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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
medullary carcinoma
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
26
tall cell variant of papillary carcinoma
tall cells with papillary nuclear features | AGGRESSIVE
27
MEN2B
medullary carcinoma
28
RET
proto-oncogene familial and sporadic medullary carcinoma MEN2A/2B
29
thyroglossal duct cyst
``` at birth or in childhood ectopic thyroid MIDLINE: btwn isthmus of thyroid and hyoid bone Sx: repeated infections NOT hormonally active ```
30
struma ovarii
mono dermal ovarian teratoma composed mostly of ectopic thyroid can cause thyrotoxicosis adenomas are common; 5% malignant
31
primary hyperparathyroid
more common than hypothyroid HYPERCALCEMIA primary: most are adenomas parathyroid carcinoma is rare
32
parathyroid adenoma
``` MOST COMMON: HYPERPARATHYROIDISM HYPERCALCEMIA elevated PTH Sx: depression, muscle weakness, fatigue, renal stones histo: NO fat MOANS, BONES, STONES ```
33
hypoparathyroidism
most often caused by accidental removal of parathyroids during surgery
34
Causes of primary hyperthyroidism
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
35
Cause of secondary hyperthyroidism
TSH secreting pituitary adenoma | RARE
36
Thyroid diseases not associated with hyperthyroidism
1. Granulomatous (de Quervain) thyroiditis 2. subacute lymphocytic thyroiditis 3. Struma ovarii 4. Factitious thyrotoxicosis
37
factitious thyrotoxicosis
exogenous thyroxine intake
38
Causes of primary hypothyroidism
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
Causes of secondary hypothyroidism
RARE 1. pituitary failure 2. hypothalamic failure
40
What is the most common cause of hypothyroidism? 1. world wide 2. US
1. iodine deficiency | 2. Hashimotos
41
Most sensitive screening test for hypothyroidism
serum TSH
42
HLA-DR3
Hashimoto | Graves
43
HLA-DR5
Hashimoto
44
anti-thyroglobulin Ab
Hashimoto
45
anti-thyroid peroxidase Ab
Hashimoto | subacute lymphocytic thyroiditis
46
PAX8 mutation
primary hypothyroidism due to genetic defect in thyroid development
47
FOXE1 mutation
primary hypothyroidism due to genetic defect in thyroid development
48
THRB mutation
primary hypothyroidism due to thyroid hormone resistance syndrome
49
thyroid peroxidase
oxidizes iodide ions to form iodine atoms for addition to tyrosine residues on thyroglobulin for T4 or T3 production
50
How does subacute lymphocytic thyroiditis differ histologically from chronic autoimmune thyroiditis?
painless thyroiditis histo: 1. more follicular disruption 2. fewer lymphocytes 3. fewer germinal centers 4. less fibrosis
51
thyroid stimulating immunoglobulin
Ab against TSH receptor | GRAVES
52
thyroid growth stimulating immunoglobulin
Ab against TSH receptor | GRAVES
53
anti-TSH receptor Ab
GRAVES
54
toxic multinodular goiter
aka: plummer syndrome subset of goiters HYPERTHYROIDISM NO infiltrative ophthalmopathy or dermopathy
55
What differentiates a multi nodular goiter from a follicular neoplasm?
neoplasm: capsule | multinodular goiter: NO capsule
56
functional nodules
HOT nodules take up radioactive iodine more likely to be BENIGN than malignant associated: hyperthyroidism
57
toxic thyroid adenoma
minority of thyroid adenomas that cause hyperthyroidism
58
TSHR
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
GNAS
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
RAS mutation
genetic alteration in minority of non-functioning follicular adenomas that are shared with follicular carcinomas
61
PIK3CA
genetic alteration in minority of non-functioning follicular adenomas that are shared with follicular carcinomas
62
lateral aberrant thyroid
ectopic thyroid that rests in lateral neck or in lymph nodes | in adults: most likely actually metastatic follicular thyroid carcinoma
63
parathyroid development
from BRANCHIAL pouch 2 superior glands: 4th pouch 2 inferior glands: 3rd pouch (gives rise to thymus too: DiGeorge association)
64
MEN1
pituitary adenoma
65
MEN2B
medullary thyroid carcinoma
66
secondary hyperparathyroidism
most commonly from renal failure
67
mammosomatroph adenoma
Prolactin, GH | combined GH/prolactin excess features
68
thyrotroph adenoma
THS hyperthyroidism RARE
69
gonadotroph
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
pituitary adenoma
``` 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
microadenoma
less than 1 cm | pituitary adenoma
72
macroadenoma
greater than 1 cm | NONFUNCTIONING are more likely to be macroadenomas (may cause hypopituitarism)
73
CDKN1B
gene associated with subset of MEN-like abnormalities | FAMILIAL ADENOMA
74
PRKAR1A
gene | FAMILIAL ADENOMA
75
AIP
gene association with GH adenoma patients that are younger
76
p53 mutation
pituitary adenoma with more aggressive behavior (invasion/recurrence) ATYPICAL ADENOMA
77
prolactinoma
MOST COMMON HYPERFUNCTIONING pituitary adenoma IHC: prolactin Sx: amenorrhea, galactorrhea, loss of libido, infertility
78
stalk effect
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
Growth hormone-producing adenoma
``` 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
insulin like growth factor (IGF-1, somatostatin C)
stimulates bone, cartilage, soft tissue growth
81
acromegaly
increased GH, IGF-1, glucose | most common cause of death: DILATED CARDIOMYOPATHY
82
adrenocorticotropic hormone producing adenoma
small, stain with PAS cell: corticotroph silent or hypercortisolism (CUSHING DISEASE), may have HYPERPIGMENTATION
83
Nelson syndrome
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
plurihormonal adenoma
pituitary adenoma that produces multiple hormones | AGGRESSIVE
85
pituitary carcinoma
RARE only know malignant because it metastasizes (appear late following multiple local recurrences) most are functional: prolactin and ACTH most common
86
hypopituitarism
75% of parenchyma lost partial or complete loss of secretion of one or more hormones causes: nonfunctioning adenoma, Sheehans, empty sella syndrome
87
pituitary apoplexy
abrupt hypopituitarism due to acute intratumoral hemorrhage
88
Sheehan syndrome
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
empty sella syndrome
any condition or Tx that destroys part or all of pituitary
90
Primary empty sella syndrome
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
secondary empty sella syndrome
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
causes of hypopituitarism
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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