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DT4-Exam 1 > Thyroid Parathyroid Disease-Melissa > Flashcards

Thyroid Parathyroid Disease-Melissa Flashcards

1
Q

Describe how the thyroid develops, its ultimate structure and location:

A

Invagination of pharyngeal mucosa–>
Bilobed organ w isthmus–>
Inferior to thyroid cartilage @ level of cricoid cartilage

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2
Q

Describe the histological appearance of the normal thyroid:

A

colloid within matrix of follicular epithelial cells and c cells

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3
Q

Define the funciton of colloid, follicular epi cells, parafollicular (c-cells) cells

A

colloid: resevoir for thyroglobulin and thyroid hormone

follicular epi cells: Thyroglobulin–> T4 + T3

C-Cells: secrete calcitonin: inhibit bone resorption; Ca sequestration by bone

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4
Q

Describe the process of Thyroid hormone release:

A

TRH (hypothalamous)–>
TSH (anterior pituitary)–>
T3 +T4 (Thyroid)–> Negative feedback on hypothalamus + pituitary

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5
Q

Define thryrotoxicosis; what is a possible cause?

A
  • Excessive leakage of T3/T4 –> Hyperthyroidism

- can be caused by thyroiditis

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6
Q

Hyperthyroidism causes what metabolic imbalance?

How does the condition present (5)?

A

Hypermetabolic state

  • GI hypermotility, malabsorption, diarrhea
  • ^ sympathetic stimulation
  • +/- CHF
  • Wide gazing state + Lid Lag
  • heat intolerance
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7
Q

What are the 5 most common causes of hyperthyroidism?

A
  • Graves disease
  • Ingestion of hormone
  • goiter
  • adenoma of thyroid
  • Thyroiditises
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8
Q

What is a struma ovarii?

A

Ovarian taratoma full of thyroid tissue–possible (RARE) cause of hyperthyroidism

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9
Q

What happens in a thyroid storm?
How does it present clinically?
What is the most common cause?

A
  • medical emergency
  • abrupt onset severe, life threatening thyrotoxicosis
  • Tachy, thermoregulatory malfxn, N/V/D
  • Seen in GRAVES DISEASE after thyroid surgery
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10
Q

How do we screen for hyperthyroidism; describe the lab findings:

A
  • ^fT4
  • Primary: LOW TSH (check T3)
  • Secondary: ^TSH
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11
Q

Most cases of hyperthyroidsim are: primary or secondary?

A

PRIMARY

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12
Q

What is endemic cretinism? What causes it?

A
  • Infants born with hypothyroidism–> MR, protruding tongue, etc.
  • Associated with Iodine deficiency or inborn metabolic error
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13
Q

What are the symptoms of HYPOthyroidism (6)?

A
  • myxedema
  • apathy
  • cold intolerance
  • constipation
  • periardial effusion and obsesity
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14
Q

What is the most sensitive laboratory test for hypothyroidism?
Which lab test will be decreased in both?

A

TSH = most sensitive test!!!

  • Primary (thyroid) = INCREASE
  • Secondary (pituitary) = DECREASED

T4 will be DECERASED in both!!

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15
Q

Waht is the #1 endogenous form of HYPERTHYROIDISM?

A

Graves disease

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16
Q

Graves Disease:

  • Population
  • Genetic association
A
  • females 20-40 yoa

- HLA-DR3, HLAB8

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17
Q

How does Graves disease present?

What is the clinical triad?

A
  • Exopthalmos (bulging eyes) + hyperthyroid sx.
  • Diffuse goiter +/- bruit over thyroid

Clinical Triad:

  • thyrotoxicosis
  • exopthalmos
  • pretibial mydedema
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18
Q

How does exopthalmos occur?

With which disease is it associated?

A

Assocated with GRAVES DISEASE:

Mononuclear infiltrate retro-orbital space–> Inflammatory edema of EO mm–>
^ ECM + ^ adipocytes

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19
Q

Describe the pathogenesis of Graves disease:

A

Autoimmune attack of thyroid autoantigens (#1= TSH-R)

*Multiple autoabs that ^ TH release

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20
Q

***Describe the histo of the graves thyroid (4):

A
  • Hypertrophy + hyperplasia
  • Crowded follicular cells
  • PAPILLAE WITHOUT FIBROVASCULAR CORE*
  • Colloid SCALLOPING*
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21
Q

Briefly describe how Graves disease manifests in the heart, eyes and skin:

A
  • cardiac hypertrophy and ischemia
  • exopthalmos w mucopolysaccharide infiltrate
  • pretibial myxedema
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22
Q

Lab findings associated with Graves (radioiodine, T4/3, TSH):

A
  • INCREASED UPTAKE on RADIOIODINE SCAN
  • ^T4, ^T3
  • DECREASED TSH
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23
Q

What is the most common thyroid disease?

What are some symptoms?

A

GOITER–simple enlargement of thyroid

- presents with cosmetic deformity, airway obstruction, dysphasia, etc. (or no complications at all)

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24
Q

What is a common cause of goiter?
Where is this a problem geographically?
How do we help it?

A

Iodine deficiency–> Impaired TH synthesis

  • common in mountainous regions (low Iodine in soil)
  • iodized salt helps
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25
Q

What is an ENDEMIC goiter?

A
  • OVER 10% of population has goiter
  • common in mountain people
  • assocated w Iodine deficiency!
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26
Q

What causes SPORADIC goiter?

A
  • many causes both environmental and genetic

- commonly idiopathic

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27
Q

What is Plummer’s syndrome?

A
  • HYPERthyroid disorder
  • multinodular goiters with hyperfunctioning nodule
  • NO optho or derm problems
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28
Q

Most goiters are…

A

EUTHYROID!

rarely HYPOthyroid, may mask or mimic neoplasm

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29
Q

Describe the pathogenesis of a goiter.

Describe the common lab findings assocated.

A

DECREASE TH–> ^TSH–> ^Thyroid size–> autonomous cell formation

  • T3/T4 wnl
  • TSH slightly ^ or wnl
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30
Q

Describe the gross morphology of a goiter:

A
  • Hypertrophy and hyperplasia
  • stimulation and involution
  • nodular/ multinodular
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31
Q

What are 4 conditions that can cause thyroiditis?

A
  • nonspecific lymphocytic thyroiditis
  • hashimotos thyroiditis
  • subacute (granulomatous) thyroiditis
  • reidel’s thyroiditis

*Infection: acute bacterial, TB, fungal, etc.

32
Q

Nonspecific lymphocytic thyroiditis:

  • Population, TH production, Genetic polymorphism
  • How does this present?
A
  • middle aged females
  • euthyroid, typically incidental finding
  • HLA-DR5

**Presents with mild symmetric thyroid enlargement + lymph infiltrate; injury of thyroid follicles may eventually lead to thyrotoxicosis

33
Q

Lab fidnings assocated with nonspecific lymphocytic thyroiditis:

A
  • ^ T4/T3
  • LOW TSH
  • DECREASED UPTAKE IN RADIOIODINE SCAN
34
Q

If you see germinal centers in the thyroid think…

A

Hashimotos thyroiditis

35
Q

Hashimotos thyroiditis:
Population?
Associated genetic polymorphisms?
How does this present?

A
  • Older adult females
  • HLA-DR5, HLA-DR3 if w atrophy
  • Autoimmune HYPOthyroidism w PAINLESS goiter (diffuse or localized)
36
Q

What is HASHITOXICOSIS?

A

Hashimotos thyroiditis–>Transient Hyperthyroidism

  • DECREASED Radioiodine scan
  • ^T4/T3
37
Q

Describe the pathogenesis of hashimoto’s thyroiditis:

A

Primary T cell defect–>
Anti-TSH AutoAbs–>
DECERASE TH synth–> HYPOthyroidism

38
Q

Describe the gross/ micro histo assocated with hashimotos thyroiditis:

A
  • Diffuse symmetiric enlargment
  • mononuclear infiltrate w GERMINAL CENTERS
  • small thyroid follicles
39
Q

Hashimotos thyroiditis is associated with ^ risk for which two malignancies?

A
  • B cell lymphomas

- Papillary ca of the thyroid

40
Q

De Quervains Thyroiditis:

Population, cause signs/ sx, histo

A
  • Older adult females
  • Viral infection–> PAIN esp w swallowing + infxn sx
  • (+/-) transient hyperthyroidism/ gland enlargement
  • Typically self limited

Histo: follicles extrude colloid; granulomatous inflammation w/ giant cells, etc.

41
Q

De Quervains Thyroiditis: Lab findings?

A
  • ^ WBC + ^ sed rate
  • ^T3/T4
  • DECREASED TSH
  • DECREASED Radioiodine uprtake
42
Q

What happens in riedel’s thyroiditis?

A

Thyroid becomes hard and fibroses; condition is rare

43
Q

Most thyroid neoplasms are most commonly malignant or benign?
Which population is most likely to get thyroid malignancies?
What is one predisposing risk factor?

A

BENIGN

  • young male patients most likely to have malignancy
  • prior radiation therapy ^ risk malignancy
44
Q

Thyroid adenoma:
Pathogenesis + Tissue of origin?
Signs/ Sx?
Histo?

A

Gs protein mutation –> Chronic ^^^ cAMP–> follicular epi mutates–> BENIGN thyroid adenoma (monoclonal)

  • Painless mass, +/- swallowing problems, +/- hyperthyroid
  • Histo: ENCAPSULATED lesion, NO papillary change, ^ follicular cells
45
Q

How do we dx thyroid adenoma?

A
  • need more than FNA to see capsule (histo slices)
46
Q

List the 4 types of thyroid carcinoma and identify most common.
Describe the population that gets this disease:

A
  • (#1) papillary
  • (#2) follicular
  • medullary
  • anaplastic

In early and middle adulthood ca more common in F.
In childhood and late adulthood M = F.

47
Q

List three risk factors for ca of the thyroid; one general + two specific

A
  • ionizing radiation
  • PTC oncogene –> papillary ca
  • RET tyrosine kinase–> medullary ca
48
Q

Papillary ca of thyroid:

  • signs + sx.
  • Histo***
  • How does it met?
A

Solitary or multifocal mass in thyroid or cervical node(s)
-Mets via LMYPHATICS

Histo: GROUND GLASS/ ORPHAN ANNIE nuclei, papillae WITH FIBROVASCULAR CORE, +/- psammoma bodies

49
Q

Follicular ca of thyroid:
- predisposing factors
- pathogenesis + tx.
+ how does it met (lymphatics vs vasculature)

A

-goiter/iodine deficiency + adenoma predispose risk
-Mets via VASCULATURE
-Pathogenesis:
Benign Adenoma–> TRANSFORMATION–> INFILTRATES capsule or vasculature
Tx: Surgery, suppression w TH

50
Q

Medullary Ca:

  • What type of tumor is this and from where does it derive?
  • What does it secrete?
A

Neoplastic Parafollicular (c-cells)–> Neuroendocrine tumor–> Secretes CALCITONIN +/- VIP, other polypeptide hormones

51
Q

What are they two types of medullary ca and when do they arise?

A
  • sporadic (5th/ 6th decade)

- MEN IIa, MEN IIb germ line mutations (younger patients; RET protooncogene mutation)

52
Q

What are the signs/ sx of sporadic medullary ca?

How do we screen for MEN?

A

Sporadic: presents w dysphasia/ sx of neck mass, +/- diarrhea due to VIP secretion

MEN screening: CALCITONIN levels, RET protooncogene testing

53
Q

Medullary Ca histology; what is common or different between the familial and sporadic types? (4)

A

Differences:

  • Solitary (sporadic) or multiple (familial) nodules
  • C cell HYPERPLASIA in FAMILIAL

Both:

  • Polygonal spindle shaped cells (nest, trabeculae, follicles)
  • AMYLOID calcitonin deposits = CONGO RED STAIN
54
Q

What is the prognosis for medullary ca?

Which is most aggressive? How does the tumor met?

A
  • Tumors met via vasculature
  • Sporadic + MEN IIb are the most aggressive
  • Familial tumors NOT MEN asstd. are less aggressive
55
Q

Which thyroid ca is the most aggressive?

In which population does it occur?

A

Anapestic ca; elderly patients in areas of endemic goiter

Very poor prognosis: death within year of dx.

56
Q

Describe the histo and morphology or anapestic ca.

From what must it be distinguished?

A
  • rapidly growing bulky lesion that invades neck structures+ commonly mets to distant sites
  • multiple cell types; if small cells present must distinguish from lymphoma
57
Q

From where are the parathyroid glands derived?
What tissue do the glands contain?
How is the gland’s function controlled?

A
  • derived from descending pharyngeal pouches
  • glands have fat interspersed
  • activity controlled by free Calcium

LOW free Ca++ = ^ PTH
^ free Ca++ = LOW PTH

58
Q

Describe the effects of PTH on bone, renal, GI systems:

A
  • ^ osteoclast activity–> ^ free Ca++
  • ^ kidney resorption of Ca++, ^ synthesis active Vit D
  • ^ urine cAMP, PO4
  • ^ GI absorption Ca++ (due to ^ vit D)

***Net effect = ^ free Ca++

59
Q

What are the three potential causes of primary hyperparathyroidism and which is most common?

Which population gets this most?

A
  • Adenoma (#1)
  • Hyperplasia
  • Carcinoma

**Conditions most common in adult females

60
Q

What are the sx of primary hyperparathyroidism?

A
  • painful bones (osteitis fibrous cystic–hemorrhage +cysts)
  • renal stones
  • abdominal groans (ulcers)
  • psychics overtones
61
Q

What are the three causes of hyperparathyroid adenoma?

A
  • sporadic (95%)
  • MEN I
  • Parathyroid adenoma 1 mutation (PRAD-1) (10-20%)
62
Q

Describe the details of PRAD-1 mutation:

A

Inversion of chrom 11–> Cyclin D GOF mutation–> proliferation of PTH producing cells

63
Q

Describe the details of MEN I disorder:

A

Homozygous LOF tumor suppressor on chrom 11q13

64
Q

Describe the histology of a primary hyperPTH adenoma.

How do we treat this?

A
  • Circumscribed lesion w loss of fat within rim of compressed normal parathyroid
  • Treat with surgical removal
65
Q

Describe the histology of parathyroid hyperplasia:

A

diffuse enlargement of 2+ glands possibly associated with MEN I or MEN Ia

66
Q

How is parathyroid carcinoma defined?

A

REQUIRES invasion or mets

67
Q

Describe pathogenesis of secondary hyperparathyroidism.

What are the signs and sx?

A

Hypocalcemia–> ^ PTH–> Parathyroid hyperplasia
(associated with ^ PO4 –> direct depression serum Ca++)

Will see bone anomalies, calciphalaxis

68
Q

What is the most common cause of secondary hyperparathyroidism? Three others?

A

RENAL FAILURE = #1

  • poor Ca++ diet
  • steatorrhea
  • Vit D deficiency
69
Q

Define pathogenesis of calciphalaxis; with what is it associated?

A

Chronic renal failure–> ^ PO4–> LOW serum Ca++ w/ calcification of vasculature–> ischemia of skin and organs

70
Q

Describe the pathogenesis of tertiary hyperparathyroidism.

How is it treated?

A

Treatment for secondary ^ PTH doesn’t work –>parathyroid hyperplasia–> secondary ^ PTH becomes autonomous, aggressive, irreversible

Tx: parathyroidectomy

71
Q

What is the most common cause of HYPOparathyroidism?

What are two others?

A
  • Surgical removal of parathyroid (#1)
  • DeGeorge syndrome
  • Primary idiopathic (possible autoimmune disease)
72
Q

Familial Hypoparathyroidism:

  • When does it present? What is the clinical triad?
  • Describe the signs and sx***
A

Presents in early childhood

  • Triad:
  • candidiasis
  • HYPOparathyroidism
  • Adolescent onset adrenal insufficiency

Signs/ Sx:
Tetany (hypocalcemia); (+) Chevostek, (+) Trousseau

73
Q

Define pseudohypoparathyroidism:

A

manifestations of hypoparathyroidism due to insensitivity to action of PTH or end organ resistance to normal/ ^ PTH

74
Q
  • **Pseudohypoparathyroidsm Type I:
  • Pathogenesis
  • clinical manifestations
A

Gs LOF mutation or PTH-R mutation–> Diminished cAMP response to PTH–> Hypoparathyroidism

Clinical Findings:

  • round facies
  • short stature, metacarpals, and metatarsals (Albright hereditary osteodystrophy)
75
Q

Pseudohypoparathyroidsim Type II:

  • Pathogenesis
  • clinical manifestations
A
  • Normal PTH induced cAMP w/ blunted second messenger response
  • Patients do not have developmental defects

DT4-Exam 1 (17 decks)

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