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Endocrine > Section 3 - Thyroid Gland > Flashcards

Section 3 - Thyroid Gland Flashcards

1
Q

Location of the thyroid gland?

A

Located below Adam’s apple. Connected by isthmus (bridge of thyroid tissue) located below cricoid cartilage.

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2
Q

Identify the following gross anatomical features of thyroid gland

A
  • right lateral lobe
  • left lateral lobe
  • pyramidal lobe
  • isthmus - bridge of thyroid tissue
  • parathyroid glands - found within the thyroid gland
  • recurrent laryngeal nerves
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3
Q

follicular epithelial cells (thyrocytes)

A

spherical cells that make up the thyroid gland

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4
Q

follicular lumen (colloid)

A

fluid within the follicles

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5
Q

parafollicular cells (c cells)

A

secrete calcitonin

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6
Q

TSH receptors

A

found on the basolateral membrane of thyroid follicular cells

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7
Q

where is the Na+/I- symporter (NIS) found?

A

found on the basal membrane

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8
Q

Pendrin

A

ion transporter that moves iodine into colloid

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9
Q

thyroglobulin

A

substrate to help make T4 and T3

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10
Q

thyroid peroxidase

A

important enzyme that helps synthesize T4 and T3. It oxidizes I- to I2. Organification occurs of I2 allowing you to add iodine to tyrosine on TGB to make MIT and DIT. Coupling of MIT and DIT leads to synthesis of T4 and T3.

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11
Q

What is the difference between T3 and T4?

A

T3 and T4 are very similar but T4 has one more iodine than T3.

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12
Q

Which is more potent T3 or T4?

A

T3 is 4-5 times more potent than T4 even though T4 gets secreted more often. However, because T4 is secreted more often, it is converted into T3.

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13
Q

Dietary and non-dietary sources of iodine?

A

Dietary sources include seafood, seaweed, kelp, iodized salt, and dairy products.

Individuals may be exposed to medications, disinfectants, and radiographic contrast agents.

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14
Q

Hypothalamic-pituitary-thyroid axis and explain the role of negative feedback on the axis.

A

Hypothalamus releases TRH which acts on thryotrophes in anterior pituitary gland.

Thyrotropes become activated and release TSH which goes and activates thyroid gland.

Thyroid then releases T3 and T4 which goes into the blood stream.

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15
Q

In T3 and T4 synthesis, what is the synthesis and structure of thyroglobulin?

A

large molecule that consists of a bunch of tyrosine molecules. These tyrosine molecules are made into thyroglobulin in the follicular cells and dumped into the colloid

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16
Q

In T3 and T4 synthesis, what is the role of iodine trapping?

A

sodium/iodine cotransport iodine and sodium into the follicular cells using ATP. Once in the follicular cells, thyroid peroxidase converts I- to I2 and is dumped into the colloid. I2 is then combined with tyrosine molecules on TGB to make MIT or DIT. MIT and DIT is cleaved and coupled to make T3 and T4.

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17
Q

In T3 and T4 synthesis, what is the role of thyroid peroxidase?

A

makes I2, MIT and DIT, and then coupled to make T3 and T4

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18
Q

In T3 and T4 synthesis, what is the role of thyroid deiodinase (5-deiodinase)?

A

deionidates MIT and DIT and recycles I- and tyrosine

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19
Q

How much of a supply of T3 and T4 can a normal thyroid store?

A

It can reserve up to one to two months

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20
Q

Explain the various ways in which TSH affects T3 and T4 synthesis and secretion?

A

Stimulates TGB synthesis, stimulates Na+/I- pump activity, activates thyroid peroxidase, and stimulates growth of thyroid follicles. Can lead to hypertrophy and hyperplasia and can manifest as a goiter in patients.

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21
Q

Explain how T3 and T4 are carried in the blood and distinguish between what is meant by free T4 vs total T4

A

Carried via transport proteins. Three main ones are thyroxine-binding globulin (TBG), thyroxine-binding pre-albumin (TBPA) and albumin. The amount of free T4 is the fraction that is responsible for hormonal activity. Total amount of thyroid hormones bound to these plasma proteins provides a substantial reservoir of T3 and T4 in the blood

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22
Q

Explain the various physiological effects of T3 and T4 on its target tissues

Growth

A
  • Helps with growth formation and works synergistically with growth hormone and somatomedins to promote bone formation
  • Bone maturation - promotes ossification and fusion of bone plates and bone maturation
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23
Q

Explain the various physiological effects of T3 and T4 on its target tissues

CNS

A
  • Maturation of CNS - extremely critical in perinatal period

- Maintains alertness, concentration , and focus

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24
Q

Explain the various physiological effects of T3 and T4 on its target tissues

BMR

A
  • increased sodium/potassium ATPase
  • increase oxygen consumption
  • increased heat production
  • increased BMR
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25
Q

Explain the various physiological effects of T3 and T4 on its target tissues

Metabolism

A
  • increased glucose absorption
  • increased glycogenolysis
  • increased glucogeneogenesis
  • increased lipolysis
  • increased protein synthesis and degradation
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26
Q

Explain the various physiological effects of T3 and T4 on its target tissues

Cardiovascular

A

increased cardiac output

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27
Q

Explain the importance of screening for congenital hypothyroidism and how this screening is performed

A

Fetal thyroid gland begins to function at 10-12 weeks of gestation.

It is a primary source of thyroid hormone in developing fetus after the first trimester, during which maternal T4 is the only source. Helps with brain development. Otherwise, can result in growth retardation and delayed cognitive development. Heel prick is given and blood is taken from screening 2-5 days after birth.

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28
Q

Various clinical manifestations of hyperthyroidism

A

Nervousness, irritability, bulging eyes (due to fibroblasts being stimulated around the eyes and causes buildup over time), goiter, menstrual irregularities, frequent bowel movements, moist palms, weight loss, rapid heartbeat, increased body temperature.

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29
Q

Graves’ disease

A

Most common primary hyperthyroidism, autoimmune disease that creates antibodies that stimulate the thyroid. Thyroid stimulating immunoglobins (TSI) bind to the thyroid gland and constantly stimulate the thyroid.

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30
Q

Toxic nodular goiter

A

primary hyperthyroidism

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31
Q

TSH - secreting adenoma

A

secondary hyperthyroidism

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32
Q

hyperfunctioning thyroid adenoma

A

primary hyperthyroidism

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33
Q

acute thyroiditis

A

primary hyperthyroidism

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34
Q

Jod-Basedow syndrome (iodine-induced thyrotoxicosis)

A

primary hyperthyroidism, due to excessive amount of iodine

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35
Q

thyrotoxicosis factitial

A

exogenous iodine

36
Q

Dental aspects of hyperthyroidism?

A

1) accelerated dental eruption in children
2) increased susceptibility to dental caries and periodontal disease
3) burning mouth syndrome
4) exacerbate patient’s response to dental pain and anxiety

37
Q

what kind of drug is methimazole?

A

thionamide drug

38
Q

what is the mechanism of methimazole

A

blocks thyroid peroxidase

39
Q

what is the major adverse, toxic effects of methimazole

A

can cause agranulocytosis and liver failure. CBC needs to be done immediately

40
Q

special considerations of methimazole

A

keep in mind that it takes time for this drug to have an effect due to the fact that the thyroid stores quite a bit of T3 and T4 already used to induce remission or control symptoms before surgery/RAI treatment. Can cause agranulocytosis and liver failure. CBC needs to be done immediately

41
Q

what kind of drug is propylthiouracil?

A

thionamide drug

42
Q

what is the mechanism of propylthiouracil?

A

blocks thyroid peroxidase.

43
Q

what is the major adverse, toxic effects of propylthiouracil?

A

can cause agranulocytosis and liver failure (much higher for this drug). CBC needs to be done immediately.

44
Q

special considerations of propylthiouracil?

A

keep in mind that it takes time for this drug to have an effect due to the fact that the thyroid stores quite a bit of T3 and T4 already. Used to induce remission or control symptoms before surgery/RAI treatment

45
Q

(RAI)

A

radioactive iodine therapy

46
Q

radioactive iodine therapy mechanism

A

administered in solution or capsule. radioactive iodine is incorporated into thyroid gland and results in extensive local tissue damage to thyroid.

47
Q

radioactive iodine therapy major adverse, toxic effects

A

can be accidentally spread so whoever is taking this should self-isolate

48
Q

special considerations of radioactive iodine therapy?

A

do NOT give to pregnant women cause it will destroy the brain of the fetus. advocate to give dosage to hypothyroidism

49
Q

beta blockers

A

control symptoms of hyperthyroidism

50
Q

beta blockers mechanism

A

decrease adrenergic manifestations (tachycardia, palpitations, tremulousness, anxiety, etc). can help alleviate symptoms until thionamide takes effect or the patient is scheduled for surgery or RAI therapy. Normally started soon after diagnosis.

51
Q

mechanism of iodine salts or solutions

A

used to overload thyroid with non-radioactive iodine. Block radioactive iodine uptake due to accidental exposure.

52
Q

corticosteroids used for?

A

specifically for Graves’ ophthalmopathy

53
Q

mechanism for corticosteroids

A

helps to treat Graves’ since decreasing thyroid hormone secretion doesn’t improve pathology of Graves’ opthalmopathy

54
Q

special considerations of corticosteroids

A

eye shades, artificial tears (saline eye drops), avoiding sleeping on the face, and raising the head of the bed should help with mild symptoms

55
Q

Surgical options for hyperthyroidism in terms of when they should be recommended and potential complications?

A

Should only have surgery for very large/obstructive goiters (Graves’ disease), those who are allergic to thioanimides, and those who are unable to or refuse to receive RAI therapy

56
Q

What are some potential complications of surgery?

A

1) transient vocal paralysis
2) prolonged post-operative hypocalcemia
3) permanent hypoparathyroidism
4) recurrent hyperthyroidism

57
Q

Various clinical manifestations of hypothyroidism?

A

1) moodiness/irritability
2) depression
3) loss of body hair
4) dry, patchy skin
5) weight gain -> decrease in basal metabolic rate
6) constipation
7) slower heartbeat
8) puffy eyes
9) swelling
10) cold sensitivity - body is producing less heat
11) accumulation of glycosaminoglycans
12) myxedema

58
Q

Hashimoto’s thyroiditis (chronic autoimmune thyroiditis)

A

most common cause!

Etiology: autoimmune system attacks thyroid gland

59
Q

Post-hyperthyroid treatment

A

Etiology: removed TOO much of thyroid during throidectomy

60
Q

iodine deficiency

A

Etiology: not enough iodine being ingested. seen more in third world countries

61
Q

Congenital

A

Etiology: thyroid gland is complete absent at birth

62
Q

lack of TSH

A

Etiology: lack of TSH produced due to a problem with the anterior pituitary or hypothalamus

63
Q

Clinically important dental aspects of hypothyroidism

A
  • Macroglossia (caused by myxedema)
  • thick lips (myxedema)
  • micrognathia (small jaw)
  • dysgeusia (alteration in taste)
  • enamel hypoplasia
  • delayed eruption in children
  • poor periodontal health
  • delayed wound healing
  • burning mouth syndrome
64
Q

what drug is taken for hypothyroidism?

A

levothyroxine

65
Q

mechanism of levothyroxine?

A

T4 analog

66
Q

major adverse effect for levothyroxine?

A

people with heart issues. not to use with obesity

67
Q

special considerations with levothyroxine?

A

make sure to start off at a lower dose, as moving from a hypothyroid to euthyroid state can cause excessive stress on the cardiovascular system since it gets the heart going. Take on empty stomach

68
Q

what is another drug for hypothyroidism?

A

liothyronine

69
Q

mechanism of liothyronine?

A

T3 analog

70
Q

major adverse effect for liothyronine?

A

people with heart issues. not to use with obesity.

71
Q

special considerations for liothyronine?

A

make sure to start off at a lower dose, as moving from hypothyroid to euthyroid state can cause excessive stress on the cardiovascular system since it gets the heart going.

72
Q

what are the different forms of thyroid cancer?

A

anaplastic, follicular, medullary, papillary

73
Q

anaplastic cancer

A

rare but extremely aggressive as it spreads to nearby structures. look much different.

74
Q

follicular cancer

A

arises from follicular cells, slow-growing but more aggressive than papillary. spreads through blood but not lymph. 2nd most common thyroid cancer. looks similar to normal follicular cells

75
Q

medullary cancer

A

arises from c-cells. fairly aggressive and can spread through lymph nodes. high secretion of calcitonin.

76
Q

papillary cancer

A

80%. arises from follicular cells, slow-growing, treatable with good prognosis. slow and treatable. most common form of thyroid cancer, females affected 3X more than males.

77
Q

Treatment for thyroid cancers?

A 
thyroidectomy
radiation therapy
radioactive iodine therapy
chemotherapy
various types of immunotherapies and chemotherapy

Potential adverse effects of treatments have been listed or covered by previous bullet poitns

78
Q

What is the etiology of thyroid storm?

A

Precipitated by an acute event such as surgery, trauma, infection or parturition (birth)

79
Q

clinical manifestations of thyroid storm?

A
  • cardiac arrhythmia
  • hypotension/shock
  • hyperpyrexia (fever)
  • agitation/anxiety/delirium/psychosis/stupor/coma
  • severe nausea, vomiting, diarrhea, abdominal pain
80
Q

treatments of thyroid storm?

A

beta blockers, thioanamides, plasmapheresis, glucocorticoids, bile acid sequestrants, abdominal pain

81
Q

dental implications of thyroid storm?

A

since this is HYPERthyroidism, you should see same dental aspects in patients with hyperthyroidism

82
Q

etiology of myxedema coma?

A

hypothyroidism

83
Q

clinical manifestations of myxedema?

A

skin and soft tissue changes with deposition of glycosaminoglycans in the dermis of the skin.

decreased mental status (mental slowness, confusion, apathy, depression) and hypothermia

84
Q

myxedema vs myxedema coma?

A

myxedema is skin changes but myxedema coma is skin changes AND decreased mental status

85
Q

treatment of myxedmea?

A

administration of electrolytes, glucose, mechanical ventilation if needed. IV T4 is also given to the body as well.

86
Q

another thing the thyroid hormone stimulates is

A

intestinal motility, allows for healthy bowel movements

87
Q

What is the difference between acute destructive thyroiditis and hashimoto’s thyroiditis

A

acute destructive thyroiditis has an initial presentation of hyperthyroidism which is followed by a hypothyroid phase and then recovery of thyroid function

in hashimoto’s thyroiditis, there is no recovery of thyroid function

Endocrine (6 decks)

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