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ENRP Exam 2 > Parathyroid Hillard > Flashcards

Parathyroid Hillard Flashcards

1
Q

the superior parathyroid glands develop from the ?

the inferior parathyroid glands develop from the?

A

fourth pharyngeal pouch

thrid pharygenal pouch

they can be ectopically located like in the mediastinum or the lateral neck

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2
Q

what does a normal parathyroid gland look like grossly and how much does it typically weigh

A

rounded red brown structure that weighs less than .5cm

gross weight will clue you into if the parathyroid is normal or if there is hyperplasia

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3
Q

describe the histology of the normal parathyroid gland

A

gland is surrounded by a thin capsule with adipose tissue and 2 cell types: chief and oxyphil

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4
Q

describe what a chief cell looks like

what do they produce?

A

chief cells have pink to clear cytoplasm with secretory granules

they produce parathyroid hormone

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5
Q

what do oxyphil cells look like and what is their function?

A

they have pink granula cytoplasm due to mitochondria

they are less endocrinogically active

similar to hurtle cells in the thyroid

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6
Q

the parathyroid gland produces _ when it senses low _

A

parathyroid hormone

low calcium

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7
Q

PTH affects bone by increasing _ activity through differentiation of progenitor cells into its mature type.

A

osteoclast (break down bone, releasing calcium)

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8
Q

PTH has affects on the kidney where it causes it to _ calcium at the distal convoluted tubule and collecting duct and _ phosphate reasbsorption

A

resorb (increase calcium)

decrease phosphate resobrptoion (pee it out)

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9
Q

PTH activates _

A

vitamin D

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10
Q

how does PTH activate vitamin D

A

it upregulates 1-alpha hydroxylase in the kidney converting inactive vitamin D to its active form calcitriol (1,25, dihydroxy vitamin D)

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11
Q

how does vitamin D increase calciim serum concentrations

A

increase kidney reabsorption, and GI abosrption of calcium

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12
Q

an elevated serum calcium will _ secretion of parathyroid hormone

A

decrease

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13
Q

the parathyroid hormone senses calcium levels through the?

A

Calcium sensing receptor

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14
Q

explain the ca sensing receptor

A

the extracellular receptor will bind calcium if levels are adequate/high in the blood and this causes PTH to be downregulated

it is a rapid continous moniotr that responds to mild changes

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15
Q

what causes sprimary hyperparaythroidism

A

parathyroid adenoma (most common)
parathyroid hyperplasia
parathyroid carcinoma

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16
Q

a parathyroid adenoma typically affects how many glands?

A

a single gland

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17
Q

parathyroid hyperplasia affects how many glands

A

multiple parathyroid glands, usually all 4

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18
Q

parathyroid carcinoma will present as?

A

a large mass lesion

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19
Q

what is primary hyperparathyroidism

A

this is when the parathyroid gland produces too much parathyroid hormone

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20
Q

1/3 of parathyroid adenomas have what mutation?

A

sporadic MEN1 mutations

a somatic mutation

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21
Q

rare germline mutation in _ can also cause parathyroid adenomas and affect every single cell in the body

A

MEN1 which will cause them to develop MEN-1 syndrome

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22
Q

MEN1 can lead to?

A

pituitary adenomas, pancreatic and endocrine tumors, parathyroid hyperplasia and rarely parathyroid adenomas

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23
Q

what cell cycle regulator mutation can lead to parathyroid adenomas

A

Cyclin D1 (CCDN1)

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24
Q

what is mutated in parathyroid carcinomas

A

CDC73

(jaw ossifying tumors as well)

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25
Q

what are the symptoms of primary hyperparathyroidsim

A

usually asymptomatic and picked up on a BMP rotuine calcium screen

if unchecked though it can cause

BONES, STONES, ABDOMINAL GROANS AND PSYCHIC MOANS
with no calcium in bones it can lead to osteoporosis and osteitis firbosis cystica (cystic areas of bony destruction)

increased circulating calcium can cause renal stones (nephrolithiasis) and gall stones along with constipation.

hypercalcemia reduces neuromusclar excitability- abdominal groans

high calcium can also lead to physciatric symptoms

lack of calcium in the bones, more calcium in the blood circulating

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26
Q

PTH increases osteoclastic activity in the bone, what can happen as a result of this

A

increased osteoclastic activity can cause a decrease in bone density, thinning of the trabeculae, and borwn tumors in the eroded bone.

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27
Q

PTH can cause “brown tumors” of the eroded bone, what is this?

A

this is when there is a loss of trabeculae in the bone and it is replaced with fibrosis, microfractures, and hemorrhage

can mimic a neoplastic process–> they progress to become completely cystic

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28
Q

when PTH causes the bone to become completely cystic what is this process termed

A

osteitis fibrosis cystica aka von recklinghuasens disease

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29
Q

when osteoclasts burrow centrally and destroy trabeculae it is referred to as?

A

dissecting osteitis

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30
Q

most of the time primary hyperparathyroidism is picked up by what?

A

routine elevated calcium

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31
Q

why is phosphorus low in primary hyperparathyroidism

A

PTH causes a decrease in phosphorous reabsorption by the kidney

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32
Q

imaging for primary parathyroid disease are used to help plan _

A

surgery

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33
Q

what imaging techniques can we use to visualize the parathryoid (when we have a known elevated calcium and PTH)

A

sestamibi scintigraphy- technetium-99m is used (radioactive)

SPECT-CT

ultrasound

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34
Q

the most reliable feature to distinguise a parathyroid adenoma from hyperplasia is?

A

the number of glands involved

1 gland in adenoma
multiple glands in hyperplasia

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35
Q

the enlargement between glands in parathyroid hyperplasia can be

A

asymmetric

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36
Q

normal weight of a parathyroid adenoma

A

.5 to 5 grams

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37
Q

multpile large parathyroid adenomas should clue you in to think?

A

MEN syndrome

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38
Q

histology of parathyroid hyperplasia and adenoma

A

both: can be hard to distinguish between the two that is why gross appearance is so important. they will have little adipose tissue with abundant chief cells and scattered oxyhphil cell nests

adenoma: can have both cells are consist of only 1 cell type; rim of normal compressed parathyroid tissue above a hypercellular nodule

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39
Q

how do you treat parathyroid hyperplasia

A

partial parathyroidectomy

  • 3 1/2 of the gland is removed and the remannt can be implanted into the forearm
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40
Q

how do you trear parathyroid adenoma

A

excision

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41
Q

how do surgeons gauge if they have removed all of the parathyroid tissue (hyperplasia/adenoma)

A

they use intraoperative parathyroid hormone levels

assess in real time

adenoma: marked drop
hyperplasia: stepwise drop with excisio of each hyperplastic gland

42
Q

what is the averaage weight of a parathyroid carcinoma

A

19grams (large mass lesion)

43
Q

is atypia a reliable criteria seperating benign tumors from malignant ones?

A

NO!

44
Q

what are the features of malignancy for the parathyroid neoplasm

A

vascular invasion, invasion of adjacent structures, metastasis

45
Q

parathyroid carcinoma is often _ _ and difficult to resect

A

poorly circumscribed

46
Q

secondary hyperparathyroidism occurs when ?

A

there is a disease or condition outside of the parathyroid gland and gives low calcium levels

47
Q

what is the most common cause of secondary hyperparathyroidism ?

A

renal failure/insufficiency

48
Q

how does renal failure cause decreased calcium levels but hyperparathyroidism

functional and absolute hypocalcemia

A

hypocalcemia- decreased renal production of the active form of vitamin D which decreases intestinal calcium absorption

decreased phosphate excretion also drives calcium levels down even further by complexing with calcium

49
Q

secondary hyperparathyroidism is compensatory _ secretion due to prolonged _

A

PTH

prolonged hypocalcemia

50
Q

what are some other causes of secondary hyperparathyroidism?

A

inadequate calcium intake
pancreatitis
vit D def.
baractic surgery

51
Q

how does secondary hyperparathyroidism look grossly and histologically

A

grossly: all 4 glands enlarged
histologically- diffuce cellular hyperplasia due to a hypocalemic state

52
Q

what are the symptoms of secondary hyperparathyroidism

A

signs of renal failure (if this is the cause)

apparent and picked up at a earlier stage than primary

bone pain, increased fracture incidence ( due to increased PTH)- renal osteodystrophy - + renal failure

calciphylaxis

53
Q

what is renal osteodystrophy

A

bone pain and fractures in the setting of renal failure

54
Q

what is calciphylaxis

A

increased vessel calcifications which cause vascular compromise and necorsis usually of the skin, fat, of lower leg

associated with secondary hyperparathyroidism

55
Q

calciphylexis is associated with?

A

hyperphosphatemia

increased calcium and phosphate complexes deposit in the skin

56
Q

what is tertiary hyperparathyroidism?

A

perisisten secretion of PTH after longstanding secondary hyperparathyroidism

57
Q

descirbe the pathology of tertiary hyperparathyroidism

A

longstanding hypocalcemia from secondary hyperparathyroidism will cause marked parathyroid gland hyperplasia and cause them to act on their own to create PTH despite calcium levels.

there is a chnage in calcium sensitivity

really high PTH, high calcium

58
Q

what are the signs of teritary hyperparathyroidism ?

A

calcipheyxis, abdominal gorans, moans, stones, cystic brown tumors, etc.

59
Q

what is the most common cause of hypercalcemia not related to parathyroid hormone?

A

hypercalcemia of malignancy

60
Q

what is hypercalcemia of malignancy

A

increased calcium with no increase in pth

PTH-related peptide tumor secretion (paraneoplastic process)
cytokine induced bone resorption by a tumor metastasis
tumors producing calcitriol that induces osteoclastic reabsorption

61
Q

what are some other causes of hypercalcemia with no increase PTH

A

excess vitamin D ingestion
excess calcium
thaizides
immobilization
GRANULOMATOUS DISEASE- EXCESS CALCITRIOL (SARCOIDOSIS)

62
Q

what is sarcoidosis

A

a non-caseating granulomatous disease that is seen in black people and bilateral hilar lymphadenopathy

involves the skin, joints, eyes, subcutenous nodules

63
Q

histology of sarcoidosis

A

giant cells with no necrosis and non-caseating granulomas

64
Q

macrophages in the granulomas of sarcoidosis creates _ which causes formation of calcitriol and forms hypercalcemia (calcitriol induces osteoclastic reabsorption)

A

1 alpha hydroxylase

65
Q

in the case of hypoparathyroidism PTH and calcium are _

A

low

66
Q

what is the primary cause of acquired hypoparathyroidism

A

removal or too much pararthyroid (iatrogenic)

67
Q

what is another cause of acquired hypoparathyroidism

A

autoummune hypoparathyroid

autoimmune parathyroid sydnrome 1*

68
Q

what is autoimmune hypoparathyroidism (autoimmune parathyroid syndrome 1)

A

a sydnrome that presents with mucocuteneous candiadisis in childhood followed by hypoparathyroidism and then adrenal insufficiency

AIRE mutation

69
Q

what are the congenital causes of hypoparathyroidism

A

digeorge syndrome

autosomal dominant hypoparathyroidism

familil isolated hypoparathyroidism

70
Q

what is familial associated hypoparathyroidism

A

issue with the production of secretion of PTH

71
Q

what are the clinical findings of hypocalcemia

A

tetany (involuntary muscle contractions, hyperstimulated peripheral nerves)- seizures, spasms

chvostek sign
troussaeu sign

anxiety

prolonged QT

paradoxical calficications

72
Q

what is chvostek sign

A

this is when you tap the facial nerve and there is contraction of the muscles that it innervates (eye, mouth nose)

73
Q

whar is trosseau sign

A

this is when you occlude the blood supply of the arm for a couple of minues and induce transient ischmeia and hypocalcemia will cause a carpal spasm to occur

74
Q

what is digeorges syndrome?

A

this is deletion of the long arm of chromosome 22 and developmental defect of the 3rd and 4th pharyngeal pouch

75
Q

what are the symptoms of digeorge syndrome

A

CATCH22

cardiac anomalies
abnormal facies
thymic aplasia
cleft palate
hypocalcemia

hypocalecmia is due to underdevelopment of the pouches and therefore the parathyroid glands, this lowers PTH and ultimately calcium as well

22q11 deletion

76
Q

what is autosomal dominant hypoparathyroidism

A

a mutation in CASR gene that increases in sensivity to calcium

PTH is inhbited even at low calcium levels

pth- low
calcium- low

usually PTH is ibhibited when calcium levels are high and bind to CASR

77
Q

what is pesuedohyperthryoidism?

A

a childhood disorder that results in end organ resistance to parathyroid hormone

hypocalcemia, hyperphosphtemia, hyperparathyrodism

78
Q

what is the mutation in pseudohypoparathyrodism and what else can it cause?

A

g protein receptor , there is resistence to PTH at end organs

affects other g protein receptors too: TSH , FSH, LH, GHRH

this means there will be hypothyroidism, infertility, short stature

albright hereditary osteodystrophy

79
Q

what is the transmission of multiple endocrine neoplasia syndromes

A

autosomal dominant (MEN)

80
Q

what are the different types of MEN syndromes

A

MEN-1
MEN2A
MEN2B
MEN4

81
Q

what organs are affected in MEN 1

A

remember the p’s

pituitary adenoma, parathyroid adenoma/hyperplasia, pacreatic/gestroenteric tumors (gastrinomas/insulinomas)

82
Q

what are the main abnormalities MEN4 can cause

A

pituitary adenomas and parathyroid hyperplasia

83
Q

MEN2A affects what

A

remember PM PHEO

parathyroid hyperplasia
medullary thyroid carcinoma
phernochromocytoma

84
Q

MEN 2B affects what

A

remember MMM Pheo

mucosal neuromas
marfanoid body
medullary thyroid carcinoma
pheochromcytoma

85
Q

MEN 1 syndrome is also known as?

mutation in?

first presentation?

A

wermer syndrome

MEN 1

hyperparathyroidism

86
Q

symptoms of men1

A

hyperparathyroidism

bones, stones, abdominal groans and psychic moans

gastrinomas

87
Q

_ _ syndrome is frequently seen in MEN1 syndrome and it presents as an increased gastrin from a gastrinoma

A

zollinger-ellison syndrome

88
Q

describe gastrinomas in men1 syndrome/zollinger ellision

A

the gastrinoma creates gastrin which stimulates gastric acid secretion from parietal cells and form peptic ulcer, reflux esophagitis, and diarrhea

89
Q

another presentation of men1 syndrome is a pituitary adenoma _

features

could be other adenoma types also like ACTH

A

prolactinoma

which causes galactorhea and amenorrhea in females and imptence in males (ED)

90
Q

what do the pancreatic tumors in men1 syndrome present with

A

an insulinoma which produces insulin and causes hypoglycemia (weakness, pale, confusion)

91
Q

when should you suspect MEN1
how do you test for it

A

suspect if: they have 2 or more primary tumors: pituitary adenoma, parathyroid adenoma, pancreatic, gastric tumor)

MEN1 DNA testing

92
Q

MEN 2A is also known as?

A

sipple syndrome

93
Q

what is the mutation in MEN2A

A

gain of function in RET proto-ooncogene

94
Q

what drive mortality in MEN2

A

medullary thyroid carcinoma

95
Q

what is medullar thyroid carcinoma

A

a mlaignant tumor of c cells in the thyroid (aka parafollicular cells)

96
Q

what are c cells/parafollicular cells of the thyroid

A

a neuroendocrine cell that secretes calcitonin to help lower lower blood calcium (prevents osteoclasts from reasorbing bone)

97
Q

what is often seen in histology of medullar thyroid carcinoma

A

amyloid due to the abundance of calcitonin polypeptides

c-cell hyperplasia

positive IHC: calcitonin

98
Q

parathroid hyperplasia presentation

medullary carcinoma presentation

pheochromocytoma presentation

all in MEN2

A

parathroid hyperplasia presentation: asymptomatic; incidental finding

medullary carcinoma presentation: thyroid nodule/lymphadenopathy

pheochromocytoma presentation - bilateral and secrete epinephrine

pheochromocytoma: episodic heacaches, sweating, tachycardia

99
Q

what is the mutation in MEN2B

A

germline missense mutation in RET

more aggressive than MEN2A

100
Q

MEN2b and MN 2B overlap with pheohromcytoma, and medullary thyroid carcinoma

what is specific to men2b

medullary thyroid carcinoma in MEN2b is miltifocal

A

mucocutenous neuromas
marfanoid hyperxtensible joints

no aortic abnormalities like in MARFANs

101
Q

almost all MEN2 patients develop _

A

medullary thyroid carcinoma

102
Q

all indivduals with medullary thyroid carcinoma should be tested for?

A

RET

MEN2B presents earlier (around 10) then MEN2A

ENRP Exam 2 (13 decks)

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