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Pathology Flashcards

1
Q

C cells

A

aka: parafollicular cells
secrete CALCITONIN
located in interstitium
IHC STAIN

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2
Q

cretinism

A

hypothyroidism that develops in infancy or early childhood
Sx: severe mental retardation, short stature, coarse facial features, protruding tongue, umbilical hernia
RARE (iodine is supplemented in food)

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3
Q

hypothyroidism in older children and adults

A

aka: myxedema
Sx: apathy and mental sluggishness (mimics DEPRESSION), constipation, pericardial effusions, cold intolerant, overweight
mucopolysaccharide rich edematous fluid build up: broad coarse facial features, large tongue, deep voice
Dx: TSH ELEVATED

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4
Q

thyroiditis

give examples

A

inflammation of the thyroid gland

  1. Hashimoto thyroiditis
  2. granulomatous (de Quervain) thyroiditis
  3. subacute lymphocytic thyroiditis
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5
Q

Hashimoto thyroiditis

A

women, 45-65 yrs
HYPOTHYROIDISM: MOST COMMON (can be hyperthyroid due to early attack and follicle rupture)
PAINLESS enlargement, followed by ATROPHY yrs later
autoimmune: depletion of thyroid epithelial cells with replacement by inflammation and fibrosis
associations: cytotoxic T cell, HLA-DR3/5
Ab: THYROID PEROXIDASE (TPO), THYROGLOBULIN
risk: B cell lymphoma

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6
Q

subacute granulomatous (de Quervain) thyroiditis

A

women, 40-60s
uncommon
after FLU-like symptoms: viral induced activation of cytotoxic T cells
PAIN
GRANULOMA (macrophages); giant cells
SELF-LIMITED: most patients fully recover in 6-8 weeks
small number remain hypothyroid permanently

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7
Q

chronic lymphocytic thyroiditis

A

Hashimotos

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8
Q

subacute lymphocytic thyroiditis

A 
aka: painless or silent thyroiditis
middle age women
variant of Hashimoto's
mild goiter, HYPERTHYROID
most don't progress to chronic (hypothyroid)
Ab: ANTI-THYROID PEROXIDASE (anti-TPO)
NO pain
excludes: women within one year after delivery, abortion, miscarriage
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9
Q

Riedel thyroiditis

A

rare
extensive FIBROSIS (possibly associated with fibrosis elsewhere in body)
WOODY

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10
Q

Graves disease

A

primary
HYPERTHYROIDISM: MOST COMMON
HLA-DR3
Ab: thyroid stimulating immunoglobulin and thyroid growth stimulating immunoglobulin to TSH RECEPTORS
Sx: diffusely enlarged thyroid, pretibial myxedema, infiltrative opthalmopathy
PAPILLARY infoldings
lab: decrease TSH, free T3/4 increased

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11
Q

infiltrative opthalmopathy

A

GRAVES
inflammation of soft tissue and muscles around eyes
causes EXOPHTHALMOS (protrusion of eyes)
inflammatory cells, accumulated ECM components, fatty infiltration

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12
Q

pretibial myxedema

A

GRAVES
aka: infiltrative dermatopathy
thickening skin over shins
due to glycosaminoglycans and lymphocytes

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13
Q

goiter

A 
enlargement of thyroid: MOST COMMON
impaired synthesis of thyroid hormone 
IODINE DEFICIENCY 
FOLLICULAR hypertrophy and hyperplasia due to increased TSH
lab: increase TSH
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14
Q

endemic goiter

A

geographic
occurs in areas where the environment is low in naturally occurring iodine (greater 10% of populations)
starts diffuse, progresses to multinodular

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15
Q

sporadic goiter

A

rare

females with increased physiologic demand for T4

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16
Q

goitregens

A

ingestion of substances that interfere with thyroid hormone synthesis
Brassicaceae (Cruciferae) family: cabbage, cauliflower, brussel sprouts, turnips

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17
Q

What factors increase the chance that a nodule is a neoplasm?

A
  1. solitary
  2. young patient
  3. male patient
  4. radiation Hx
    NOT hot nodules
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18
Q

hot nodules

A

take up radioactive iodine

more likely to be BENIGN

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19
Q

thyroid adenoma

A 
aka: FOLLICULAR adenoma
MOST COMMON: BENIGN thyroid tumor
solitary, encapsulated
does NOT breach capsule
most non-functional
not considered forerunner for carcinoma but has shared genetic alterations
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20
Q

Hurthle cell adenoma

A

follicular adenoma with lots of Hurthle cells

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21
Q

pathogenesis of toxic adenoma and toxic multi nodular goiter

A

somatic mutation of TSH receptor signaling pathway: TSHR, GNAS
HYPERTHYROIDISM; functional HOT node

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22
Q

papillary carcinoma

A 
most often: 25-50 years
MOST COMMON: MALIGNANT thyroid tumor
prognosis: excellent
PSAMMOMA bodies, ORPHAN ANNIE 
metastasis: lymph
association: previous ionizing radiation
Dx: nuclear features
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23
Q

follicular carcinoma

A

women, older
more frequent in areas with iodine deficiencies
BREACH CAPSULE, cold imaging
Sx: slow enlarging painless nodule
metastasis: HEMATOGENOUS
prognosis: good, depends on invasion/stage

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24
Q

anaplastic carcinoma

A 
older
undifferentiated, follicular epithelium
RAPID
AGGRESSIVE: mortality near 100%
often have Hx of well-differentiated thyroid CA
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25
Q

medullary carcinoma

A

40-50s yrs for sporadic and familial not associated with MEN2A/2B
C cells/ PARAFOLLICULAR cells
secrete CALCITONIN
most sporadic, rest: MEN2A/2B or FMTC (familial medullary thyroid carcinoma)
activating point mutation in RET proto-oncogenes
AMYLOID

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26
Q

tall cell variant of papillary carcinoma

A

tall cells with papillary nuclear features

AGGRESSIVE

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27
Q

MEN2B

A

medullary carcinoma

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28
Q

RET

A

proto-oncogene
familial and sporadic medullary carcinoma
MEN2A/2B

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29
Q

thyroglossal duct cyst

A 
at birth or in childhood
ectopic thyroid
MIDLINE: btwn isthmus of thyroid and hyoid bone
Sx: repeated infections
NOT hormonally active
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30
Q

struma ovarii

A

mono dermal ovarian teratoma composed mostly of ectopic thyroid
can cause thyrotoxicosis
adenomas are common; 5% malignant

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31
Q

primary hyperparathyroid

A

more common than hypothyroid
HYPERCALCEMIA
primary: most are adenomas
parathyroid carcinoma is rare

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32
Q

parathyroid adenoma

A 
MOST COMMON: HYPERPARATHYROIDISM
HYPERCALCEMIA
elevated PTH
Sx: depression, muscle weakness, fatigue, renal stones
histo: NO fat
MOANS, BONES, STONES
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33
Q

hypoparathyroidism

A

most often caused by accidental removal of parathyroids during surgery

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34
Q

Causes of primary hyperthyroidism

A
  1. diffuse hyperplasia (Graves)
  2. hyper-functioning (toxic) multinodular goiter
  3. hyper-functioning (toxic) adenoma
  4. iodine-induced
  5. neonatal thyrotoxicosis associated with maternal Graves
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35
Q

Cause of secondary hyperthyroidism

A

TSH secreting pituitary adenoma

RARE

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36
Q

Thyroid diseases not associated with hyperthyroidism

A
  1. Granulomatous (de Quervain) thyroiditis
  2. subacute lymphocytic thyroiditis
  3. Struma ovarii
  4. Factitious thyrotoxicosis
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37
Q

factitious thyrotoxicosis

A

exogenous thyroxine intake

38
Q

Causes of primary hypothyroidism

A
  1. genetic defects in thyroid development (PAX8, FOXE1, TSH receptor mutations)
  2. thyroid hormone resistance syndrome (THRB mutations)
  3. surgery, radioactive iodine, external radiation
  4. autoimmune (Hashimotos)
  5. iodine deficiency
  6. drugs (lithium, iodides, p-aminosalicylic acid)
  7. congenital biosynthetic defect (dyshormonogenetic goiter)
39
Q

Causes of secondary hypothyroidism

A

RARE

  1. pituitary failure
  2. hypothalamic failure
40
Q

What is the most common cause of hypothyroidism?

  1. world wide
  2. US
A
  1. iodine deficiency

2. Hashimotos

41
Q

Most sensitive screening test for hypothyroidism

42
Q

HLA-DR3

A

Hashimoto

Graves

43
Q

HLA-DR5

44
Q

anti-thyroglobulin Ab

45
Q

anti-thyroid peroxidase Ab

A

Hashimoto

subacute lymphocytic thyroiditis

46
Q

PAX8 mutation

A

primary hypothyroidism due to genetic defect in thyroid development

47
Q

FOXE1 mutation

A

primary hypothyroidism due to genetic defect in thyroid development

48
Q

THRB mutation

A

primary hypothyroidism due to thyroid hormone resistance syndrome

49
Q

thyroid peroxidase

A

oxidizes iodide ions to form iodine atoms for addition to tyrosine residues on thyroglobulin for T4 or T3 production

50
Q

How does subacute lymphocytic thyroiditis differ histologically from chronic autoimmune thyroiditis?

A

painless thyroiditis histo:

  1. more follicular disruption
  2. fewer lymphocytes
  3. fewer germinal centers
  4. less fibrosis
51
Q

thyroid stimulating immunoglobulin

A

Ab against TSH receptor

GRAVES

52
Q

thyroid growth stimulating immunoglobulin

A

Ab against TSH receptor

GRAVES

53
Q

anti-TSH receptor Ab

54
Q

toxic multinodular goiter

A

aka: plummer syndrome
subset of goiters
HYPERTHYROIDISM
NO infiltrative ophthalmopathy or dermopathy

55
Q

What differentiates a multi nodular goiter from a follicular neoplasm?

A

neoplasm: capsule

multinodular goiter: NO capsule

56
Q

functional nodules

A

HOT nodules
take up radioactive iodine
more likely to be BENIGN than malignant
associated: hyperthyroidism

57
Q

toxic thyroid adenoma

A

minority of thyroid adenomas that cause hyperthyroidism

58
Q

TSHR

A

gene for TSH receptor
mutation: cause follicular cells to secrete thyroid hormone independent of TSH stimulation
TOXIC GOITER, TOXIC ADENOMA
rare in follicular carcinoma

59
Q

GNAS

A

gene for alpha-subunit of Gs
mutation: cause follicular cells to secrete thyroid hormone independent of TSH stimulation
TOXIC GOITER, TOXIC ADENOMA
GNAS1: ANTERIOR PITUITARY ADENOMA (40% of somatotroph adenomas, minority of ACTH secreting)
rare in follicular carcinoma

60
Q

RAS mutation

A

genetic alteration in minority of non-functioning follicular adenomas that are shared with follicular carcinomas

61
Q

PIK3CA

A

genetic alteration in minority of non-functioning follicular adenomas that are shared with follicular carcinomas

62
Q

lateral aberrant thyroid

A

ectopic thyroid that rests in lateral neck or in lymph nodes

in adults: most likely actually metastatic follicular thyroid carcinoma

63
Q

parathyroid development

A

from BRANCHIAL pouch
2 superior glands: 4th pouch
2 inferior glands: 3rd pouch (gives rise to thymus too: DiGeorge association)

64
Q

MEN1

A

pituitary adenoma

65
Q

MEN2B

A

medullary thyroid carcinoma

66
Q

secondary hyperparathyroidism

A

most commonly from renal failure

67
Q

mammosomatroph adenoma

A

Prolactin, GH

combined GH/prolactin excess features

68
Q

thyrotroph adenoma

A

THS
hyperthyroidism
RARE

69
Q

gonadotroph

A

FSH, LH
non-functioning typically: difficult to recognize
if suppressed production: LH most commonly suppressed
if producing hormone: FSH most commonly produced
hypogonadism, mass effect, hypopituitarism

70
Q

pituitary adenoma

A 
classified based on the hormone
functional or non-functional
most sporadic
BENIGN
Sx: bitemporal hemianopsia, headaches, production of hormones
histo: RETICULIN on SILVER STAIN
71
Q

microadenoma

A

less than 1 cm

pituitary adenoma

72
Q

macroadenoma

A

greater than 1 cm

NONFUNCTIONING are more likely to be macroadenomas (may cause hypopituitarism)

73
Q

CDKN1B

A

gene associated with subset of MEN-like abnormalities

FAMILIAL ADENOMA

74
Q

PRKAR1A

A

gene

FAMILIAL ADENOMA

75
Q

AIP

A

gene association with GH adenoma patients that are younger

76
Q

p53 mutation

A

pituitary adenoma with more aggressive behavior (invasion/recurrence)
ATYPICAL ADENOMA

77
Q

prolactinoma

A

MOST COMMON HYPERFUNCTIONING pituitary adenoma
IHC: prolactin
Sx: amenorrhea, galactorrhea, loss of libido, infertility

78
Q

stalk effect

A

any mass in the area of the pituitary can disturb prolactin secretion (mild elevations in serum prolactin do not necessarily indicate prolactinoma)
cell: lactotrophs

79
Q

Growth hormone-producing adenoma

A 
SECOND most common
acromegaly, gigantism
cell: somatoroph
stimulates hepatic secretion of IGF-1
other: gonadal dysfunction, diabetes mellitus (GH inhibits peripheral glucose uptake, and increases gluconeogenesis causing hyperinsulinism which leads to insulin resistance), weakness, HTN, arthritis, CHF, increased risk GI CA
80
Q

insulin like growth factor (IGF-1, somatostatin C)

A

stimulates bone, cartilage, soft tissue growth

81
Q

acromegaly

A

increased GH, IGF-1, glucose

most common cause of death: DILATED CARDIOMYOPATHY

82
Q

adrenocorticotropic hormone producing adenoma

A

small, stain with PAS
cell: corticotroph
silent or hypercortisolism (CUSHING DISEASE), may have HYPERPIGMENTATION

83
Q

Nelson syndrome

A

large destructive pituitary adenoma
develops after surgical removal of adrenal glands: loss of inhibitory effect of corticosteroids on pre-existing ACTH micro adenoma
NO hypercortisolism (because no adrenal glands)
HYPERPIGMENTATION

84
Q

plurihormonal adenoma

A

pituitary adenoma that produces multiple hormones

AGGRESSIVE

85
Q

pituitary carcinoma

A

RARE
only know malignant because it metastasizes (appear late following multiple local recurrences)
most are functional: prolactin and ACTH most common

86
Q

hypopituitarism

A

75% of parenchyma lost
partial or complete loss of secretion of one or more hormones
causes: nonfunctioning adenoma, Sheehans, empty sella syndrome

87
Q

pituitary apoplexy

A

abrupt hypopituitarism due to acute intratumoral hemorrhage

88
Q

Sheehan syndrome

A

pituitary gland expands in pregnancy without increase in blood supply to the ANTERIOR PITUITARY from the LOW PRESSURE VENOUS system: hypoxia
post partum hemorrhage leads to hypotension and DIC leads to necrosis
Sx: lactation failure, amenorrhea, adrenal insufficiency, hypothyroid
posterior pituitary receives blood from arterial braces and is less susceptible to ischemia

89
Q

empty sella syndrome

A

any condition or Tx that destroys part or all of pituitary

90
Q

Primary empty sella syndrome

A
  1. anatomic defect present
  2. subarachnoid space extends into sella: increase CSF pressure compresses gland
  3. increase in press on pituitary gland causes it to atrophy
    OBESE, HTN, MULTIPLE PREGNANCIES
91
Q

secondary empty sella syndrome

A

mass, such as a pituitary adenoma, enlarges the sella and is then either surgically removed or undergoes infarction, leading to loss of pituitary function

92
Q

causes of hypopituitarism

A
  1. tumors: pituitary, adenoma, craniopharyngioma, cerebral tumor
  2. hypothalmic disorder: tumor, functional disturbance (anorexia), isolated GH and GnH secretion due to impaired secretion of hypothalamic releasing hormones
  3. sarcoidosis
  4. vascular disease: Sheehan, infarction, severe hypotension, cranial arteritis
  5. infection: meningitis (TB, syphilis)
  6. iatrogenic: surgery, irradiation, prolonged glucocorticoids or TH (ACTH or TSH suppression)

Endocrine (7 decks)

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