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Endo II > Pituitary and thyroid > Flashcards

Pituitary and thyroid Flashcards

1
Q

PIT-1

A

TF which regulates differentiation of
somatotrophs
mammosomatotrophs
lactotrophs

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2
Q

SF-1 and GATA-2

A

TFs which regulates differentiation of gonadotrophs

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3
Q

What is most common cause of hyperpituitarism of ant pit

A

pituitary adenoma

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4
Q

what is the peak incidence of pituitary adenomas

A

35-60

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5
Q

genetic abnormaliites of pituitary adenomas

A

GPCR mutations -> GNAS

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6
Q

GNAS

A

codes for Galpha subunit

these mutation are also present in corticotroph adenomas

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7
Q

morphology of pituitary adenoma

A
  • well circumscribed and soft (d/t lack of reticulin)
  • if breaks thru diaphgragma sella its invasive
  • CELLULAR MONOMORPHISM AND LOSS OF RETICULIN distinguished from nonneoplastic surrounding cells
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8
Q

Mass Effect signs

A
  • radiographic abnromaliites of sella turcia
  • bitemporal hemianopsia
  • elevated intracranial pressure
  • acute hemorrhage into adenoma leading to pituitary apoplexy
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9
Q

lactotroph adenoma

A

prolactin secreting

most frequent type of fnx pituitary adenoma

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10
Q

sparsely granulated lactotroph adenomas

A

most common

chromophobic cells w/juxtanuclear PIT-1

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11
Q

densely granulated lactotroph adenomas

A

diffuse cytoplasmic PIT-1

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12
Q

other morphological features of lactotroph adenomas

A

psammoma bodies or calcification of entire tumor

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13
Q

symptoms of lactotroph adenoma

A

amenorrhea
galactorrhea
loss of libido and fertility

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14
Q

other causes of pathologic prolactinemia

A 
truama to pituitary stalk
DR2 antagonists
any mass in suprasellar compartment
renal failure
hypothyroidism
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15
Q

Tx of prolactinemia

A

surgery

bromocriptine

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16
Q

somatotroph adenomas

A

GH secreting

2nd most common type of fnx pituitary adenoma

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17
Q

densely granulated somatotroph adenomas

A

monomorphic acidophillic cells

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18
Q

mammosomatotroph

A

bihormonal: GH and prolactin

usually dense granulated variant

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19
Q

acromegaly

A

bone density may increase in spine and hips

sausage fingers

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20
Q

other issues associated with GH excess

A 
gonadal dysfunction
DM
mm weakness
HTN
arthritis
CHF
GI CA
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21
Q

Dx of somatotroph adenoma

A

elevated GH and IGF1

FAILURE OF GLUCOSE load to suppress GH

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22
Q

corticotroph adenomas

A

excess ACTH -> adrenal hypersection of cortisol -> cushings disease

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23
Q

corticotroph adenomas morphology

A

stain with PAS due to CHO in POMC

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24
Q

Nelson syndrome

A

large destructive adenomas develop post adrenal gland removal
do not present until mass effect bc cannot become symptomatic

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25
Q

pleurihormonal

A

very rare and usually aggressive

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26
Q

gonadotroph adenomas

A

secrete hormones inefficiently and variably
usually discovered d/t mass effect
FSH usually dominantly secreted hormone
usually express SF-1 and GATA-2

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27
Q

thyrotroph adenomas

A

rare

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28
Q

non-fnx pituitary adeomas

A

aka silent or null-cell

most common type of pituitary adenoma

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29
Q

pituitary carcinomas

A

rare
presence of craniospinal or systemic mets
most are functional: prolactin and ACTH most common

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30
Q

when does hypopituitarism become symptomatic

A

when 75% of parenchyma is lost

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31
Q

Where is the likely pathology in neurogenic DI

A

hypothalmus

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32
Q

what is the most common cause of neurogenic DI

A

trauma

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33
Q

Pituitary apoplexy

A

sudden hemorrhage into pituitary gland
sudden onset of HA and diploplia
CV collapse, loss of conciousness, sudden death
neurosurgical emergency

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34
Q

sheehan syndrome

A

aka postparum necrosis of ant pit
most common cause of ant pit necrosis
pit enlarges during preg without increased blood supply, if blood loss occurs during labor ant pit at risk

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35
Q

other causes of pit necrosis

A 
DIC
Sickle cell
elevated intracranial pressure
trumatic injury
shock
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36
Q

Rathke cleft cyst

A

lined by ciliated cuboidal epi w/occaision goblet and ant pit cells
proteinacious fluid

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37
Q

empty sella syndrome

A

any condition or Tx that destryoys all or part of pit gland

radiation or surgery

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38
Q

hypothalamic lesion

A

DI
tumors
inflammatory disorder and infections (TB and sarcoidosis)
genetic defects (PIT-1)

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39
Q

Post pit syndromes

A

DI

SIADH

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40
Q

SIADH

A

most common cause is SSC of lung

can also be caused by drugs

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41
Q

hypothalamic suprasellar tumros

A

may induce hypo or hyper fnx of ant pit, DI, or combos

gliomas and craniopharyngiomas most common

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42
Q

craniopharyngiomas

A 
arise from vestigial remnants of Rathke pouch
biomodal: 5-15 and 65
HA and visual disturbances
WNT and beta catenin mutationa
excellent prognosis
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43
Q

morphology of craniopharyngiomas

A

most commonly cystic and mulitloculates

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44
Q

2 variants of craniopharyngiomas

A

adamantinomatous

papillary

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45
Q

adamantinomatous craniopharyngiomas

A

kids
calcification (psomma bodies)
cysts of machine oil fluid

46
Q

papillary craniopharyngiomas

A

adults

calcifications and cysts rare

47
Q

parafollicular cells

A

aka C cells
in thyroid
secrete calcitonin

48
Q

3 most common causes of thyrotoxicosis

A

Diffuse hyperplasia associated with graves (85%)
hyperfunctional multinodular goiter
hyperfunctional thyroid adenoma

49
Q

Thyrotoxicosis and BMR

A

increased
skin warm, soft, flushed
heat intolerance and sweating
weigh loss despite increased appetite

50
Q

Thyrotoxicosis and heart

A 
earliest and most consistent features
elevated contractility and CO
tachy, palps, cardiomegaly
arrhythimia (a-fib) in older patients
CHF
51
Q

Thyrotoxic cardiomyopathy

A

left ventricular dysfunction -> decreased CO

52
Q

Thyrotoxicosis and NS

A 
tremor
hyperactivity
emotional lability
anxiety
inability to concentrate
insomnia
mm weakness and decreased mm mass
53
Q

Thyrotoxicosis and eyes

A

wide staring gaze with lid lag

exopthalmus only in graves

54
Q

Thyrotoxicosis and skeleton

A

over stimulation of bone resorption -> osteoporosis

55
Q

Thyroid storm

A 
abrupt onset of severe Thyrotoxicosis
most common in graves
febrile and tachy
medical emergency b/c arrhythmias fatal
predisposing factors: infection, surgery, stress, cessation of meds
56
Q

apathetic hyperthyroidism

A

older adults and various co-morbidities blunt features of excess TH

57
Q

Tx of Thyrotoxicosis

A 
beta blockers
thionamide
iodine
radioiodine ablation 
surgery
58
Q

congenital hypothyroidism

A

worldwide d/t endemic iodine deficiency

59
Q

autoimmune hypothyroidsim

A

most common in developed countries

almost all are hashimotos

60
Q

Abs against thyroid

A

antimicrosomal
antithyroid peroxidase
antithyroglobulin

61
Q

drugs which can induce hypothyroidsim

A

methimazole
PTU
lithium
p-aminosalcylic acid

62
Q

myxedema

A 
hypothyroidism in developing in older child or adult
slowing of physical and mental activity
listless, cold intolderant, overweight
constipation, decreased sweating
reduced CO -> SOB 
atherogenic profile
deepening of voice, non pitting edema
63
Q

histo of myxedema

A

glycosaminglycans and hyaluronic acid in skin

64
Q

Dx of myxedema

A

TSH

65
Q

hashimotos thyroiditis

A

women 45-65
CTLA4 and PTPN22 (regulate T cells)
progressive apoptosis or thyroid epi replaced by mononuclear cells and fibrosis

66
Q

morphology of hashimotos

A

diffusely enlarged, with intact capsule and pall surface
extensive mononuclear infiltrates with germinal centers
Hurthle cells
fibrosis does NOT extend beyond capsule

67
Q

hashitoxicosis

A

transient thyrotoxicosis d/t disruption of thyroid follicles and release of TH

68
Q

hashimotos at risk for what CA

A

extranodal marginal zone B cell lymphomas in thyroid

69
Q

subacute lymphocytic thyroiditis

A

postpartum thyroiditis is in this category
autoimmune (Abs)
lymphocytic infiltrates w/large germinal centers
unlike hasimotos NO fibrosis or Hurthle cells

70
Q

granulomatous thyroiditis

A 
aka dequervain thyroiditis
40-50
tirggered by viral infection, Hx of URI
painful
u/l or b/l enlarged firm thyroid with intact capsule that may adhere to surrounding structures
multinucleated giant cells
lasts 2-6 weeks
elevated TH, decreased TSH
radioactive I uptake diminished
71
Q

graves

A

most common cause of endogenous hyperthyroidism

peak 20-40

72
Q

graves triad

A

hyperthyroidism with diffuse enlargement of gland
exopthalamus
pretibial myexedema

73
Q

Ab in graves

A

TSI- thyroid stimulating immunoglobulin

74
Q

Pathogenesis of graves

A

linked to CTLA4 and PTPN22 and HLA-DR3

75
Q

morphology of graves

A

-symmetrically enlarged with diffuse hypertrophy and hyperplasia of follicular epi cells
-soft meaty appearance resembling mm
small papillae project into lumen, but NO fibrovascular core
T cell and B cell infiltratates
germinal centers
colloid scalloped

76
Q

Tx of graves

A 
beta blockers
thionamides
PTU
radioiodine ablation
thyroidectomy
77
Q

what is TH in most goiters

A

euthyroid

78
Q

diffuse nontoxic/simple goiter

A

aka colloid goiter
2 categories:
endemic
sporadic

79
Q

endemic diffuse nontoxic/simple goiter

A

10%+ of pop must be affected
mountainous areas
can be d/t goitrogens

80
Q

sporadic

A

less frequent the endemic

mostly idiopathic

81
Q

goiterogens

A 
cabbage, cauliflower, brussel sprouts, turnips
cassava root (thiocyanate)
82
Q

phases of goiter

A

hyperplastic: symmetrically enlarged

colloid involution: when I is again available

83
Q

multinodular goiter

A

virtually all long standing simole goiters progress to multinodular
produce most extreme thyroid enlargements
polyclonal and monoclonal nodules
can be complicated by follicular rupture, hemorrhages, cysts scarring, calcification

84
Q

multinodular goiter morphology

A

pressure on midline structures
intrathroacic/plunging goiter: grows behind sternum
brown gelantinous colloid

85
Q

mass effects of multinodular goiter

A

airway obstruction
dysphagia
compression of large vessels
SVC syndrome

86
Q

plummer syndrome

A

less common presentation of goiter
hyperthyroidism (toxic)
exopthalmus and dermopathy of graves absent

87
Q

determining malignancy in thyroid

A
  • solitary nodules more likely to be neoplastic
  • nodules in young more likely to be neoplastic
  • noduels in males more likely to be neoplastic
  • Hx of radiation more likely malignant
  • fnx noduels more likely benign
88
Q

thyroid adenomas

A

from follicualr epi
usually not forerunners to carcinomas
most are non functional

89
Q

common mutations in thyroid adenomas

A

gain of fnx in TSHR or GRAS

these are RARE in follicular carcinomas

90
Q

rare mutatuion in thyroid adenomas

A

RAD or pIK3CA mutation
PAX8-PPARG fusion
these ARE shared with follicualr carcinomas

91
Q

morphology of thyroid adenomas

A

solitary spherical, encapsulated lesion
areas of hemorrhage, fibrosis, cystic changes common
HALLMARK is well formed capsule
integrity of capsule is only way to determine if it is truly benign

92
Q

Dx of thyroid adenomas

A

surgical removal for capsule integrity determination

93
Q

prognosis of thyroid adenomas

A

excellent

do not recur

94
Q

thyroid carcinomas

A

uncommon
in kids M=F
types: papillary, follicular, anaplastic, medullary

95
Q

which thyroid carcinomas arise from follicular epi

A

papillary
follicular
anaplastic
mutation in TK -> RAS -> MAPK pathway

96
Q

papillary carcinomas

A

most common 85%
25-50
usually have radiation Hx

97
Q

mutations in papillary carcinomas

A

gain of fnx in RET, NTRK1, or BRAF

98
Q

RET mutations

A

part of MAP kinase pathway
RET/PTC fusion
more common in radiation
NOT seen in follicular adenomas or carcinomas

99
Q

BRAF

A

in MAP pathwya
adverse prognosis
NOT seen in follicular adenomas or carcinomas

100
Q

morphology of papillary carcinomas

A

GRAY WHITE
areas of fibrosis and cysts
papillae have fibrovascular stalk
nuclei of OPTICAL CLEARING (ground glass or orphan Annie nuclei)
psudoinclusions in nuclei of invading cytoplasm
psammoma bodies in papillay (never seen in follicular or medullary CA)
LYMPH invasion, but NOT blood
METS to cervical nodes

101
Q

Dx of papillary carcinomas

A

on cellular findings alone

excellent prognosis

102
Q

follicular carcinomas

A

more common in areas with I deficiency

40-60

103
Q

mutation in follicular carcinoma

A
  • RAS or PI3K/AKT TK pathway
  • loss of fnx in PTEN
  • PAX8-PPARG fusion
104
Q

morphology of follicular carcinoma

A 
usually well circumscribed but may rupture capsule
gray-tan-pink
central fibrosis and calcification
hurthle cells
NO psammoma bodies
Dx with capsular invasion
105
Q

spread of follicular carcinoma

A

lymph rarely involved, but common thru blood with mets to bone, liver, and lungs

106
Q

Tx of follicular carcinoma

A

total thyroidectomy
radioactive iodine ablation
TH to suppress TSH

107
Q

anaplastic carcinomas

A

aggressive 100% mortality
65
25% previous Hx of thyroid CA
25% concurrent CA in adjacent cells

108
Q

anaplastic carcinomas mutations

A

TP53

beta catenin

109
Q

anaplastic carcinomas morphology

A

lots of cell types (giant, spindle, mised, foci of papillary or follicular differentiation)

110
Q

medullary carcinoma

A

neuroendocrine neoplasm derived from parafollicular C cells
secrete calcitonin
can also secrete serotonin, ACTH, VIP

111
Q

familial causes of medullary carcinoma

A

MEN-2

germline RET mutations (not translocations)

112
Q

morphology of medullary carcinoma

A 
sporadic solitary, familial mulitple
necrosis and hemorrhage
AMYLOID
CALCITONIN
adjacent C cell hyperplasia -> MEN2

Endo II (15 decks)

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