Thyroid and Parathyroid Histology Flashcards

1
Q

Describe the formation of the thryoid gland.

A

Endodermal mass of cells invaginates into the underlying mesoderm, creating the thyroid diverticulum that is positioned between anterior 2/3 and posterior 1/3 of the developing tongue.

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2
Q

What pharyngeal arches do the thyroid diverticulum grow in between?

A

2nd and 3rd

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3
Q

During what week of embryonic development does thyroid gland respond to TSH?

A

week 22.

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4
Q

What’s Cretinism

A

Congenital absence of thyroid gland causing irreversible neurologic damage in the infant

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5
Q

Describe the steps in synthesis of thyroid hormone.

A
  1. TSH binds, and the cell actively transport aa and iodide ions across the cell membrane. Iodide ions concentration inside the cell increase = Iodide trap
  2. Oxidation (organification) takes places in the lumen of colloid
  3. Iodine is added to tyrosine residues on TGB
  4. MIT and DIT binds. if two DIT binds = T4. if a MIT and a DIT binds = T3
  5. The TGB bound T3 and T4 is stored until stimulation.
  6. Upon TSH stimulation the complex is endocytosed and via lysosomes TGB is broken down releasing T4 and T3 and Iodide. T4 and T3 are relased into the blood, and the rest are reccyled.
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6
Q

What enzyme is responsible for the addition of iodine to tyrosine residues of TGB

A

Tyrosine peroxidase

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7
Q

Thyroid peroxidase activity and the iodination process can be inhibited by what drugs?

A

Propylthiouracil and methyl mercaptoimidazole

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8
Q

What is the MOA of mercaptoimidazole and PTU?

A

Inhibits the binding of I (organizfiaiotn)

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9
Q

Thyroxine-binding protein functions to _.

A

it’s a capillary transport protein that transports T3 and T4 in the blood.

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10
Q

What is the ratio of bounnd vs unbound thyroid hormone int he blood?

A

> 1% is free

99% is bound to Thyroxine binding globulins, to albumins or others

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11
Q

What is the basic functions of thyroid hormones?

A

Stimulates basic metabolic rate, augment thermogenesis, ,augments glucose production, and is required for normal development of the CNS

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12
Q

What are some symptoms of hyperthyroidism?

A

Increased metabolic rate, weight loss, hyperactivity and heat intolerance

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13
Q

What are some common causes of hyperthyroidism?

A
  1. excessive stimulation by adenohypophysis
  2. loss of feedback control by thyroid gland (graves disease)
  3. ingestion of T4 (used for weight loss)
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14
Q

What is Grave’s disease caused by?

A

Autoimmune disorder that produces antibodies to the receptors for TSH on the follicular epithelium . the bound antibody chronically stimulate thyroid gland to release thryoid hormone. Feedback loop doenst work to inhibit it.

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15
Q

what are some symptoms of Graves disease?/

A
  1. enlargement of the thyroid gland (goiter), bulding of the eyes (exophthalmos), tachycardia, warm skin, fine finger tremors are typical clinical features
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16
Q

How can graves disease be treated?

A

Surgical removal, radioactive iodine. Post Tx regimen requires supplementation of thyroid hormones.

17
Q

What are some symptoms of low hypothyroidism?

A

low metabolic rate, feeling of being cold, weight gain (some patients). In adults coarse skin with puffy appearance due to accumulation of proteoglycans and retention of fluid in the dermis of the skin (myxedema) and msucle.

18
Q

What is Hashitomo’s disease?

A

autoimmune disease associated with hypofunction of the thyroid gland, caused by autoantibodies (antimicrosoaml antibodies) to thyroid peroxidase and thyroglobulin.

19
Q

How can Hashitomo’s disease be treated?

A

oral thyroid medication

20
Q

Condition of severely stunted physical and mental growth due to untreated congenital deficiency of thyroid hormones is characteristics of what disorder?

A

FKA cretinism aka congenital hypotheyroidism

21
Q

Bone maturation and puberty are severely delayed and ovulation is impeded and interility is common, neurological impairment with reduced muscle tone, and cognitive impairment are all characteristics of what type of disorders.

A

COngential hypothyroidism aka FKA cretinism.

22
Q

Calcitonin are made where?

A

In parafollicular cells (C cells) in the follicular epithelium of thyroid gland

23
Q

Calcitonin binds to receptors on what types of cells?

A

Osteoclasts

24
Q

What gland originates from the interaction of the endoderm of the third and fourth pouch?

A

parathyroid gland

25
Q

The position of the parathyroid gland switches during development such that the pair of glands which is ultimately inferior develops from which pouch?

A

Third pouch. superior ones are from 4th pouch.

26
Q

What’s responsible for the switching of the parathyoid pouches?

A

Migration of the thymus

27
Q

Which cell type are more numerous in the parathyroid glands?

A

Chief or principal cells

28
Q

what are two cell types found in the parathyroud gland?

A

Chief cells and oxyphil cells.

29
Q

What cell types secrete PTH?

A

chief (principal) cells.

30
Q

What receptors on the chief cells sense Ca and then riggers the release of intracellular signals suppressing the secretion of parathyroid horone.

A

Ca-sensing receptor (CaSR)

31
Q

What cells in the bone do PTH act on?

A

Acts on osteoblast to prmote osteoclast activity –> increase in circulating Cal levels.

32
Q

How does PTH control rate of Ca uptake in the GI tract?

A

By regulating production of vitamin D in the kidneys.

33
Q

In response to PTH, vitamin D production is stimulated, vit D then acts on the intestinal mucosa to do what two things?

A

Absorb Ca and synthesize Calbindin (carrier protein)

34
Q

Ca deficiency resulting in spontaneous depolarization of neurons and muscle fibers resulting in tetany is seen what condition that which cannot sense low blood calcium.

A

Hypoparathyroidism

35
Q

What are the consequences of hyperparathyroidism?

A

High blood calcium, bone loss leading to osteomalacia and osteitis fibrosis cystica; abnormal calcium deposition in arteries and kidneys.

36
Q

The calcification of the bone matrix osteoid is deficient in rickets and osteomalacia due to _

A

Deficiency of vitamin D

37
Q

Rachitic rosary at the costochondral junction, poor calcification of the long bones causing bowlegs or knock-knees are associated with which Vitamin D deficient disease?

A

Rickets