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D&T3 Exam 1 > Thyroid-denning > Flashcards

Thyroid-denning Flashcards

1
Q

Thyroid

Development

A

Eva GI nation of the developing pharyngeal mucosa

Bilobed organ with isthmus

Found in neck, inf to thyroid cartilage, same level as cricoid cartilage

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2
Q

Normal thyroid

Micro

Colloid

A

Reservoir of materials for thyroid hormone production

Lesser extent, reservoir of hormones themselves

Rich in thyroglobulin

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3
Q

Normal thyroid

Micro

Follicular epithelial cells

A

Convert thyroglobulin into T4 and T3

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4
Q

Thyroglobulin is converted to T4 and T3 by

A

Follicular epithelial cells

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5
Q

T4 and T3

Effect on metabolism

A

Inc BMR

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6
Q

Normal thyroid

Micro

Parafollicular cells (C cells)

Secrete

A

Calcitonin

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7
Q

Normal thyroid

Micro

Calcitonin effect

A

Causes absorption of Ca by the skeletal system

Inhibits resorption of bone by osteoclasts

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8
Q

Hyperthyroidism

Define

A

Inc in free T4 and/or Free T3

Hyperfunction of thyroid (graves disease)

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9
Q

Thyrotoxicosis

A

Excessive leakage of thyroid hormone

Thyroiditises

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10
Q

Hyperthyroidism results in

A

Hypermetabolic state

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11
Q

Hyperthyroidism

Causes (MC)

A

Graves’ disease

Ingestion of xs thyroid hormone (for Rx of hypothyroidism)

Hyperfunction multinodular goiter

Hyperfunction adenoma of the thyroid

Certain thyroiditises

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12
Q

Hyperthyroidism

Less common causes

A

TSH producing pituitary adenoma

Stroma Ovarii (thyroid tissue in the ovary)

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13
Q

Hyperthyroidism

S&Sx

A

Due to inc thyroid hormones

Inc BMR

GI: hypermotility, malabsorption, diarrhea

Sympathetic sx

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14
Q

Hyperthyroidism

Sympathetic sx

A

Due to overactive sympathetic nervous system

Nervousness, tremor, tachycardia, palpatations, hyperreflexia and irritability

Possible CHF

Wide gazing stare and lid lag (levator palpebrae superioris)

Heat intolerance

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15
Q

Hyperthyroidism

Thyroid storm

A

Medical emergency

Abrupt onset of severe and life threatening thyrotoxicosis with exaggeration of usual symptoms of hyperthyroidism

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16
Q

Thyroid storm

Clinical presentation

A

CV-marked tachycardia (140bpm)

Thermoregulatory dysfunction-(104-106)

GI-N/v, diarrhea

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17
Q

Thyroid storm

Common cause

A

Graves’ disease

Can also be seen following surgery on thyroid (release of xs hormone)

May cause death

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18
Q

Hyperthyroidism

Screen

A

Measure fT4 and TSH

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19
Q

Hyperthyroidism

Findings on screen

A

Inc fT4

Dec TSH (primary—thyroid)

Sometimes due to T3 (then measure T3)

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20
Q

Hyperthyroidism

Rx

A

Beta blockers for adrenergic tone

Thionamides to BLOCK new hormone synthesis

Agents to PREVENT CONVERSION of T4 to T3

Radioiodine to ABLATE thyroid function

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21
Q

Hypothyroidism

Most cases are

A

Primary (thyroid)

Surgery

Hashimoto’s thyroiditis

Primary idiopathic

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22
Q

Hypothyroidism

Myxedema

A

Applied to older child or adult

Generalized apathy and mental sluggishness (mimics depression)

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23
Q

Hypothyroidism

Myxedema

Sx

A

Listlessness; COLD INTOLERANT

Mucopolysaccharide-rich edema (skin and subcutaneous tissue)

Constipation

Pericardial effusions; obesity

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24
Q

Hypothyroidism

Labs

A

TSH is most sensitive

Inc in primary (thyroid)

Dec in secondary (pituitary)

T4 dec in both

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25
Q

Graves’ disease

Pt

A

20-40

Females

60% concordance

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26
Q

MC cause of endogenous hyperthyroidism

A

Graves’ disease

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27
Q

Graves’ disease

Genetics

A

HLA-DR3 and -B8

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28
Q

Graves’ disease

S&Sx

A

Triad:
Thyrotoxicosis (100%) (hyperthyroidism)

Exopthalmus (40%)

PRETIBIAL myxedema (LOCALIZED, infiltration dermopathy)

Thyroid enlargement (diffuse), bruit over thyroid

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29
Q

Exopthalmus

A

Marked infiltration of the retro-orbital space by mononuclear cells

Inflammatory edema and swelling of extraocular mm

Accumulation of ECM components

Inc number of adipocytes

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30
Q

Graves’ disease

Pathogenesis

A

Breakdown in self tolerance to thyroid auto ags, most important is the TSH receptor

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31
Q

Graves’ disease

Autoantibodies

A

TSI (Binds TSH receptor) stimulates TH production

TGI (binds TSH receptor) stimulates growth

TBII–TSH binding inhibitor immunoglobulin
-prevents binding of TSH:: may stimulate or inhibit

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32
Q

Graves’ disease

Morphology

Thyroid

A

Diffuse hypertrophy and hyperplasia

Follicular cellls: tall, columnar, and crowded

May have papillae WITHOUT FIBROVASCULAR CORE (papillary cancer has fibrovascular cores)

Colloid: shows scalloping

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33
Q

Graves’ disease

Organ manifestations

A

Heart: hypertrophied and ischemia

Opthalmopathy: mucopolysaccharides and lymphocytes (autoimmune not direct effect)

Dermopathy: pretibial myxedma: mucopolysaccharides and lymphocytes, orange-peel texture

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34
Q

Graves’ disease

Labs

A

Radioiodine scan: diffuse uptake

Inc fT4 and T3

Dec TSH

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35
Q

Graves’ disease

Rx

A

Beta blockers

Thionamides (propylthiouracil)

Radioiodine ablation

Surgery

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36
Q

Goiter

A

Simple enlargement of the thyroid

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37
Q

MC thyroid disease

A

Gaiters

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38
Q

Goiters

Due to

A

Impaired synthesis of TH

Iodine deficiency

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39
Q

Goiters

Endemic

A

MC in mountainous areas

Endemic=10% of population

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40
Q

Goiters

Sporadic

A

Many causes

Environmental and genetic

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41
Q

Goiters

S&Sx

A

Enlargement may cause

Cosmetic problems

Or

Airway obstruction, dysphasia, compression of large vessels in the neck and thorax (mass effect)

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42
Q

Goiters

S&Sx

Related syndrome

A

Plummer’s syndrome

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43
Q

Goiters

Plummer’s syndrome

A

Hyperfunctioning nodule forms in long standing goiter, results in hyperthyroidism

No opthalmopathy or dermopathy

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44
Q

Goiters

Effects

A

Overall most euthyroid

Hypothyroid less common

May mask or mimic neoplasms

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45
Q

Goiters

Pathogenesis

A

Dec thyroid hormones cause inc TSH

Result: thyroid enlargement (eventually get autonomous groups of cells forming)

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46
Q

Goiters

Common cause

A

Iodine deficiency

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47
Q

Goiters

Morphology

A

Due to hypertrophy and hyperplasia (caused by inc TSH)

T3, T4 wnl; TSH wnl or slightly high

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48
Q

Nodular or multi nodular goiters arise from

A

Stimulation and involution

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49
Q

Goiters

Stimulation and involution causes

A

Nodular or multi nodular goiter

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50
Q

Thyroiditis (inflammation)

Types

A

Nonspecific lymphocytic thyroiditis

Hashimoto’s thyroiditis

Subacute (granulomatous) thyroiditis :: de quervain’s

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51
Q

Thyroiditis (inflammation)

Other types

A

Acute bacterial

Mycobacterium tuberculosis or Fungi

Riedel’s thyroiditis

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52
Q

Nonspecific lymphocytic thyroiditis

Common presentation

A

Incidental

Euthyroid

Middle aged females

Possibly autoimmune:: HLA-DR5

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53
Q

Nonspecific lymphocytic thyroiditis

Morphology

A

Mild symmetric enlargement

Multifocal small lymphocytes

if germinal centers are present, think hashimotots

54
Q

Thyroiditis

With germinal centers present

A

Hashimotos

55
Q

Nonspecific lymphocytic thyroiditis

Labs

A

Thyrotoxicosis (due to injury of thyroid follicles)

Inc T4 and T3

Dec TSH

Radioiodine scan: dec uptake
(Graves’ has inc uptake)

56
Q

Hashimoto’s thyroiditis

Presentation

A

Autoimmune: HLA-DR5

Female 45-65

Transient hyperthyroidism:: Hashitoxicosis

57
Q

Hashimoto’s thyroiditis

With atrophy

Gene ass

A

HLA-DR3

58
Q

Hashimoto’s thyroiditis

S&Sx

A

Painless enlargement

Symmetric and diffuse

May be localized (suspicion of neoplasm)

59
Q

Hashimoto’s thyroiditis

Pathogenesis

A

Similar abs as graves

But anti-TSH receptor Ab blocks action of TSH

Result: hypothyroidism

Primarily a T-cell defect

60
Q

Hashimoto’s thyroiditis

Morphology

A

Diffuse, symmetric enlargement

Mononuclear infiltrate WITH GERMINAL CENTERS

Mall thyroid follicles

61
Q

Hashimoto’s thyroiditis

Labs

Hashitoxicosis

A

Inc T4 and T3; dec TSH

Radioiodine scan: dec uptake (graves-see inc uptake)

62
Q

Hashimoto’s thyroiditis

Labs

Hypothyroid (MC)

A

Dec T4 and T3

Inc TSH

63
Q

Hashimoto’s thyroiditis

Ass risk

A

Inc risk of developing B-cell lymphomas

Predisposition to papillary carcinoma

64
Q

De Quervains thyroiditis

Common presentation

A

Females 30-50

Due to viral infection

65
Q

De Quervains thyroiditis

S&Sx

A

PAIN in neck (esp. when swallowing)

Fever

Malaise

Variable enlargement of thyroid

Transient hyperthyroidism (6-8wks)

66
Q

De Quervains thyroiditis

Morphology

A

PMN infiltrate

Scattered lymphocytes and plasma cells

Macrophages

Disrupted follicles with extruded colloid

Result::: Granulomatous Rxn

67
Q

De Quervains thyroiditis

Labs

A

Inc leukocytes
Inc sedimentation rate
Inc T4 and T3 (disrupted follicles)
Dec TSH

Radioactive iodine uptake DEC
Low TSH

Self limited

68
Q

Riedel’s thyroiditis

Presentation

A

Rare

“Woody Hard” Fibrosis

69
Q

Thyroid Neoplasms

A

Benign 10:1

Carcinomas 10%

70
Q

Thyroid neoplasms

Clinical clues

A

Solitary nodules

“Hot” nodules more likely benign

Younger pts>neoplasm

Males>neoplasm

Radiation>incidence of malignancy

71
Q

Thyroid Adenomas

Characteristics

A

Derived from follicular epithelium

Solitary

72
Q

Thyroid Adenomas

S&Sx

A

Painless mass

Inference with swallowing

Minority hyperfunction

Most are “COLD”—up to 10% of “cold” nodules are malignant (rare in hot)

Hot=hyperfunctioning

73
Q

Thyroid Adenomas

Pathogenesis

A

Somatic mutations- chronic stimulation of cAMP pathway

Result: autonomously functioning MONOCLONAL thyroid adenoma

Mutations of Gs-alpha mimic exaggerated TSH stimulation

74
Q

Thyroid Adenomas

Mutation

A

Mutations of Gs-alpha mimic exaggerated TSH stimulation

75
Q

Thyroid Adenomas

Morphology

A

Solitary, spherical, encapsulated

Various histologic types

Usually NO papillary changes (unlike encapsulated papillary CA)

Well defined, intact Capsule

76
Q

Thyroid Adenomas

Dx

A

Careful histologic examination

Malignant transformation does not occur except in exceptional circumstances

77
Q

Carcinoma of the Thyroid

Presentation

A

Female

Childhood and late adult

78
Q

MC Carcinoma of the Thyroid

A

Papillary CA

79
Q

Carcinoma of the Thyroid

Pathogenesis

A

Ionizing radiation

PTC Oncogene

RET (tyrosine kinase) proto-oncogene

80
Q

Carcinoma of the Thyroid

Types

A

Papillary

Follicular

Medullary

Anaplastic

81
Q

Papillary CA

A

MC

82
Q

Papillary CA

S&Sx

A

Mass in neck

Thyroid

Or

Cervical LN–isolated involved cervical LN doesn’t change prognosis

83
Q

Papillary CA

Morphology

A

Solitary or multifocal

Nuclear features-ground glass or orphan Annie nuclei

Have papillae with dense fibrovascular core

Psammoma bodies

Mets by lymphatics

84
Q

Papillary CA

Prognosis

A

10 yr survival 85%

85
Q

Follicular CA

A

2nd MC

86
Q

Follicular CA

Presentation

A

Middle age

Predisposed: iodine deficient areas, nodular goiter

87
Q

Follicular CA

S&Sx

A

Solitary “cold” nodule

88
Q

Follicular CA

Morphology

A

DIFFERENTIATED FROM ADENOMA

Microscopic invasion of the capsule and vasculature

Mets via vasculature

89
Q

Follicular CA

Tx

A

Surger

Better differentiated: suppression by thyroid hormones (suppresses TSH)

90
Q

Medullary CA

Characteristics

A

Neuroendocrine tumor

Derived from parafollicular cells (C Cells)

Secrete calcitonin

91
Q

Medullary CA

Sporadic

A

80%

5th-6th decade

92
Q

Medullary CA

Mutation

A

MEN IIa and IIb

Germ line mutations of RET protooncogene

Younger pts

93
Q

Medullary CA

S&Sx

Sporadic

A

Mass in neck

Dysphagia or hoarseness

May secrete VIP causing Diarrhea

94
Q

Medullary CA

MEN

A

Screen for calcitonin level and mutations of RET

95
Q

Medullary CA

Morphology

A

Multiple common in familial type

Polygonal to spindle shaped cells–nests trabeculae, or follicles

AMYLOID deposits of calcitonin

See ass c-cell hyperplasia in familial not sporadic

96
Q

See ass C-cell hyperplasia

A

Familial NOT sporadic Medullary CA

97
Q

Medullary CA

Prognosis

A

Sporadic and MEN IIb: aggressive

MET via blood

Familial that are NOT MEN: less aggressive

98
Q

Anaplastic CA

Characteristics

A

Most aggressive

Elderly

Areas of endemic goiter

99
Q

Anaplastic CA

Morphology

A

Bulky

Grows rapidly beyond thyroid (into neck structures)

Giant cells or squamoid cells or sarcomatous cells

Small cell (distinguish from lymphoma)

100
Q

Anaplastic CA

Prognosis

A

Grow with wild abandon

Met to distant sites

Death in <1yr

101
Q

Parathyroids

Derived

A

From descending pharyngeal pouches

102
Q

Parathyroids

Controlled by

A

Free (ionized) ca

Dec ionized ca causes inc PTH

Inc ionized ca causes dec PTH

103
Q

PTH

Function

A

Activates osteoclasts: ca released from bone (resorption)

Kidney: reabsorption of ca, inc cAMP in urine, conversion of 25OH-Vit D to 1,25 diOH-VitD, inc urinary PO4

GI: get in ca absorption with 1,25diOH VitD

Net: inc ionized ca

104
Q

Primary hyper-PTH

Causes

A

MC autonomous ADENOMA

Hyperplasia 2nd

Carcinoma

105
Q

Primary hyper-PTH

Presentation

A

Adults: females

Sporadic or MEN

Cause bone resorption and renal disease (stones and nephrocalcinosis)–inc ionized ca

106
Q

Primary hyper-PTH

S&Sx

A

MC: inc ionized ca: can be picked up in asymptomatic pt::: mets to bone MC cause of clinically significant hyper ca

Painful BONES, renal STONES, abdominal GROANS (ulcers) and psychic MOANS

107
Q

Primary hyper-PTH

Pathogenesis

A

Sporadic (95%)

Inherited: MEN I

Genetic alteration: parathyroid Adenoma 1 (PRAD 1)

108
Q

Primary hyper-PTH

Parathyroid Adenoma 1 (PRAD 1)

A

Encodes cyclin D1

Inversion of Chromosome 11

Overexpression of cyclin D1

109
Q

Primary hyper-PTH

Pathogenesis

MEN I

A

Homozygous loss of putative suppressor gene on chromosome 11q13

110
Q

Primary hyper-PTH

Morphology

A

Adenoma: circumscribed lesion with loss of fat. RIM OF COMPRESSED NORMAL PARATHYROID

Hyperplasia: see diffuse enlargement of 2 or more glands: sporadic or MEN I or IIa

111
Q

Primary hyper-PTH

Morphology

CA

A

Dx by invasion or metastasis

112
Q

Primary hyper-PTH

Morphology

Other organs

A

Bone–osteitis fibrosa cystica: thinned bone with hemorrhage and cyst formation

Kidney–stones (nephrolithiasis); nephrocalcinosis

113
Q

Primary hyper-PTH

Rx

A

Surgery req to remove adenoma

May have to go into MEDIASTINUM

114
Q

Secondary hyperparathyroidism

Due to

A

Excessive secretion of PTH caused by hypocalcemia

Results in parathyroid hyperplasia

115
Q

Secondary hyperparathyroidism

Common pt

A

Pts with CHRONIC DEPRESSION of serum calcium leading to overactivity of parathyroid gland

Ass with inc po4. Directly depresses serum Ca

116
Q

Secondary hyperparathyroidism

MC cause

A

Renal failure

117
Q

Secondary hyperparathyroidism

Other causes

A

Inadequate diet of ca

Steatorrhea (fat binds ca)

Vit d deficiency

118
Q

Secondary hyperparathyroidism

S&Sx

A

Parathyroid glands are hyperplastic

Bone abnormalities and other changes less severe than primary

Calciphalaxis

119
Q

Secondary hyperparathyroidism

Calciphalaxis

A

Seen in chronic renal failure

Due to inc phosphate (PPT. Ca in blood vessels:: may cause ischemia to skin and other organs)

120
Q

Tertiary hyperparathyroidism

Due to

A

Occurs when tx for secondary hyper-PTH either quits working, does not respond or pt not treated

Due to hyperplasia

See hypercalcemia

121
Q

Tertiary hyperparathyroidism

Relation to secondary…

A

Secondary hyper-PTH becomes autonomous and excessive

Can no longer reverse condition

122
Q

Tertiary hyperparathyroidism

Rx

A

May need parathyroidectomy

123
Q

Hypoparathyroidism

A

Less common that hyper-PTH

124
Q

Hypoparathyroidism

Causes

A

Surgery (MC)

Congenital absence (Di George syndrome)

Primary (idiopathic)

125
Q

Hypoparathyroidism

Primary (idiopathic)

A

60% have auto-abs directed against ca-sensing receptor:: may prevent release of PTH

126
Q

Hypoparathyroidism

Causes

Familial hypoparathyroidism

A

Presents in childhood with the onset of CANDIDIASIS

Then hypoparathyroidism

In adolescence adrenal insufficiency develops

127
Q

Hypoparathyroidism

S&Sx

A

Tetany due to hypocalcemis

Neuromuscular irritability, tingling to spasm to laryngospasm to seizures

Chvostek sign: tap along facial nerve, induce contractions of mm of eye, mouth or nose

Trousseau sign- inflate BP cuff, induce carpal spasm, goes always when deflate the cuff

128
Q

Pseudohypo-PTH

A

Hypocalcemia, inc phosphate

Generally inc PTH (can be normal)

Insensitivity to action of PTH

Get end-organ RESISTANCE to normal or elevated PTH

129
Q

Pseudohypo-PTH

Defects

Pseudohypoparathroidism Type 1

A

Diminished cAMP respons to PTH due to

Deficiency of Gs-Alpha protein

Or

Abnormalities of hormone receptor complex

130
Q

Pseudohypo-PTH

Pseudohypoparathyroidism Type 1

Clinical

A

Round facies, short stature, short metacarpal and metatarsal bones (Albright hereditary osteodystrophy)

131
Q

Pseudohypo-PTH

Defects

Pseudohypoparathyroidism Type 2

A

Normal PTH-induced cAMP

Blunted response to second messenger

Do not have developmental defects

132
Q

Pseudohypo-PTH

Results in

A

Hypocalcemia results

Causes secondary parathyroid hyperfunction: inc PTH

D&T3 Exam 1 (19 decks)

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