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Hannah Endo/Repro year 2 > Endo- parathyroid pathology > Flashcards

Endo- parathyroid pathology Flashcards

1
Q

Mechanisms by which malignancy can cause hypercalemia

A
  1. humoral hypercalcemia of malignancy (HHM)/ blood mediated
    - 80% increased PTHrP seen in squamous carcinomas
    - Vitamin D-mediated (increased) seen in lymphomas
  2. local osteolytic hypercalcemia / bone mediated
    - release of Ca2+ from osteoclastic bone resorption seen in breast carcinomas, lung cancers, and myelomas
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2
Q

most “telltale” sign of parathyroid carcinoma? highly suggestive features?

A

sign: metastasis!

Fts: invasion of adjacent tissues, vascular invasion, and elevated PTH that doesn’t go down after surgery

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3
Q

Congenital causes of primary hypoparathyroidism

A
  1. Di Georges Syndrome
  2. CaSR germline mutation (GOF type)
  3. Familial Isolated Hypoparathyroidism
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4
Q

benign neoplasm of parathyroid chief or oxyphil cells. typically solitary. can be surrounded by rim of normal parathyroid tissue due to clonal nature of cells

A

parathyroid adenoma -MCC os primary hyperparathyroidism

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5
Q

what is Di Georges Syndrome

A
  • Chr 22q11.2 deletion syndrome
  • developmental defects in 3rd and 4th pharyngeal ouches that causes absent or hypoplastic parathyroid glands, thymus and heart outflow defects (trunks arteriosus or Tet of Fallot)
  • results in immune deficiency and increased risk of illness, HYPOCALCEMIA and tetany, cyanosis, facial anomalies (small mouth),

*TYPE OF PRIMARY HYPOPARATHRYOIDISM

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6
Q

most common cause of non-parathyroid hypercalcemia? other possible causes?

A

MC: malignancy

others:
- Vitamin D toxicity (hypervitaminosis)
- granulomatous Dz (sarcoidosis)
- excess Ca2+ ingestion
- meds (thiazide diuretics)

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7
Q

define pseudohypoparathyroidism

A

-NL to Elevated PTH; hypocalcemia, hyperphosphatemia
-caused by resistance to PTH via the GPCR pathway
(no renal response, or bone, or intestine) related to a genetic mutations of PHP and “ALBRIGHTS HEREDITARY OSTEODYSTROPHY”
-can affect other hormone pathways (TSH, LH/FSH)

*kind of resembles secondary parathyroid hyperplasia with labs but is not due to chronic renal failure or other extrinsic dz and there is no hyperplasia of gland

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8
Q

define the two types of germline CaSR mutations and implications

A
  1. Loss of Function/ inactivating CaSR mutation
    - “never thinks there is enough Ca, even when there is”
    - turns on PTH = HYPERCALCEMIA
    - reduces renal excretion= HYPOCALCIURIA
    * * aka Familial Hypocalciuric Hypercalcemia (is not a type of primary hypoparathyroidism!!!)
  2. Gain of Function/activating CaSR mutation
    - “thinks there is plenty Ca, when when there isn’t”
    - turns off PTH = HYPOCALCEMIA
    - increases renal excretion = HYPERCALCIURIA
    * ** aka Autsomal Dominant HypoPTH (hypercalciruic hypocalcemia; IS a type of primary hypoparathyroidism)
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9
Q

what is tertiary hyperparathyroidism ? what is the value of Ca2+?

A
  • rare
  • excessive and autonomous (unregulated) parathyroid activity due to a prolonged period of secondary hyperplasia and prolonged hypocalcemia causing persistent parathyroid stimulation (occurs even after Calcium level normalizes)
  • results in hypercalcemia!!!
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10
Q

hyperparathyroidism vs non-parathyroid source of hypercalcemia: which is more likely to be asx? overtly sx? and they are most commonly due to ?

A

hyperparathyroidism is usually asx and due to parathyroid adenoma MC

other: more likely very symptomatic (mental status changes, N/V, EKG changes - short QT) ; most commonly due to malignancy ( other less common causes are vitamin D toxicity, or thiazide diuretics, or sarcoidosis)

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11
Q

the ____ regulates the amount of PTH secreted from the parathyroid glands

A

Calcium-sensing receptor (CaSR)

*low serum Ca2+ = increased PTH secretion and vice versa

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12
Q

what two lab values help you distinguish parathyroid gland disorders

A

Calcium and PTH

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13
Q

What is the most common cause of primary hyperparathyroidism ? and two other causes? and what would the lab values of Serum Ca2+, serum PTH, serumPhosphate, urinary cAMP, and serum Alkaline phosphatase be?

A

1 = parathyroid adenoma (usual single gland, 1/4, affected)

others: parathyroid hyperplasia (all 4 glands enlarge to some extent) and parathyroid carcinoma (very large growth of usually 1 gland)

  • high calcium, PTH, urinary cAMP, Alk Phos
  • decreased serum phosphate
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14
Q

clinical features and physical exam findings of hypocalcemia

A

clin: behavioral disturbances/ stupor, lethargy, numbness, tingling, parathesias, muscle cramps, spasms (tetany), convulsions, poor appetite

PE:
 trousseau sign (flexed wrist tetany from BP cuff) 
Chvostek sign (face twitching from tapping Facial N.)
Prolonged QT interval on EKG
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15
Q

___ maybe be responsible for primary parathyroid hyperplasia, which is almost always seen in multiple glands, and ______(primary or secondary) hyperplasia is more common. Additionally they usually lack ___ that is seen in parathyroid adenomas

A

MEN Syndromes may be responsible (sporadic forms are rare)

SECONDARY hyperplasia is more common than primary (due to kidney disease)

lack NL RIM of parathyroid tissue ( and adipose tissue)

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16
Q

principle function of parathyroid gland

A

main fxn: calcium homeostasis

  • releases PTH which exerts its calcium raising affects by:
    1. release calcium and phosphate from bone stores (osteoclast activity)
    2. induces kidneys to reabsorb more calcium (block phosphate reabsorption)
    3. induces kidneys to convert 25(OH)D to active 1,25(OH)D which allows more calcium reabsorption from the intestines and bones
17
Q

difference in lab values from hypercalcemia of other causes vs hypercalcemia of primary hyperparathyroidism

A

primary hyperparathyroidism : high PTH and Ca2+

other: NL PTH, high Ca2+

18
Q

are germline or somatic MEN1 mutations more often seen in the setting of parathyroid adenomas

A

sporadic parathyroid adenomas are more common than familial and they have SOMATIC MEN1 mutations in 20-30% of them

19
Q

what will you see on a technetium scan of a parathyroid adenoma

A

an area of increased uptake (hotter, brighter in color) that is disproportionate to the other glands
-fused CT help localize the area

20
Q

mechanism of secondary parathyroid hyperplasia? lab values of PTH, alkaline phosphatase, and serum phosphate, and Ca2+?

A
  • renal disease/dysfunction !
  • kidneys continually excrete calcium and reabsorb phosphorous which decreases serum Ca2+ causing parathyroid cells to increase function to try to maintain levels (and subsequent 4 gland hyperplasia), however, even with increasingly high PTH levels, calcium is is still low, and the constant PTH release causes renal osteodystrophy
  • High PTH, low calcium, high phosphate, high alk phos
21
Q

define Osteitis Fibrosis Cystica

A

(a common side effect seen in primary hyperparathyroidism)

  • starts as a BROWN TUMOR (type of OFC that are bone lesions that arises in the setting of excess osteoclast activity)
  • it is resorption of bone due to increased osteoclast activity, that leads to fibrosis and cystic spaces in bone
  • results in small fractures, hemorrhage in bone space, and reactive tissues (bone pain)
  • can appear like metastatic disease on imaging

aka “von Recklinghausen Disease of bone”

22
Q

sx of primary hyperparathyroidism (which largely derive from chronic hypercalcemia)

A

the RAPP: “Painful bones, Renal stones, Abdominal groans, Physic moans”

  • osteoporosis (fractures, decreased density)
  • osteitis fibrosis cystica
  • nephrolithiasis (kidney stones)
  • constipation
  • PUD
  • gallstones
  • depression, lethargy, seizures
23
Q

intraoperative monitoring of ____ predicts a successful outcome in parathyroidectomy

A

PTH

24
Q

(histology question) the predominant cell types of the parathyroid gland

A
  1. chief cells (endocrine cell; central round, purple, uniform nuclei; light pink or white cytoplasm, secretory granules that release PTH)
  2. oxyphil cells (endocrine cell; smaller, darker purple nuclei; eosinophilic granular material in cytoplasm -i.e darker pink cytoplasm-; less endocrinology active than chief cells)
  3. adipocytes
25
Q

what is the first sign that usually presents in the dx of primary hyperparathyroidism

A

incidental high calcium found on routine lab work
(usually pts are asx for a while, sx arise due to chronic, protracted hypercalcemia)
-after high Ca2+ seen, follow up with PTH levels

26
Q

define calciphylaxis

A

-secondary hyperparathyroidism can lead to extensive VASCULAR CALCIFICATION and occlusion of blood vessels which can result in ischemia, ischemic gangrene, infection, and DEATH BY SEPSIS

online definition: calcium accumulates in small blood vessels of the fat and skin tissues. Calciphylaxis causes blood clots, painful skin ulcers and may cause serious infections that can lead to death

27
Q

T/F

Diarrhea is a common sx of primary hyperparathyroidism

A

NO: the abdominal sx are gallstones and constipation and PUD

28
Q

define Albright’s hereditary osteodystrophy

A
  • associated with genetic mutations of PHP genes leading to pseudohypoparathyroidism (and other conditions)
  • Main PE findings: short stature, obese, short phalanges of UE and LE
  • other PE findings: dental abnormalities, subcutaneous ossification, cataracts, occasionally seizures and tetany
29
Q

define renal osteodystrophy

A

(*seen in the setting of secondary parathyroid hyperplasia due to renal dysfunction)

=bone disease that occurs when kidneys fail to maintain proper levels of calcium in the blood

  • aka “dissecting osteitis”
  • can lead to skeletal abnormalities and “rugged jersey sign” of the vertebral bodies

Hannah Endo/Repro year 2 (11 decks)

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