug treatment
Young adults

64
Q

Before iodide or surgery, why should the patient be made euthyroid?

A

To prevent thyrotoxic crisis due to dangerously high levels of T4 released into system

65
Q

What is an adjuvant therapy in hyperthyroism

A

Beta-blockade

Propanolol, Nadolol

66
Q

How does Iodine induce thyroid disease?

A

Overdose:
Acute - inhibits T3/T4 release
Prolonged - suppresses T3/T4 production

67
Q

How does Amiodarone induce thyroid disease?

A

Contains organic iodine
Hypo: inhibits synthesis and release of T3/T4 (start replacement therapy)
Mild hyper: Blocks T4 to T3 conversion (increases TSH and T4)
Severe hyper: increased production of T4 (do to iodine content) - stop/carbimazole

68
Q

How does Lithium induce thyroid disease?

A

Hypo: inhibits iodine uptake and prevents T3/T4 release (replace T4)
Hyper:rare

69
Q

Give examples of Ca2+ homeostasis diseases

A 
Primary hyperparathyroidism
Secondary hyperparathyroidism
Osteoporosis
Rickets
Calcium Stones
Receptor mutations
Paget's disease
70
Q

What are the two types of cells in the parathyroid gland?

A

Chief calls

Oxyphil cells

71
Q

Which cells produce parathyroid hormone?

A

Chief cells

72
Q

What is the function of parathyroid cells?

A

Increase blood Ca2+ conc when it gets too low

73
Q

How is low Ca2+ detected?

A

By G-protein coupled Ca2+ sensing receptors (CaSR)

74
Q

How does PTH work?

A

Raises blood Ca2+:
Indirectly stimulates osteoclasts to release more Ca from bone (resorption)
Increased renal Ca reabsorption
Increased Vit D production (stimulates Ca uptake from intestine and above)

75
Q

How is PTH regulated?

A

Negative feedback

Increase in blood Ca decreases PTH and increases bones formation

76
Q

How does calcitonin work?

A

Reduces blood Ca2+

Reduces osteoclast activity to reduce bone resorption and allows rapid bone deposition by osteoblast

77
Q

How is calcitonin regulated?

A

Negative feedback

Decrease in blood Ca decreases calcitonin secretion and reduces bone formation

78
Q

Which diseases are caused by calcitonin?

A

None

Pharmacy Y3S1 (14 decks)

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