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CAS 3 > Disorders of the Parathyroid Gland > Flashcards

Disorders of the Parathyroid Gland Flashcards

1
Q

MOA of chief cells

A

have secretory granules containing parathyroid hormone (PTH)

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2
Q

MOA of oxyphil cells

A

found throughout the normal parathyroid either singly or in small clusters. They are slightly larger than the chief cells, have acidophilic cytoplasm, and
are tightly packed with mitochondria

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3
Q

third pharyngeal pouch forms the

A

inferior parathyroid gland

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4
Q

fourth pharyngeal pouch forms the

A

superior PTH gland

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5
Q

pathogenesis of CASR gene calcium in homeostasis

A

Decrease in extracellular calcium concentration
extracellular fluids (ECF) ——>
diminishes the activity CaSR parathyroid
Release of PTH——–>
PTH acts on kidney and bone to increase renal and
bone Ca2+ resorption + favors vitamin D synthesis
in kidney.——–>
Vitamin D promotes Ca2+ absorption in small
intestine.———->
These effects contribute altogether to return
extracellular Ca2+ levels to the normal level, thus
activating the CaSR and inhibiting release of PTH.

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6
Q

list 4 effects of PTH

A
  • Increased renal tubular reabsorption of calcium
  • Increased urinary phosphate excretion,
  • Increased conversion of vitamin D to its active
    dihydroxy form in the kidneys,
  • Enhanced osteoclastic activity
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7
Q

what is the role of fibroblastic growth factor 23 (FGF 23)

A

FGF 23
* Phosphaturic hormone
* Reduces expression of sodium phosphate
cotransporters in kidney PCT
* reducing 1,25 dihydroxy Vit D levels

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8
Q

what is the role of fibroblastic growth factor 23 (FGF 23)

A

FGF 23
* Phosphaturic hormone
* Reduces expression of sodium phosphate
cotransporters in kidney PCT
* reducing 1,25 dihydroxy Vit D levels

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9
Q

what is the function of RANKL (receptor activator of nuclear factor κB ligand)

A

Membrane-bound protein of osteoblasts that stimulates osteoclasts by interacting with RANK
Ensures fusion and differentiation into activated osteoclasts and prevents their apoptosis

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10
Q

what is the function of RANK

A

receptor on osteoclasts and osteoclast precursors, for interaction with osteoblasts

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11
Q

what is the function of Osteoprotegerin (OPG)

A

A regulatory protein secreted by osteoblasts that binds RANKL
Inhibits RANK-RANKL interaction, leading to decreased osteoclast activity.

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12
Q

__________ :
-Secreted by osteoblasts
-Promotes the proliferation of osteoclast precursor cells
-Simultaneous binding and fusion of ______and RANKL on the surface of precursor osteoclasts on the synovium→ differentiation of precursor osteoclasts into osteoclasts

A

M-CSF(macrophage colony-stimulating factor)

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13
Q

Interaction of membrane bound or soluble _______with RANK ____________ cells induces their differentiation and activation into mature osteoclasts.

A

RANKL , RANK-expressing osteoclast precursor cells

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14
Q

vitamin D3, prostaglandin E2 (PGE2), parathyroid hormone (PTH) and several cytokines - (TNFα) and
interleukin (IL)-1, -11 and -17. induced ___________ expression

A

RANKL expression by osteocytes and osteoblasts

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15
Q

Expression of the decoy receptor osteoprotegerin (OPG) is induced by :

A

17-β oestradiol,
IL-4
TGF-β

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16
Q

OPG ___________ with RANK/RANKL interaction thereby _________bone degradation

A

interferes, inhibition

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17
Q

list 3 inducers of RANKL expression

A

progesterone
PTH
calcitriol (vit. D3)

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18
Q

estrogen, induces the expression of the _______

A

decoy receptor OPG

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19
Q

____________ important cause of hypercalcemia.

A

Primary hyperparathyroidism

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20
Q
  • Adults, more common in women than men 4 : 1.
    !Adenoma: 85% to 95%:

primary or secondary hyperPTH

A

1º hyper-PTH

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21
Q

pathogenesis of PRIMARY HYPERPARATHYROIDISM

A

Excess production of PTH → Hypercalcemia

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22
Q

Clinically silent – cause of hypercalcemia

A

Primary hyperparathyroidism

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23
Q

Clinically apparent – causes of hypercalcemia

A

Cancer – PTH like polypeptide + Osteolytic bone metastasis

24
Q

Persistent hyperplasia in long standing secondary
hyperparathyroidism even with correction

Calcium and phosphate increased

Requires parathyroidectomy

A

teritary hyper-PTH

25
Q

Compensatory hyperplasia of all parathyroids because
of prolonged hypocalcemia - CKD or Vit D def

Calcium levels low / normal

A

secondary hyperparathyroidism

26
Q

Primary Hyperparathyroidism is most common in adults or children
women or men
4:1 ratio
adenoma 85-95%

A

ADULTS , WOMEN

27
Q

list 3 genetic abnormalities in primary hyperparathyroidism

A
  1. Cyclin D1 gene rearrangements – overexpressed in 40% parathyroid adenoma
    Cyclin D1 – normal cell cycle regulator, gene
    located at 11q Inversion Chr 11 repositions this
    gene adjacent to PTH gene located at 11p drives
    abnormal expression of Cyclin D1 in PTH
    producing cells
  2. MEN mutations: MEN-1,MEN-2a ( parathyroid tumors)
  3. Familial hypocalciuric hypercalcemia (CASR inactivating mutations)
28
Q

determine diiagnosis:
-rare autosomal dominant condition.
-(CASR inactivating mutations) decreasing sensitivity
to extracellular calcium leading high PTH levels.

A

Familial hypocalciuric hypercalcemia (FHH)

29
Q

diagnosis of FHH

A
  • asymptomatic hypercalcemic patient with a family history of hypercalcemia,
  • asymptomatic hypercalcemia before the age of 40 years
  • serum calcium values from first-degree relatives in the absence of family history.
30
Q

FHH patient typically have electrolyte imbalances of:

A
  • mild hypercalcemia
  • hypocalciuria
  • hypermagnesemia
  • hypophosphatemia.
30
Q

FHH patient typically have electrolyte imbalances of:

A
  • mild hypercalcemia
  • hypocalciuria
  • hypermagnesemia
  • hypophosphatemia.
31
Q

Increased PTH secretion despite
increased Serum Calcium
= Hypercalcemia

is seen in?

A

in parathyroid ; reuced CASR function

32
Q

Increased calcium reabsorption
despite increased Serum Calcium
= Hypercalcemia & Hypocalciuria
is seen in?

A

in kidney; reduced CASR function

33
Q

Determine Diagnosis:

A
  • 24 hours urinary calcium excretion is less than 100 mg/24 hours.
  • Ca/Cr excretion ratio is low. (0.020 or less)- should be tested for CaSR gene mutations.
  • Serum Magnesium is in the upper-normal range or mildly elevated
34
Q

Morphologic findings in Primary hyperparathyroidism: parathyroid adenoma GROSS:

A
  • solitary nodule confined to single gland;
  • other glands normal/shrunken (feedback inhibition by calcium)
  • well-circumscribed – delicate capsule
  • soft, tan to reddish-brown
  • 0.5-5g
35
Q

Morphologic findings in Primary hyperparathyroidism: parathyroid adenoma Microscopically:

A
  • fairly uniform, polygonal chief cells with small, centrally placed nuclei- endocrine
    atypia
  • Absence of adipose tissue that is seen in normal parathyroid.
36
Q

Morphologic findings in Primary hyperparathyroidism: parathyroid HYPERPLASIA:

A

All 4 glands involved - asymmetry (together not >1g)
Chief cell predominant- nodular / diffuse
Fat may be inconspicuous

37
Q

Morphologic findings in Primary hyperparathyroidism: parathyroid CARCINOMAS:

A

involves one parathyroid
circumscribed lesions / clearly invasive neoplasms

Gross:
* gray-white, irregular masses weighing up to 10g

Microscopy
* dense, fibrous capsule
* cells usually are uniform and resemble normal parathyroid cells nodular or trabecular
patterns.
* Diagnosis of carcinoma based on cytologic detail is unreliable, invasion of surrounding
tissues and metastasis are the only definitive criteria

38
Q

bones marrow contains fibrous tissue accompanied by foci of hemorrhage and cyst formation

A

(osteitis fibrosa cystica- Brown tumor of hyperparathroidism)

39
Q

clinical features of 1º hyperPTH

A

-painful bones ( abnormal remodeling, osteolysis & fractures)
-renal stones ( renal colic)
-abdominal groans ( hypercalcemia induced ileus, constipation, pancreatitis, peptic ulcer)
-psychic moans ( malaise, fatigue, depression)

40
Q

lab diagnosis for 1º hyper-PTH

A
  • Elevated serum Calcium and PTH
    D/D:
    Paraneoplastic syndrome (e.g., squamous cell cancer of the lung) and Renal cell carcinoma
    distinguishing factors: serum PTH levels will be low due to negative feedback
41
Q

what is the renal pathogenesis for secondary hyper-PTH

A

renal insufficiency –> Reduced α 1 hydroxylase –>
Reduced synthesis of active Vit D–> Reduced Calcium absorption in GIT - chronic hypocalcemia —> Parathyroid stimulation —>PTH

42
Q

describe the gross morphology of 2º hyperparathyroidism

A

glandular enlargement

43
Q

describe the microscopic morphology of 2º hyperparathyroidism

A

hyperplastic glands with increased water clear chief cells, fat decreased
Metastatic calcification in various tissues.
Vascular calcification – ischemic damage to skin and other organs.
Bone: as seen in primary hyperparathyroidism

44
Q

what are the 5 main lab dx. for 2º hyperparathyroidism

A

➢Hypocalcemia*
➢Hyperphosphatemia *
➢Increased PTH levels
➢Decreased Vit D
➢Increased ALP

45
Q

Disorder : Primary hyperparathyroidism
Serum calcium
Serum PTH
Serum phosphorus
Serum 1,25(OH)2

A

Increased
Increased
Decreased
Increased

46
Q

Disorder: secondary hyperparathyroidism (renal vit D. Def)
Serum calcium
Serum PTH
Serum phosphorus
Serum 1,25(OH)2

A

Decreased
Increased
Increased
Decreased

47
Q

Disorder: malignancy induced hypercalemia
Serum calcium
Serum PTH
Serum phosphorus
Serum 1,25(OH)2

A

Increased
Decreased
Normal
Decreased

48
Q

Disorder: hypoparathyroidism
Serum calcium
Serum PTH
Serum phosphorus
Serum 1,25(OH)2

A

decreased
decreased
increased
decreased

49
Q

what are 4 main causes for hypoparathyroidism

A
  • Acquired - inadvertent consequence of surgery of thyroid / neck dissection
    Autoimmune hypoparathyroidism- assc. w/ APS1
  • Autosomal-dominant hypoparathyroidism is caused by gain-of-function mutations in
    the calcium-sensing receptor (CASR) gene.
  • Congenital absence of parathyroid glands: Associated malformations like thymic aplasia and cardiovascular defects, or as a component of the 22q11 deletion syndrome – DiGeorge Syndrome
  • hypomagnesemia
50
Q

determine dx:
* Defective response in renal tubule to PTH ( PTH resistance)
* Due to defects in G protein receptor
Type IA ( Albrights hereditary osteodystrophy)
* May be associated with end organ resistance to TSH/ FSH/LH

A

Pseudohypoparathyroidism

51
Q

lab findings for pseudohypoparathyroidism

A
  • Increased PTH
  • Hypocalcemia
  • Hyperphosphatemia
  • increased Alkaline phosphatase
52
Q

what are to signs for neuromuscular irrirabilty

A
  • Chvostek sign: twitch of the facial muscles that occurs when gently tapping an
    individual’s cheek, in front of the ear
    Trousseau sign - carpopedal spasm
53
Q

ACUTE clinical features for hypo-PTH

A

Acute- surgical ablation
* neuromuscular irritability : tingling, muscle spasms, facial grimacing and sustained
carpopedal spasm (tetany)
- chvostek sign
- trousseau sign
- cardiac arrythmas
- increased ICP & seixures

54
Q

CHRONIC clinical features for hypo-PTH

A

Cataract, calcifications of the basal ganglia, dental abnormalities
* Mental status changes - emotional instability

55
Q

Disorder: pseudohypoparathyroidism
Serum calcium
Serum PTH
Serum phosphorus
Serum 1,25(OH)2

A

dec
inc
inc
inc

CAS 3 (10 decks)

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