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Endocrine and Reproductive Systems > P- Thyroid and Parathyroid > Flashcards

P- Thyroid and Parathyroid Flashcards

1
Q

Describe the normal gross anatomy of the thyroid. What happens if there is incomplete migration in development?

A

There are two lobes straddling the trachea with the isthmus.
The normal thyroid should be just inferior and lateral to the Adam’s apple.
If there is incomplete migration–> lingual thyroid at the base of the tongue

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2
Q

Describe normal histology of the thyroid.

A
  1. follicles that are variably sized and lined by single layer of thyrocytes and full of thyroglobulin [colloid]
  2. parafollicular C-cells interspersed with the follicular cells [derived from neural crest]
  3. rich capillary network
  4. thin fibrous septa
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3
Q

What is the role of the follicular cell in the thyroid.

A
  1. make T3, T4
  2. store T3,T4 in colloid
  3. secrete T3. T4
T3= triiodothyronine
T4= thyroxin
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4
Q

What must T3 and T4 be incorporated with to facilitate storage in colloid?

A

TBG - thyroid binding globulin

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5
Q

How is the release of thyroid hormones regulated?

A
  1. hypothalamus secretes thyrotropin releasing hormone [TRH]
  2. Ant pituitiary thyrotropes release thyrotropin [TSH]
  3. TSH binds GPCR on follicular cell which promotes T3, T4 synthesis AND release of preformed T3, T4 into the bloodstream
  4. T3 and T4 in the blood are bound to TBG and albumin
  5. unbound T3 and T4 are biologically active
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6
Q

Which is more active, T3 or T4?

Which is more prevalent in blood, T3 or T4?

A

T3 is more active, T4 is more prevalent [by 20x]

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7
Q

What do T3 and T4 regulate?

A
  1. body temp
  2. metabolism and O2 consumption
  3. HR, cardiac output
  4. protein synthesis
  5. carb, fat breakdown
  6. maturation of CNS and PNS
    7, body growth/development
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8
Q

If there is high T3/4 in the blood, what happens to TRH and TSH?
If there is low T3/4 what happens to TRH/TSH?

A

high T3/4 = both decrease

Low T3/4 = both increase

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9
Q

What is the most clinically useful marker of thyroid axis function?

A

Serum levels of TSH

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10
Q

When doing an assay for T3/4 why is it important to calculate free T3/4 and not total?
How do you make this measurement?

A

Extraneous factors like drugs and illness can affect binding to TBG.
To account for this you can do a thyroid hormone binding ratio using the T3-resin uptake test.

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11
Q

How do you determine the thyroid hormone binding ratio [THBR]?

A

Use the T3- resin uptake test.
If the patients TBG is loaded with T3, little radiolabeled T3 will be able to bind TBG so more will be on the resin.

When you have THBR multiply it by total T3 or T4 to give the FREE T3/4 index

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12
Q

What is meant by primary hyperthyroidism? What is an example?

A

Primary = in the thyroid
so it means that a disorder intrinsic to the thyroid gland that results in excessive thyroid function

ex. Grave’s

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13
Q

What is meant by secondary hyperthyroidism? What is an example?

A

Excessive thyroid function due to extrinsic disorder like a TSH-producing adenoma in the pituitary.

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14
Q

What is an example of primary hypothyroidism? Secondary hypothyroidism?

A

Primary hypothyroidism - hashimotos

Secondary hypothyroidism = HP failure

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15
Q

You are suspicious a person has thyroid dysfunction. You do a lab test and get a normal TSH. What does this rule out?

A

This means that it is not likely to be a primary thyroid abnormality.

If it was a hyperfunctioning thyroid, TSH would be low
If it was a low functioning thyroid, TSH would be high

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16
Q

What is a situation where you have low TSH and hypothyroidism?

A

Secondary hypothyroidism caused by HP dysfunction

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17
Q

What is thyrotoxicosis? How does it differ from hyperthyroidism?

A

Hyperthyroidism can CAUSE thyrotoxicosis, but they can exist separately too.
Thyrotoxicosis is where there is elevated circulating free T3 and T4 leading to a hypermetabolic state

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18
Q

What are the 3 primary causes of thyrotoxicosis that are associated with hyperthyroidism?

A
  1. Diffuse toxic hyperplasia [graves]
  2. hyperfunctioning multinodular goiter
  3. hyperfunctioning adenoma
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19
Q

What is the secondary cause of thyrotoxicosis that is associated with hyperthyroidism?

A

TSH-secreting pituitary adenoma

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20
Q

What are the 4 causes of thyrotoxicosis NOT associated with hyperthyroidism?

A
  1. subacute granulomatous thyroiditis
  2. subacute lymphocytic thyroiditis
  3. struma ovarii [thyroid tissue in ovarian teratoma]
  4. factitious thyrotoxicosis [drugs, intake of T3]
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21
Q

What are the “general effects” of thyrotoxicosis?

A
  1. metabolism increase
  2. sweating
  3. weight loss though eating more
  4. heat intolerance
  5. nervous, irritable
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22
Q

What is the effect of thyrotoxicosis on the eyes?

A

exophthalmos- bulging eyes

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23
Q 
What are the effects of thyrotoxicosis:
1. skin
2. heart
3. neuromuscular
4. GI
5 eyes
A
  1. red, warm, velvety
  2. tachycardia, palpitation
  3. tremor, muscle weakness
  4. increased motility, diarrhea, malabsorption
  5. exophthalmos
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24
Q

What is a thyroid storm?

A

Severe thyrotoxicosis leads to massive release of catecholamines causing cardiac arrhythmia and death

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25
Q

What is apathetic hyperthyroidism?

A

blunted thyrotoxicosis symptoms in the elderly

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26
Q

What are the primary causes of hypothyroidism?

What is the most common cause worldwide?

A
  1. radiation, ablation, surgery
  2. hashimotos
  3. iodine deficiency***
  4. congenital biosynthetic defect/developmental abnormalities
  5. lithium
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27
Q

What are many of the symptoms of hypothyroidism due to?

A

accumulation of mucopolysaccharides in tissues and subsequent non-pitting edema [myxedema]

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28
Q

What are the symptoms of hypothyroidism:

  1. generally
  2. skin
  3. GI
  4. heart
  5. larynx
  6. eyes
  7. hair
A
  1. apathy, depression, cold intolerance, weight gain, low libido
  2. dry, brittle, coarse facial features, decreased sweat
  3. enlarged tongue, slow motility, poor appetite
  4. effusion, enlarged heart
  5. deeper voice due to edema
  6. puffy due to edema
  7. dry, brittle, loss
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29
Q

A child in Africa presents with short stature, mental retardation, coarse facial features, protruding tongue and belly and sparse hair. What is the likely disorder? What caused it?

A

Cretinism- due to lack of iodine –> hypothyroidism

If the mother had low iodine intake during development there is exceptionally impaired skeletal and CNS function

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30
Q

What is the most common cause of hypothyroidism in the US? What sex and age range does it tend to present?
How do they typically present?

A

Hashimoto’s thyroiditis [chronic lymphocytic thyroiditis]

Women 10x more than men and in the 45-65 range

They present either with classic hypothyroid signs [lethargy, dry brittle skin, low GI motility, etc] or they present with a small goiter.

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31
Q

Why does Hashimoto cause a small goiter?

A

In Hashimoto there is destruction of the thyroid by autoimmune function.
This initially leads to thyrotoxicosis [increased T3/4] but then eventually it progressed to hypothyroidism.

Low T3/4 stimulates TSH secretion which acts on the thyroid causing small goiter.

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32
Q

What 3 parts of the thyroid do CD4 T cells react against in Hashimoto’s?

A
  1. thyroid peroxidase
  2. thyroglobin
  3. TSH receptor
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33
Q

Describe the autoimmune attack of Hashimoto’s.

A

CD4 T cells react against thyroid antigens like thyroglobin and thyroid peroxidase and:

  1. attract macrophages to damage thyrocytes like a type IV hypersensitivity rxn
  2. induce CD8 to destroy thyrocytes
  3. induce plasma cell release of antibodies to coat the thyrocyte and lead to NK cell attack
34
Q

What happens to T3/4 and TSH initially when thyroid follicles are damaged in Hashimoto? What happens over time?

A

Initially :
Increased T3/4 and decreased TSH [because the attack on thyrocytes release stored T3/4

Over time:
T3/4 decrease and TSH increases

35
Q

What do you see histologically in Hashimoto?

A
  1. lymphoid follicles with germinal centers
  2. macrophages, plasma cells
  3. infiltrate is symmetrical and diffue
  4. inflamed thyrocytes become pink [Hurthle cells]
  5. fibrosis and atrophy
36
Q

What tumor does Hashimoto put people at risk for?

A

B cell lymphoma

37
Q

What is the most common hyperthyroidism in the US?
What sex is more affected and what age group?
What is the mechanism of this disease?
How do the patients present?

A

Graves disease affects women 20-40.
It is constitutive activation of a TSHR because autoantibodies bind to it and keep it turned on.

Patients present with thyrotoxicosis, diffuse thyroid enlargement, exophthalmos, and pretibial myxedema with orange peel look.

38
Q

What are the 3 types of antibodies that can be found in patients with Graves disease?
Which result in hyperthyroidism?
Which result in goiter?

A
  1. Thyroid-stimulating IgG - mimics TSH, binds TSHR and stimulates it to release T3/4 [LATS-long acting thyroid stimulator]
    - hyperthyroidism
  2. Thyroid growth stimulating Ig- bind TSHR and stimulate growth of the thyroid follicles
    - goiter
    - hyperthyroidism
  3. TSH-binding inhibitory Ig- bind TSHR preventing TSH binding. Some stimulate, others paradoxically inhibit
    - hyperthyroidism
    - transient hypothyroidism
39
Q

How does Graves disease look histologically?

A
  1. diffuse and nodular hyperplasia/hypertrophy
  2. papillary structures inside follicles
  3. columnar follicular cells
  4. colloid becomes scalloped
  5. lymphocytic infiltrate throughout
40
Q

What is the mechanism by which goiters form? What is a goiter?

A

Goiter is enlargement of thyroid tissue.
If T3/4 is low, the pituitary will secrete TSH.
TSH will cause hypertrophy and hyperplasia of follicular cells to increase T3/4 output

41
Q

What is the #1 cause of goiters worldwide?

A

Iodine deficiency [decreased T3/T4–> increased TSH–> hypertrophy/hyperplasia of follicular cells–>goiter]

42
Q

What is the difference between a diffuse and multinodular goiter?

A

Diffuse = symmetric with same size nodule, both lobes

Multinodular = irregular, lumpy

43
Q

What is the difference between a simple and toxic goiter?

A

Simple = no thyrotoxicosis, no large nodules

Toxic = thyrotoxicosis

44
Q

How do diffuse goiters appear histologically?

A

hyperplastic columnar epithelial cells form papillary structures that extend into colloid [like Graves].

If iodine is added to the diet and thyroid stimulation decreases, the epithelium can involute back to cuboidal.
There is increased colloid in involuted areas [colloid goiters]

45
Q

How do multinodular goiters form?

How do they look histologically?

A

Different follicles respond differently to stimulatory factors. In long standing goiters:

  1. irregular distribution of proliferation and involution combine
  2. multinodular appearance
  3. areas of hemorrhage
  4. areas of fibrosis
  5. prominent cystic changes
46
Q

A 30-50 year old woman presents with a painful thyroid, especially when swallowing, after an upper respiratory tract infection.
Her thyroid is palpable and enlarged and she has a fever.
What is the problem and what is the pathogenesis?

A

Subacute Granulomatous Thyroiditis [de Quervain]

  1. Neutrophilic infiltrate damages follicles–>brief hyperthroidism
  2. later, chronic infiltrate replaces the acute and forms granulomas –> hypothyroidism, fibrosis
  3. inflammation settles and euthyroid state returns several weeks later
47
Q

What thyroiditis are you likely to get post-partum?
What is the mechanism?
What is the recurrence risk?
What is the histology?

A

Subacute lymphocytic thyroiditis:
Painless/silent due to autoimmune problem postpartum.
Throtoxicosis is followed by euthyroid state in a few months. Recurs with subsequent pregnancies

Histology:

  1. lymphoid infiltrates
  2. germinal centers
  3. NO thyroid follicle atrophy
48
Q

What is Reidel thyroiditis?

A

Fibrosing thyroiditis due to autoimmune etiology.

Thyroid and adjacent neck tissue become inflamed and fixed to each other

49
Q

What is palpation thyroiditis?

A

When the doctor palpates too hard and ruptures the thyroid follicles causing inflammation

50
Q

Most thyroid nodules are benign but what 5 factors increase the risk of malignancy?

A
  1. solitary thyroid nodule
  2. male
  3. young patient
  4. previous radiation on neck
  5. cold [non-functioning] nodule on thyroid scan
51
Q

What clinical tools can be used to est. diagnosis of a thyroid neoplasm?

A
  1. physical exam
  2. FNA
  3. radionucleotide thyroid scan
  4. US
  5. microscopic examination
52
Q

When doing a radioactive iodine scan, what thyroid lesions will be “hot”? What will be “cold”?

A

Hot = thyroiditis, benign goiter because it shows uptake and retention

Cold= tumors because they are non-functioning

53
Q

What is the benign thyroid neoplasm? What are the 5 malignant?
What cells are they all derived from?

A 
Benign - follicular adenoma
Malignant:
1. papillary carcinoma
2. follicular carcinoma
3. medullary carcinoma - C-follicular cell 
4. anaplastic carcinoma
5. lymphoma
54
Q

Will follicular adenomas be cold or hot on radioactive iodine scans?
Who are they most commonly seen in?
Are they single or multiple?
Describe gross and histologic appearance.

A

They are usually cold because they are non-functional and asymptomatic [except for the lump]

Most commonly seen in middle aged women and are usually single.

Grossly- single, encapsulated [thick fibrous capsule]

Histologically:

  1. resemble normal thyroid except for growth pattern inside capsule
  2. Hurthle cells
55
Q

How can follicular adenoma and follicular carcinoma be differentiated?

A 
Adenoma = do not invade capsule, vessels 
Carcinoma= invade THICKER capsule, vessels

To make a definitive differentiation you need to have histologic examination of the resected thyroid/lobe.

56
Q

What mutation is associated with follicular adenomas?

A

RAS

57
Q

What is the most common thyroid malignancy?

What sex and age group are most affected?

A

papillary carcinoma of the thyroid affects women more than men. They are seen in teens, twenties and after 50.

58
Q

A patient with past history of radiation exposure presents with a palpable neck mass.
What is the likely malignancy? Will it be hot or cold?
Do they tend to metastasize?
What is the prognosis?

A

Papillary carcinoma
Cold
metastasizes to local lymph nodes, but hematogenous mets are rare

Prognosis is good because they are slow growing except in:

  1. elderly
  2. distant mets
  3. invasion of soft tissue/vital neck structures
59
Q

What is seen histologically on a papillary carcinoma?

A
  1. finger-like projections with fibrovascular core [core differentiates it from papillary sprigs in Graves and diffuse goiters]
  2. can form follicles
  3. orphan annie eye nuclei
  4. pseudoinclusions in the nucleus
  5. psamomma bodies [calcium deposits]

Can be papillary, cystic, solid or follicular. It is diagnosed based on nuclear features.

60
Q

What are the mutations are associated with papillary carcinoma?

A
  1. translocation involving RET [tyrkinR] and PTC [papillary thyroid carcinoma] –> fusion protein that activates MAPK pathway and replication
  2. BRAF point mutation V600E that is specific for papillary carcinoma of the thyroid. Do DNA sequencing for it
61
Q

What is the usual cause of follicular carcinoma? What age group and sex is affected?
It this carcinoma hot or cold?
Does it invade or metastasize?

A

It is usually caused by iodine deficiency in older age women.
The lesion is cold
It metastasizes hematogenously to lungs, liver, bones

62
Q

Describe the microscopic appearance of follicular adenoma.

What is needed for diagnosis?

A
  1. tumor cells resemble normal follicular cells
  2. thick fibrous capsule
  3. tumor follicles invade through the capsule
  4. vascular invasion in the carcinoma

To diagnose follicular adenoma from carcinoma you need a lobectomy or total thyroidectomy. FNA cannot differentiate the two

63
Q

What mutations are associated with follicular carcinoma?

A
  1. RAS point mutation

2. PAX8-PPARg translocation

64
Q

How does medullary carcinoma differ from the other thyroid carcinomas?

A
  1. arises from parafollicular C cells, not follicular
  2. functional tumor that secretes
    - calcitonin [lowers serum Ca]
    - serotonin, somatostatin
  3. can be single, multiple, bilateral
65
Q

Most medullary carcinomas are sporadic but 20% are associated with what?

A
  1. MEN2 and MEN2b

2. RET

66
Q

What is the histology of a medullary carcinoma?

A
  1. polygonal or spindle cells
  2. AMYLOID
  3. necrosis and hemorrhage
67
Q

A patient presents with a past history of multinodular goiters. What type of carcinoma are you concerned about?
What mutation is associated with it?

A

Anaplastic carcinoma is a high-grade, undifferentiated carcinoma with a high mortality rate.
It arises in older patients that have previously had multinodular goiters and/or prior will differentiated carcinomas of the thyroid.

It is associated with p53 mutation

68
Q

Describe the gross and histologic appearance of parathyroid.

A

Parathyroid derives from 3 and 4 branchial pouches and is 4 tiny, encapsulated glands.
Histologically:
1. nests and cords of purple chief cells that make PTH
2. pink oxyphil cells with granular cytoplasm and lots of mitochondria [no known function]

both cell types contain a small amount of fat and have a rich vascular supply

69
Q

What is the role of the parathyroid gland?

What are the 4 jobs of PTH?

A

It sences free calcium ion concentration in serum and releases PTH when calcium is low.

PTH can increases calcium via:

  1. increased bone resorption
  2. gut dietary absorption
  3. renal tubule reabsorption
  4. initiate actions of vit D
70
Q

Describe primary, secondary and tertiary hyperparathyroidism.

A

Primary = problem with parathyroid itself [most common clinically silent hypercalcemia]

Secondary = extra parathyroidal factors causing excess PTH release [renal failure]

Tertiary= autonomous and excessive hyperfunctioning of a parathyroid likely due to a transformation to monoclonal state

71
Q

What 3 conditions cause primary hyperparathyroidism?

A
  1. parathyroid adenoma [75%]
  2. parathyroid glandular hyperplasia
  3. parathyroid carcinoma

All three elevate PTH, increase serum Ca

72
Q

What symptoms are associated with symptomatic primary hyperparathyroidism?

A

Psychic moans, abdominal groans, painful bones, renal stones

  1. osteoporosis, osteitis fibrosa cystica–> painful fracture
  2. peptic ulcers, constipation, pancreatitis, gallstones
  3. renal stones from calcium precipitating out in calyces
  4. prox muscle weakness, hypotonia, depression, lethargy, seizures
73
Q

What age and sex are more likely to get a primary parathyroid adenoma?
What is the gross appearance of the parathyroid?
Histologic?
What does radionucleotide scan show?

A

It most commonly affects women 20-40.

Grossly: a solitary adenoma that secretes PTH and elevates serum Ca causing atrophy of the other 3 glands.
The gland with the adenoma is encapsulated
Histologically: adenoma is composed of chief cells and is encapsulated and presses against normal tissue

Radionucleotide shows greater uptake in the gland with the adenoma compared to the other 3

74
Q

Describe the gross appearance of the parathyroid in primary parathyroid hyperplasia.
What does histology show?
What do you see on the radionucleotide scan?

A

Gross: 4 enlarged, hyperactive glands

Histology: loss of normal intraglandular fat and higher density of chief cells

Radionucleotide: equal uptake in all 4 glands

75
Q

What is the familial component of primary parathyroid hyperplasia?

A

MEN1, MEN2A

76
Q

What age group is affected by parathyroid carcinoma?
What is the gross appearance?
What is the histology?
How is it differentiated from primary parathyroid adenoma?

A

It affects men and women equally from 25-70

Gross: solitary nodule infiltrating adjacent tissue through the thin capsule

Histology: lower intraglandular fat, high density of chief cells. It looks the same as parathyroid adenoma

Differentiate from parathyroid adenoma because:

  1. invades surrounding tissue in the neck and mets
  2. calcium levels are often higher
77
Q

What is overexpressed in parathyroid adenoma, carcinoma AND hyperplasia?

A

cyclin D1

78
Q

What is the most frequent cause of secondary hyperparathyroidism?

A

Renal failure–>

  1. prevents phosphate excretion
  2. elevated phosphate chronically lowers calcium levels in serum activating the feedback loop
  3. stimulates PTH production
79
Q

How do the symptoms associated with primary hyperparathyroidism compare to secondary?

Describe the gross and histologic appearance of secondary.

A

secondary presents with many of the same symptoms [bones, stones, groans, moans] but are less severe

In secondary, however, there are metastatic calcifications in lungs, heart, vessels [which can lead to tissue ischemia–>calciphylaxis]

Grossly, all 4 glands hypertrophy and there is increased chief cell density and decreased intraluminal fat.

80
Q

What is calciphylaxis?

A

when hypercalcemia leads to calcified vessels causing tissue ischemia

81
Q

What are the possible inherited causes of hypoparathyroidism?
What are acquired causes?
What are the symptoms?

A

Inherited:

  1. isolated
  2. di George syndrome [defective thymus]
  3. MEN syndromes

Acquired
1. surgical removal of thyroid accidentally take parathyroid too

Symptoms:
tetany, tingling, spasms, arrhythmias, seizures

Endocrine and Reproductive Systems (27 decks)

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