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LMP301 > LMP301 Lecture 8: Thyroid Disease > Flashcards

LMP301 Lecture 8: Thyroid Disease Flashcards

Thyroid diseases

1
Q

What is symptom of goiter?

A

Enlarged thyroid gland

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2
Q

Is goiter due to hypo, hyper, or eu-thyroid?

A

Can be anything

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3
Q

Goiter is due to…

A

Lack of iodine

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4
Q

Thyroid gland secretes…

A

T3 and T4

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5
Q

What is more abundant in the blood, T3 or T4?

A

T4

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6
Q

What makes 2/3 of the circulating T3?

A

Peripheral tissues (liver, kidney) deiodinate T4

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7
Q

What stimulates the production of thyroid hormones?

A

TSH

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8
Q

What is more biologically active, T3 or T4?

A

T3

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9
Q

What is the inactive form of T3?

A

rT3 (reverse)

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10
Q

How is rT3 produced

A

metabolised from T4

T4 can make both T3 and rT3

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11
Q

How can local thyroid status be modulated?

A

Balance production of T3 and rT3

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12
Q

Thyroid hormones are needed for…

A

all tissue maturation and metabolism

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13
Q

Precursor for thyroid hormones

A

tyrosine

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14
Q

MIT structure

A

1 iodide attached to tyrosine

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15
Q

DIT structure

A

2 iodides attached to tyrosine

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16
Q

T4 is made up of

A

DIT + DIT

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17
Q

T3 is made up of…

A

MIT + DIT

T4 - 1 iodine (at first benzene)

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18
Q

rT3 is made up of…

A

T4 - 1 iodine (at second benzene)

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19
Q

T4 is also called…

A

thyroxine

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20
Q

Hypothalamus-pituitary-thyroid axis for T3, T4 control

A

Hypothalamus: TRH
a. pituitary: TSH
Thyroid: TSH binds on TSH receptor -> T4 and T3 production

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21
Q

Feedback of thyroid hormones

A

TSH neg feedback on hypothalamus (short loop feedback)

T4 + T3 neg feedback on hypothalamus, a. pituitary (long loop feedback)

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22
Q

How do thyroid hormones travel? Give some examples.

A

Bound to carrier proteins in plasma (e.g. albumin, TBG)

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23
Q

TBG

A

T4-binding globulin

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24
Q

Which thyroid hormones are active?

A

The ones not bounded to carrier proteins in the plasma

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25
Q

% of free T3 + T4

A

T3: 0.3% of all T3
T4: 0.03% of all T4

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26
Q

What may change the concentration of free thyroid hormones?

A

Changes in the [ ] or affinity of carrier proteins

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27
Q

Are FT3 + FT4 better or worse markers of thyroid function? Why?

A

Better

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28
Q

Effects of increasing TBG

A

More T4 + T3
Same FT4
Same TSH

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29
Q

What compounds increase TBG?

A
  • estrogen

- oral contraceptives

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30
Q

Effects of decreasing TBG

A

Less T4 + T3
Same FT4
Same TSH

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31
Q

Effect of inhibiting binding of thyroid hormones to TBG

A

Less T4

Same FT4

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32
Q

What compounds decrease TBG?

A
  • androgens

- glucocorticoids

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33
Q

What compounds inhibit thyroid hormones from binding to TBG?

A

Salicylates

34
Q

Myxedema

A

Dry, waxy swelling of the skin with abnormal deposits of glucosaminoglycans

35
Q

Glucosaminoglycans

A

unbranched polysaccharides

36
Q

What is myxedema a strong indication of?

A

hypothyroidism

37
Q

key symptoms of hypothyroidism

A
  • Weight gain
  • fatigue
  • myxedema
  • high cholesterol
  • slow HR
38
Q

Hypothyroidism is a _____ syndrome

A

hypometabolic

39
Q

What do thyroid hormones control in the body?

A

metabolism

40
Q

Why is a symptom of hypothyroidisms high cholesterol?

A

Less LDL receptors produced, so less liver uptake

41
Q

Types of hypothyroidism

A
  1. Primary hypothyroidism
  2. Secondary hypothyroidism
  3. Tertiary hypothyroidism
42
Q

Primary hypothyroidism

A

Problem at thyroid gland

43
Q

Examples of problems at the thyroid gland

A
  • autoimmune destruction (Hashimoto’s disease)
  • iodine deficiency
  • treatment of hyperthyrodism
  • congenital defects in hormone
  • antithyroid drugs (side effect of some drug therapy)
44
Q

Secondary hypothyroidism

A

Problems at pituitary gland (TSH)

45
Q

Tertiary hypothyroidism

A

Problems at the hypothalamus (TRH)

46
Q

Diagnosis for hypothyroidism:
High/normal TSH
High fT4

A

not hypothyroidism

47
Q

Diagnosis for hypothyroidism:
High TSH
Low fT4

A

Primary hypothyroidism

48
Q

What feature must be present for actual hypothyrodism to be diagnosed?

A

low fT4

49
Q

Diagnosis for hypothyroidism:
High TSH
Normal fT4

A

subclinical hypothyrodism (high risk, but not yet hypo)

50
Q

Diagnosis for hypothyroidism:
Low/normal TSH
Low fT4

A

Secondary hypothyrodism

51
Q

Complications of hypothyroidism vary depending on…

A

When during the lifetime patient has the disease

52
Q

Complications of hypothyroidism:

Pregnancy

A

Affect fetal development (irreversible)

53
Q

Complications of hypothyroidism:

Infancy, childhood

A
  • bad brain development
  • can’t grow tall
  • low IQ
  • bad psychomotor development
  • cretinism (if severe)
54
Q

Complications of hypothyroidism:

Adult

A
  • death from myxedema coma (if severe)
55
Q

Myxedema coma

A
  • long-term hypothyrodism + another factor
  • cold body (<80 F)
  • loss of consciousness
56
Q

Creatinism is ____ ___thyroidism

A

congenital

hypo-

57
Q

Creatinism can be caused by…

A
  • absence of thyroid gland

- thyroid hormone synthesis defects

58
Q

Is creatinism fatal?

A

No

  • Creatinism happens if diagnosed too late
  • Early diagnosis can completely reverse effect
59
Q

Symptoms of creatinism

A
  • mental retardation
  • short
  • deaf
  • neurological problems
  • tongue sticking out
  • flat nose bridge
60
Q

How to treat creatinism?

A

replacement thyroid hormone

61
Q

Diagnosis of creatinism

A

screening tests for newborns (can’t usually tell from clinical symptoms)

  • Screen TSH (should be high if T3 + T4 is low)
  • High TSH = creatinism
62
Q

Treatment for primary hypothyrodism

A

Replacement therapy with synthetic T3 + T4

- Monitor by observing TSH levels after a few weeks (should be normal)

63
Q

Key symptoms of hyperthyrodism

A
  • Weight loss
  • Fatigue
  • Glucose intolerance
  • Tremor
  • Infected eye
  • Sweating
  • Rapid heart rate
  • High BP
64
Q

Why is weight loss a symptom of hyperthyroidism?

A

Too much metabolic activity

65
Q

Why is fatigue a symptom of hyperthyroidism? Why is it a symptom of hypothyrodism?

A

Hyper: high metabolic activity cause muscle overwork
Hypo: hormones not available, so no stimulation for metabolism

66
Q

Causes of hyperthyrodism

A
  1. Graves’ disease
  2. Plummer’s disease
  3. Thyroid tumour
  4. Thyroiditis
  5. Pituitary tumour
  6. HCG secreting trophoblastic tumour
  7. Iodine / iodine drugs
  8. Excessive T4 + T3
67
Q

Plummer’s disease

A

toxic multinodular goiter:

excess production of thyroid hormones from functionally autonomous thyroid nodules

68
Q

Graves’ disease

A

Diffuse toxic hyperplasia:

  • Autoimmune disease that affects the thyroid
  • Antibodies bind to TSH receptor
69
Q

Thyroiditis

A

inflammation of thyroid gland

70
Q

HCG secreting trophoblastic tumour

A

HCG has same a-unit as TSH, so during prenancy, the excess HCG might bind to TSH receptor and stimulate T3 + T4 production

71
Q

Why might high iodine cause hyperthyroidism

A

Iodine is a substrate needed to make T3 and T4

72
Q

Symptoms of Grave’s disease

A
  • retracted eyelids
73
Q

Diagnosis of Graves’ disease

A
  • Very low TSH
  • Very high fT4
  • Anti-TSH receptor antibodies
  • Radionucleotide uptake and scan (will accumulate in the thyroid)
74
Q

Treatment for Graves’ disease

A
  • Antithyroid drugs
  • radioiodine / radiosodium (destroy thyroid gland)
  • surgery to remove thyroid gland
75
Q

Antithyroid drugs

A
  • Block iodide uptake
  • inhibit T4 synthesis
  • inhibit T4 -> T3 conversion
76
Q

Diagnosis for hyperthyroidism:
Normal TSH
Normal fT4

A

not thyrotoxicosis

77
Q

Diagnosis for hyperthyroidism:
High / normal TSH
High fT4

A

Pituitary tumour

Thyroid hormone resistance syndrome

78
Q

Diagnosis for hyperthyroidism:
Low TSH
Normal fT4
Normal fT3

A

subclinical thyrotoxicosis

79
Q

Diagnosis for hyperthyroidism:
Low TSH
Normal fT4
High fT3

A

T3 toxicosis

80
Q

Diagnosis for hyperthyroidism:
Low TSH
High fT4
T3 toxicosis

A

Primary thyrotoxicosis

81
Q

thyrotoxicosis

A

hyperthyroidism

82
Q

Why is glucose intolerance a symptom of hyperthyroidism?

A

Insulin is quickly cleared due to high metabolic rate

LMP301 (18 decks)

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