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Pathology > Endocrine Part I > Flashcards

Endocrine Part I Flashcards

1
Q

What are factors released the pitutiary gland that stimualts the production of hrmones from endocrine glands?

A

Trophic factors

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2
Q

What are the general classification of ALL endocrine disorders?

A

Hypo/hyperfunctioning of the endocrine organ
Mass lesions/neoplasms
Autoimmune disorders
Infections —> these are rare

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3
Q

WHat is ADH for?

A

Water retention, Na excretion

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4
Q

What are the 4 clinical manifestations of pituitary diseases?

A

Hyperpituitarism
Hypopituitarism
Local mas effects
Decreaesd & Increased secretion of AHD

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5
Q

What are the 2 types of neoplasms of hyperitutarism? What is their difference?

A

Pituitary adenoma - functioning/non-functioning
Pitutiary carcinoma - hyperfuncitoning pituitary (PRL & ACTH)

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6
Q

What is the diff between functioning and non-functioning pituitary adenomas?

A

Functioning - hormone excess & clinical manifestations
Nonfunctioning - w/o clinical sx of hormone excess

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7
Q

What are the genetic alteration in pituitary hormones? There are 7 genes

A

GNAS - GH adenomas
PKAR1A - GH adenomas & PRL adenomas
CYclin D1 = Aggresive adenomas
HRAS = Pituitary adenomas
MEN1 = GH adenomas, PRL adenomas, ACTH adenomas
CDKN1B = ACTH adenomas
AIP = GH adenomas
RB (retinoblatoma) = Aggressive adenomas

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8
Q

What genetic alterations is one of the most common alterations seen in pituitary adenomas?

A

G-protein mutations

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9
Q

WHat is the gross morphology of pituitary adenomas?

A

Typical: soft & well-circumscribed
Smaller = confined to the sella turcica
Larger = extend superiorly thorugh the diaphram of sella into the suprasellar region

Invasive/Aggressive = could infiltrate the neighboring tissues

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10
Q

What is the histology of pituitary adenomas?

A

Only one typical cell
Uniform polygonal cells arranged in sheets or cords
Soft gelatinuous consistency

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11
Q

What is the key characterisitc of pituitary adenomas?

A

cellular monomorphism + absence of reticular network

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12
Q

What is the most common type of hyperfunctioning adenoma?

A

Lactotroph adenomas

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13
Q

What are the histological features of lactotroph adenoma?

A

Sparsely granulated
Has chromophobe cells

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14
Q

What are the diff pituitary adenomas?

A

Lactotoroph adenoma
Somatotroph adenomas
Corticotroph adenoma
GOnadotroph adenomas
Thyrotoph adenoma
Non-funcitoning adenoma

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15
Q

What is the clinical cours eof lactotoroph adenoma?

A

GAL = common in girls sooo…..

Galactorrhea
Amenorrhea
Loss of libido & sexual function

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16
Q

How do u differentiate physiologic hyperprolactinemia from Lactotroph hyperplasia?

A

If physiologic HYPERprolactinemia —> seen often in pregnancy & breastfeeding women

Lactototrph hyperplasia => Pathologic

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17
Q

What is the 2nd most common funcitoning adenoma and presents w/ GIGANTISM in children & ACROMEGALY in adults?

A

Somatotroph adenomas

-> remember sa GH to

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18
Q

What is the morphology of Somatotroph adenomas?

A

Monomorphic => Densely granulated
Sparsely granulated => Chromophobe cells
Bihormonal => Mammosomatotrophs (PRL & GH)

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19
Q

WHat are the causes of HYPOpitutarism?

A

Tumors & other masses
Traumatic brain injury & subarachnoid hemorrhage
Pituitary surgery or radiation
Pitutiary apoplexy
Ischemic necrosis or Sheehan’s syndrome
Rathke’s cleft cyst
Empty sella syndrome
Hypothalamic lesions
Inflammatory disorders & infections
Genetic Defects

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20
Q

What are the 2 types of Empty sella syndrome?

A

Primary empty sella => defect in the dipahragm sella allows the arachnoid mater & CSF to HERNIATE into the sella —> women w/ hx of multiple pregnancies

SEcondary empty sella => mass enlarges the sella —> loss of pitutiary function

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21
Q

What are the manfiestations of hypopituitarism?

A

Gonadotropin loss —> amenorrhea, inferitlity in women, loss of libido in men

TSH & ACTH def -> simialr to hypothyroidism
PRL deficiency
MSH deficiency

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22
Q

What are the different local mass effects in the pituitary gland?

A

Visual field abnormlaities

Elevated ICP —> headache, nausesa, vomiting
Obstructive hydrocephalus & seizures

Pituitary apoplexy —> acute hemorrhages into an adenoma —> rapid enlargement of lesion

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23
Q

What are the diff posterior pitutary syndromes?

A

Diabetes inspidus —> Central & Nephrogenic DI
SIADH

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24
Q

How do u diffenretiate Diabetes inspidus from SIADH?

A

Urinary output
= HIGH: Diabetes Inspidius
= LOW: SIADH

Levels of ADH
= HIGH: SIADH
= LOW: DI

Serum Na
= HIGH: DI
= LOW: SIADH

Hydration status
= HIGH (over hydrated): SIADH
= LOW: DI

Both will present with excessive thirst

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25
Q

What neoplasm may present as DI or SIADH? What are the common implicated tumors of this neoplasm?

A

Hypothalamic Suprasellar tumors

Implicated tumors:
- Gliomas
- Cranipharyngiomas

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26
Q

What are the different pathologies of the thyroid gland?

A

Hyperthyroidism
Hypothyroidism
Thyroiditis
Riedel’s thryoiditis
Graves’ disease
Goiters
Neoplams of the TG

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27
Q

How would u characterize thyrotoxicosis?

A

Elevated levels of free T3 & T4
Hypermetabolic state

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28
Q

What are the most common causes of thyrotoxicosis?

A

Diffuse hyperplasia of the thyroid assoc w/ Graves dis
Hyperfunctional multinodular goiter
Hyperfunctional thyroid adenoma

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29
Q

WHat are the clinical features of thyrotoxicosis?

A

INC in the basal metabolic rate
Cardiac manifestations
Overactivity of the sympathetic NS
Ocular changes
Thyroid storm
Apathetic hyperthyroidism

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30
Q

How do we diagnose px w/ THyrotoxicosis?

A

Low TSH, INC T3 & T4

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31
Q

What causes hypothyroidism?

A

structural or functional derangement that interferes with the production of thyroid hormone

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32
Q

WHat are the 3 causes of primary hypothyroidism?

A

Congenital hypothyroidism
Autoimmune hypothyroidism
Iatrogenic hypothyroidism

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33
Q

What are possible defective steps of congenital hypothyroidism? Other causes?

A

Iodide transport into thyrocytes
Organificaiton of iodine
Processing to form hormonally active T3&T4

Other causes:
- Complete absence of thyroid parenchyma (thyroid agenesis)

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34
Q

Whata causes secondary hypothyroidism?

A

Central hypothyroidism

Deficiencies of TSH
Deficiencies of TRH

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35
Q

What is cretinism? What are its clinical manfiestations?

A

hypothyroidism that developed during infancy/childhood

common in regions where dietary iodine deficiency is endemic

Severe intellectual disability, short stature, coarse facial features, protruding tongue, umbilical hernia

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36
Q

What type of hypothyroidism develops in older children/adult aka Gull’s disease? What are the clin manifestations of this dis?

A

Myxedema

Mimic depression
Listless, cold intolerant, frequently overweight, DEC sympathetic activity

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37
Q

What is the histologic feature of Myxedema?

A

Accumulation of Glycosaminoglycans, & hyaluronic acid

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38
Q

What are the 3 groups of thyroiditis?

A

Hashimoto’s thyroiditis
Granulomatous thyroiditis
Subacute lymphocytic thyroiditis

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39
Q

What type of thyroiditis is an autoimmune disorder that results in destruction of the TG & major cause of non-endemic goiter in the pediatric population?

A

Hashimoto’s thyroiditis

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40
Q

What causes Hashimoto’s thyroiditis?

A

Breakdown in self-tolerance to thyroid autoantigens

INC suscpetibility to CTLA4, PTPN22, & IL2RA

CD8 CTX Tcell med death

Cytokine-mediated cell death

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41
Q

What are the morphological features of Hashomoto’s thyrodiitis?

A

Gross:
- Thyroid is diffusely enlarge, capsule intact

Histology:
- Extensive inflammation of the parenchym
- Thyroid follicles are atrophic
- Hurthle cells w/ heterogenous lymphocytes

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42
Q

What cells are pathognomonic for Hashimotos thyroiditis?

A

Hurthle cells

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43
Q

What are the clinical features of Hashimotos thyroiditis?

A

painless enlargement of thyroid
INC T3, T4, uptake of radiactive iodine
DEC TSH

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44
Q

What is aka as De Quervain Thyroiditis & occurs less frequently as Hashimoto?

A

Granulomatous thyropiditis

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45
Q

What causes Granuloamtous thyroiditis? What is its morphology?

A

Viral infections (URTI)

Gross: unilateral or bilateral enlargement & firm TG

Histo
- patchy and depends on stage of disease
- multinucleated Giant cells enclose pools of coloid

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46
Q

What are the clinical features of Granulomatous thyroiditis?

A

most common cause of thyroid pain
self-limiting
INC T3, T4, DEC TSH

normal TG functions return after 6-8 wks of recoery

47
Q

What is aka painless thyroiditis? What is the cause of this condition?

A

Subacute lymphocytic thyroiditis

Circulating antithyroid peroxidase antibodies

48
Q

What are the morphologic features of Subacute lymphocytic thyroiditis? Clinical features?

A

Gross: normal

Histo: Lymphocytic infltration with large germinal centers & patchy disruption & collapse of thyroid follicles

Clinical features:
- mild transient HYPERthyroidism, painless goiter

49
Q

What is the difference betw Hashimotos thyroiditis & Subacute lymphocytic thyroiditis?

A

SCLT: Fibrosis & Hurthle cell metaplasia not prominent

50
Q

What is a rare condition of the TG with chronic inflammation, fibrosis, obstructive symptoms with invasiono of surrounding structures?

A

Riedel’s thyroiditis
Aka Riedel struma, Chronic invasive fibrous thyroiditis, or Ligneus struma

51
Q

What is the hallmark of RIedel’s thyrodiitis?

A

Replacement of thyroid tissue with dense fibrotic tisue

52
Q

What is the diagnostic confirmation of the biopsy of Riedel’s thyroiditis?

A

Dense fibrous tissue with characteristic eosinophilic infiltrate

53
Q

Whta are the clinical manifestation sof RIedel’s thyroiditis?

A

PE: hard & enlarged thyroid, (+) Chvostek or Trousseau sign

S/Sx:
Dyspnea, Dysphagia, Stridor, Venous sinus thrombosis, Exophthalmos

54
Q

What are the diagnostic criteria of RIedel thyroiditis?

A

Extrathyroidal extension of inflammatory process
Occlusive phlebitis
Absence of granulomas, giant cells, lymphoid follicles, or Oncocytes

Absenceof thyroid malignancy

55
Q

What are the 3 tx options for Riedel’s thyroiditis?

A

Glucocorticoid tx
Tamoxifen
Mycophenolate Mofetil

56
Q

What is an autoimmune disorder with production of autoAbs against multiple thyroid proteins (TSH receptor) & is the most common cause of endogenous HYPERthyroidism?

A

Graves’ disease

GRAVEEEE yern

57
Q

What triad of clinical findings are seen in Graves’ dis?

A

HYPERthyroidism
Opthalmopathy
Infiltrative dermopahty (pretibial myxedema)

58
Q

WHat are the morphological features of Graves dis?

A

Symmetrical enlargement of thyroid gland

Gross: Beefy red parenchyma
Histo: Follicles are lined by tall, columnar epithelium, crowded, enlarged epithelial cells

59
Q

What are the clinical features of Graves disease?

A

Diffuse enlargement of thryoid present in all cases

Ophthalmopathy —> exophthalmos

Infiltrativedermpathy —> scaly thickening & induration

INC free T4, T3, DEC TSH

60
Q

What are the tx options for Graves disease?

A

B-blockers
Thionamides
Radioiodine ablation, thyroidectomy
Surgery

61
Q

What condition has an enlargement of the TG caused by impaired synthesis of thyroid hormone due to deficiency of Iodine in the diet?

A

Goiter

62
Q

What is the pathophysiology of Goiters?

A

DEC TH production —> compensatory INC in serum TSH —> Hypertrophy & Hyperplasia of Thyroid follicles —> Enlargement of TG

INC in functional mass —> Euthyroid metab state (overcomes hormone def)

Severe dis —> inadequate compensatory response —> Goitrous hypothyroidism

63
Q

What are the 2 types of Goiter?

A

Diffuse non-toxic
Multinodular

64
Q

What causes Diffuse nontoxic (simple goiter)/Colloid goiter?

A

Enlargement of TG w/o producing nodularity

Occurs in geographic areas where water, soil, and food contain low levels of Iodine

65
Q

What are substances that interfere with thyroid hormone synthesis in Simple Goiter/Diffuse Nontoxic Goiter?

A

Thiocyanate that inhibits Iodide transport

66
Q

What are the 2 phases in evolution of diffuse nontoxic goiter?

A

Hyperplatic phase
Colloid involution phase

67
Q

What is the difference betw Hyperplastic phase & COlloid involution phase of Simple goiter?

A

Hyperplastic -> follicles are lined by crowded columnar cells (piles up)

Colloid involution-> happens when dietary Iodine INC or if demand for TH decreases

68
Q

WHat are the clinical features of Simple Goiter/Diffuse nontoxic goiter?

A

Normal serum T3, T4
Elevated TSH

69
Q

What type of Goiter reuslts from recurrent episodes of hyperplasia and involution that ocmbine to produce irregular enlargement of the TG/

A

Multinodular goiter

70
Q

What is the morphology of Goiters?

A

Multilobulated, asymmetrically enlarged glands
Pressure on midline structures (trachea & esophagus)

Brown, gelatinous colloid on cut surface

Hemorrhage, fibrosis, calcification, & cystic changes

Histo: Colloid-rich follicles lined by flattened inactive epithelium & areas of follicle hyperplasia w/ degenerative changes

71
Q

What are the 2 types of neoplasms in the TG?

A

Adenoma
Thyroid carcinoma

72
Q

What is a benign neoplasm of the TG w/ discrete solitary masses derived from follicular epithelium?

A

Follicular adenomas

73
Q

What is the gross morphology of Follicular adenoma?

A

Intact, well-formed fibrous capsule encircling the tumors

Well-demarcated nodule, typically encapsulated

74
Q

What is the diff betw Adenoma & Hyperplasia?

A

Both have INC in # of cells
Adenoma:
- there’s crowding but cells are cuboidal in shape, (+) - (+) Fibrous capsule

75
Q

What cell is a histologic feature of Follicular adenoma?

A

Hurthle cell/Oxyphil adenoma

Also seen in Hashimoto’s thyroiditis

76
Q

What is a malignant tumor of the thyroid gland? What are the diff subtypes under this?

A

Thyroid carcinoma

Subtypes:
Papillary TCA
Follicular TCA
Anaplastic TCA
Medullary TCA

77
Q

What genetic alteration is seen in each subtype of THyroid carcinoma?

A

Papillary TCA = MAP kinase, RET/PTC translocation, BRAF point mutation

Follicular TCA = RAS point mutation, PTEN point mutation, PI3K point mutation, PAX8:PPARG translocation

ANaplastic TCA: RAS point mutation, PTEN point mutation & PI3K point mutation

Medullary TCA: MEN 2 with RET mutations

78
Q

What is the most comomn type of cancer in the TG?

A

Papillary carcinoma

79
Q

What is the distinguishing feature of follicular adneomas from follicular carcinomas?

A

Integrity of the capsule

80
Q

What is the morphology of papillary carcinoma? Dx feature?

A

Gross: discernable papillary structures
Histo:
- Finger-like/Papillary-like projections
- Orphan Annie eyes (empty-appearing nuclei w/ optical clearing) - Dx feature

81
Q

What are concentirc calcified structures seen in Papilary CA usuall seen at the core of the papilla, not a dx feature of papillary CA/

A

Psamomma bodies

82
Q

What are the 4 cell variants of Papillary carcinoma of thyroid gland? What are its distinguishing features?

A

Follicular variant => Orphan ANnie nuclei
Tall-cell variant => Follicle is lined w/ tall columnar cells w/ intensely eosinophilic cytolasm

Diffuse-sclerosing variant => youger px, might have Psamomma bodies, prominent lymphocytic infiltration

Papillary microcarcinoma => contains Orphan annie nuclei, good prognosis, distant metastasis

83
Q

In what pop is Follicular carcinoma more frequent? What are the morphologic features of Follicular carcnoma?

A

Areas w/ iodine deificiency

Gross: replacement of entire thyroid parenchyma, light in appearance but contains small foci of hemorrhage

Histo: Recognizable colloids

84
Q

WHat are the clinical manifestations of Follicular carcinoma?

A

Solitary cold thyroid nodules
Tend to metastasize through the bloodstream to the lungs, bone, & liver

85
Q

WHat are the 3 diff cell variants of FOllicular carcinoma?

A

Hurthle cell variant
Minimally invasive follicular CA => infiltation of thyroid parenchyma & capsule

Vascular invasion follicular CA => fibrous capsule, compressed normal thyroid parenchyma

86
Q

What type of TG carcinoma is higliy aggresive, seen in older px, well-differentiated papillary or follicular carcinoma?

A

Anaplastic carcinoma

87
Q

What are the morphological features of ANaplastic carcinoma?

A

Gross: bulky mass, grows rapidly beyond the thyroid capsule into adjunct structures of the neck

Histo: Large pleomorphc giant cells, osteoclat-like multinucleated giant cells, Spindle type, Mixed spindle & giant cell type

88
Q

From what cells is Medullary carcinoma derived from? What hormones do it secrete?

A

Parafollicular C cells
Calcitonin, ACTH, VIP, Serotonin

89
Q

WHat are the morphologic features of Medullary carcinoma?

A

Gross: Solid pattern of growth
Histo: remnants of thyroid follicle, abundant deposition of AMYLOID

90
Q

What are the clincial manifestationsof Medullary carcinoma?

A

ACTH: cushing-like syndrome
Serotonin: CArcinoid tumor
VIP: GI manifesations
Mass in neck -> Dysphagia/Hoarseness

91
Q

What are the 3 types of hyperparathyroidism?

A

Primary, secondary, & tertiary hyperparathyroidism

92
Q

What are the causes of hyperthyroidism?

A

Primary => secretion of excess PTH by chief cells in adenoma, DEC TSH, INC T4, T3

Secondary => renal disease results i impaired PO4 excretion, PTG enlarged, INC TSH, T4, T3

Tertiary => INC TSH, INC T4, T3

93
Q

What is the most important cause of hypercalcemia?

A

Primary hyperthyroidism

Usual cause of hyperfunctioning parathyroid

94
Q

What are the diff causes of primary hyperparathyroidism?

A

Parathyroid adenoma
Primary Hyperplasia
Parathyroid carcinoma

95
Q

What is the most common cause of primary HYPERPARAthyroidism? What are the molecular defects of this dis?

A

Prathyroid adenoma

Molecular defects:
Cyclin D1 gene inversions
MEN1 mutations

96
Q

What are the morphological features of Parathyroid adenomas?

A

Gross: Often solitary, mostly composed of Chief cells, well-circumscribed, soft, tan to reddish brown

Histo: Chief cells:, inconspicuou adipose tissue

97
Q

What is primary hyperplasia and what are its morphological features (histo)?

A

4 glands are involved

Histo:
Chief cell hyperplaia
Water-clear cell hyperplasia => abundant glycogen

98
Q

What are the morphological features of Parathyroid carcinoma?

A

PTG enlarged, gray-white irregular mass

Histo Dx: Invasion of surrounding tissues & metastasis

99
Q

What are the diff bone changes in HYPERparathyroidism?

A

Osteoporosis
Brown tumor
Osteitis fibrosa cystica

100
Q

What type of bone change in hyperparathyroidism results in DEC bone mass, INC osteoclast activity which produces dissecting Osteitis?

A

Osteoporosis

101
Q

What causes brown tumor?

A

Bone loss predisposes to microfactures & secondary hemorrhages

Vascularity, hemorrhage, hemosiderin deposition

Not really a tumpr

102
Q

What is a hallmark of severe hyperparathyroidism?

A

Osteitis fibrosa cystica
Aka Von Recklinghausen’s disease of the bone

Combination of INC osteoclast activity, peritrabecular fibrosisis, Cystic brown tumors

103
Q

What are the clinical features of hyperparathyroidism?

A

Nephrolithiasis => Metastatic calcification

104
Q

What causes secondary hyperparathyroidism?

A

Compensatory state due to prolonged hypocalcemia

Renal failure

Other causes: Inadquate Ca intake, VIt D def, Steatorrhea

105
Q

What is the most common cause of 2ndary hyperparathyroidism

A

Renal failure

106
Q

What are the clinical manifestations of 2ndary hyperparathyroidism?

A

Skeletal abnormalities (milder compaired to primary)

Cacliphylaxis - vascular calcification

107
Q

What condition is caused by end organ resistance to the action of PTH & presents with hypocalcemia, hyperphosphatemia, INC PTH?

A

Pseudohypoparathyroidism

108
Q

What are the diff causes of HYPOparathyroidism?

A

Surgically induced (thyroidectomy) -> most common
AI hypoparathyroidism
Autosomal dominant hypoparathyroidism
Familial isolated hypoparathyroidism
Congenital absence of PTG -> Digeorge syndrome

109
Q

What causes AI hypoparathyroidism, Autosomal dominant Hypoparathyroidsim & familial isolated hypoparathyroidism?

A

AI hypoparathyroidism => Autoimmune polyendocrine system syndrome (APS-1 => Autoimmune regulator gene

Autosomal dominant hypoparathyroidism => Ca snesing receptor gene

Familial isolated hypoparathyroidism => PTH precursor peptide

110
Q

What conditions are assoc w/ AI hypoparathyroidism?

A

Chronic mucocutaneous candidiasis ff by hyperparathyroidism & primary adrenal insufficiency

111
Q

What happens in autosomal dominant hypoparathyroidism?

A

SUppress parathyroid hormone ==> HYPOCALCEMIA, HYPERcalcemia

112
Q

What are the clinical manifestaions of HYPOCalcemia? What is the hallmark of hypocalcemia?

A

CATS love milk ==> Ca in milk ==> Hypocalcemia

Convulsions
Arrhythmias
Tetany => hallmark of hypocalcemia
Spasms & Stridor

113
Q

What are the classifc findigns on PE of HYPOparathyroidism?

A

Chvostek sign => tapping along facial nerve
Trousseau sign => carpal spasms

Pathology (8 decks)

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