Parathyroid gland REVISION NOTES

Parathyroid gland
TONY SCARIA 2010 KMC

Normal calcium metabolism

• Normal calcium level in the body
• Normal serum Ca = 9 – 11 mg%,
• Ionized Ca = 50%,
• Ca bound to protein = 40%,
• Ca bound to anions - 10%

ALP is raised in conditions a/w increased
osteoblastic activity
Raised ALP (d/t osteoblastic activity) ALP is normal in
• Paget disease,
• Bone metastases,
• Rickets, osteomalacia*,
• osteoporosis and
• multiple myeloma

Action of PTH
• ↑osteoclast activity releasing Ca2+ & phosphate from bones
• ↑Ca2+ & ↓phosphate reabsorption in the kidney;
• ↑Active 1,25 dihydroxy-vitamin D3 production

Primary hyperparathyroidism Secondary hyperparathyroidism Tertiary hyperparathyroidism
• Autonomous secretion of PTH,
usually by a single parathyroid
adenoma
• physiological increase in PTH
secretion to compensate for
prolonged hypocalcaemia (such
as in vitamin D deficiency)
continuous stimulation of the
parathyroids over a prolonged
period of time
adenoma formation and
autonomous PTH secretion

Types of hyperparathyroidism

Primary hyperparathyroidism

Primary hyperparathyroidism
• ↑Ca, ↓PO4, ↑PTH
• The most common cause of primary hyperparathyroidism is
parathyroid solitary adenoma.
• A single solitary abnormal gland is the cause of approximately 80% of patients
• Adenomas are most often located in the inferior parathyroid gland.
• Chief cells are predominant in both hyperplasia and adenoma.
• The abnormality of the gland is usually a benign neoplasm or adenoma and
rarely a parathyroid carcinoma.

Types of primary hyperparathyroidism
Sporadic Familial
Most common type Less common
• Cyclin D1 gene inversions leading to
overexpression of cyclin D1
• MEN1 mutations
• Multiple Endocrine Neoplasia, type 1 (MEN1 gene
on chromosome 11
• Multiple Endocrine Neoplasia, type 2(RET gene on
chromosome 10
• familial hypocalciuric hypercalcemia  autosomal
dominant disorder caused by loss-of-function
mutations in the parathyroid calcium-sensing
receptor gene (CASR), which results in decreased
sensitivity to extracellular calcium

CF
• bones, stones and abdominal groans
• PTH-induced hypercalcemia favors formation of urinary tract stones
(nephrolithiasis) as well as calcifcation of the renal interstitium
and tubules (nephrocalcinosis)

Brown tumour in primary
hyperparathyroidism
• Osteitis fibrosa cystica
• Bone loss predisposes to microfractures and secondary
hemorrhages that elicit an inﬂux of macrophages and an
ingrowth of reparative fibrous tissue, creating a mass
of reactive tissue, known as a brown tumor

Brown tumour

Generalised generalized osteitis fbrosa cystica (von
Recklinghausen disease of bone)

• d/t raised PTH
• Increased osteoclastic activity ↑ca2+
• Increased osteoblastic activity ↑ ALP
• ↓PO4

Radiological features of primary
hyperparathyroidism
• Irregular diffuse rarefaction of bone
• Salt & pepper appearance of skull
• Subperiosteal resorption of phalanges
• Multiple cyst in pelvis & other bones
• Brown tumour

Salt & pepper appearance of skull

Loss of lamina dura

Subperiosteal resorption of phalanges

Multiple cyst in pelvis & other bones

Brown tumour in hyperparathyroidism

Cod fish spine
Intervertebral disk becomes
ballooned as they indent soft
vertebral bodies forming the
'Cod Fish spine

To localise adenoma
• 99_Tc sestamibi scan.
• After one hour of injection, uptake is done by both thyroid and parathyroid
gland.
• After 3 hrs uptake evidence is there only in parathyroid. So by computer
subtraction adenoma is located.

Indications for surgical removal of adenoma
• individuals aged less than 50 years,
• with clear-cut symptoms or documented complications (such as
peptic ulceration, renal stones, renal impairment or osteoporosis),
• (in asymptomatic patients) signifcant hypercalcaemia (corrected
serum calcium > 2.85 mmol/L (> 11.4 mg/dL))

Secondary hyperparathyroidism

Causes of secondary hyperparathyroidism
• chronic renal failure  MC cause
• Low vitamin D intake,
• Rickets,
• osteomalacia,
• malabsorption

CKD
Decrease in GFR
Increased phosphate
load in blood
Defective conversion of 25hydroxyvitamin D
to its active metabolite,1,25-
dihydroxyvitamin D,
• due in part to renal tubular cell damage
• elevated FGF23 levels
hypocalcaemia
increased PTH production by the parathyroid glands
Elevated FGF23
The FGF23 promotes
phosphate excretion,
thereby compensating in
part for the reduced
glomerular fltration of
phosphate.

• Rugger Jersey spine is
seen in CRF
• d/t 2*
hyperparathyroidism

Secondary hyperparathyroidism
• In CRF
• Ca2+↓
• PTH↑
• ↑PO4
• In malnutrition, ricket osteomalacia
• Ca↓
• PTH ↑
• ↓ PO4

TERTIARY HYPERPARATHYROIDISM
• Occurs after prolonged secondary hyperparathyroidism, causing
glands to act autonomously having undergone hyperplastic or
adenomatous change.
• This causes Ca2+ from secretion of PTH unlimited by feedback
control. Seen in chronic renal failure.

TERTIARY HYPERPARATHYROIDISM
• Ca2+↑,
• PTH↑
• ↓PO4

Malignant hyperparathyroidism
• Hypercalcemia in malignancy occur due to increase level of PTHrp. In
this PTH level are not raised
• Parathyroid-related protein (PTHrp)
• squamous cell lung cancers,
• breast
• renal cell carcinomas

CF of hyperparathyroidism
• Most of them are asymptomatic
General Renal Skeletal GIT Cardiovascular
• Fatigue
• Mental
confusion
(Psychic
moans)
• Polyuria
• nocturia
• Renal colic
from
stones(abdo
minal
groan)
• Bone pain
• Bone cysts
• Brown
tumor
• Anorexia
• Nausea
• Vomiting
• Peptic
ulceration
(abdominal
groan)
• HTN
• Short QT
interval

Calciphylaxis
metastatic calcification of blood
vessel
(secondary to
hyperphosphatemia) may lead to
ischemia damage
to skin & other organs.

Nephrogenic DI in hypercalcemia
• Polyuria results from effect of hypercalcemia on renal tubules
reducing their concentrating ability, a form of nephrogenic diabetes
insipidus

Hypercalcemia

Causes of hypercalcemia

• Lithium may cause hyperparathyroidism by reducing the sensitivity of
the calcium-sensing receptor (CaSR)

CF
• Mild
• Asymptomatic
• vague neuropsychiatric symptoms
• Trouble concentrating, personality changes, or depression
• peptic ulcer disease
• Nephrolithiasis
• nausea, anorexia, constipation, or pancreatitis
• NEPHROGENIC DI
• POLYURIA POLYDYPSIA
• electrocardiographic changes
• bradycardia, AV block, and short QT intervalTONY SCARIA 2010 KMC

Mx of A/C hypercalcemia
Mild hypercalcemia • Adequate hydration
Severe hypercalcemia (13-15mg/dl) • IV 0.9% saline 2–4 L/day
• use of loop diuretics to enhance sodium and
calcium excretion
• Zoledronic acid 4 mg IV or pamidronate 60–90 mg
IV
• IM/SC calcitonin 100 U 3 times daily for frst 24–48
hours in life-threatening hypercalcaemia

Management of c/c hypercalcemia
• Bisphosphonates
• Glucocorticoids :
• Effective in particular situations such as Vitamin D intoxication, Sarcoidosis,
Malignancy
• Calcitonin
• Phosphate*:
• 5. *Dialysis* - Quick and effective and is likely to be needed in
• severe cases with renal failure
• 6. *Plicamycin*
• 7. *Gallium Nitrate*

Cinacalcet
• Cinacalcet
• calcimimetic which enhances
the sensitivity of the calcium-
sensing receptor, so reducing
PTH levels, and is licensed for
tertiary hyperparathyroidism
and as a treatment for patients
with primary
hyperparathyroidism who are
unwilling to have surgery or are
medically unft

Familial hypocalciuric hypercalcemia
• AD
• Loss of function mutation of CaSR gene resulting in decreased
sensitivity to extracellular calcium  increased PTH secretion 
increased renal absorption of ca2+

Hypoparathyroidism

Primary (due to gland
failure)
Secondary Pseudohypoparathyroidism Pseudopseudohypoparathyr
oidism
• Infantile
hypoparathyroidism: It is
associated with thymic
aplasia (Di George
syndrome)
• Idiopathic (Autoimmune)
(associated with other
autoimmune disorders),
• Post operative : surgery
(thyroidectomy).
• Post radio iodine therapy
• Hypomagnesemia – (Mg
is required for PTH
secretion)
It is a group of disorders
characterized by
hypocalcemia due to renal
resistance to PTH.
PTH levels are high.
Various phenotypic
abnormalities may be
associated—classically,
short stature, round face,
obesity, short fourth
metacarpals,ectopic bone
formation, and mental
retardation. *Cataract*.
Treatment is same as for
primary
Patients without
hypocalcemia but sharing
the phenotypic
abnormalities (as of
pseudohypoparathyroidism).
These patient have normal
serum calcium and high
serum PTH. In
pseudohypoparathyroidism,
defect lies at PTH receptor
level. While in pseudo
pseudohypoparathyroidism
defect lies at gene
transcription level beyond
the PTH receptors.

Alberts hereditary osteodystrophy

Albert hereditary osteodystrophy
• short stature,
• round face,
• obesity,
• short fourth metacarpals,
• ectopic bone formation,
• mental retardation
• Cataract

• AHO occurs in both
pseudohypoparathyroidism type Ia
& also in
pseudopseudohypoparathroidism

• females affected by either PHP-Ia or PPHP will have offspring with
PHP-Ia, if these children inherit the allele carrying the GNAS
mutation; in contrast, if the mutant allele is inherited from a male
affected by either disorder, the offspring will exhibit PPHP

PHP Ia PPHPP PHP Ib PHP II
• hypocalcemia due to
renal resistance to PTH.
• PTH levels are high.
• normal serum calcium
and high serum PTH
hypocalcemia and
hyperphosphatemia
Elevated serum PTH
• Epigenetic mutation in
Gsα allele from mother
• Epigenetic mutation in
Gsα allele from father
• there is reduced
synthesis of cAMP in
response to PTH so
there is no appropriate
increase in the urinary
cAMP occurs
• there is increased
synthesis of cAMP in
response to PTH so
there is increase in the
urinary cAMP occurs
Decreased cAMP release Normal cAMP in urine
• Albert hereditary
osteodystrophy
• Albert hereditary
osteodystrophy

• Pseudopseudohypoparathyroidism (PPHP)
• Patients without hypocalcemia but sharing the phenotypic abnormalities (as
of pseudo hypoparathyroidism)
• Serum PTH is normal
• Serum Ca2+ PO4 is normal

Hypocalcemia

Chvostek’s sign
Chvostek’s sign (twitching of the circumoral
muscles in response to gentle tapping of the facial nerve just
anterior
to the ear)

Carpal spasm may be induced by inflation of a blood
pressure cuff to 20 mmHg above the patient’s systolic blood
pressure for 3 min (Trousseau’s sign)

Tetany
• Increase excitability of peripheral nerve due either to a low serum
calcium or low serum magnesium or alkalosis
Low serum Ca2+ Low serum Mg2+ Alkalosis
• Malabsorption
• Osteomalacia
• Hypoparathyroidism
• Acute pancreatitis
• Repeated vomiting
• Hyperventilation
• Primary
hyperaldosteronism

• In CRF, Hypocalcemia is a feature but tetany does not occurs due to
acidosis which prevents tetany

• In children
• Carpopedal spasm
• Stridor
• Convulsions.
• In adults
• Tingling sensation in the hands,
feet and around the mouth.
• Carpopedal spasm (Main
d’accoucheur position)

• Latent tetany signs are
• 1. Trousseau’s sign
• 2. Chvostek sign

• Treatment of tetany
• Injection calcium gluconate I/V
• In case of persistent vomiting – I/V saline
• In hyperventilation – Re breath from same bag

Magnesium

• Normal serum magnesium = 1.5 to 2.3 mg

• Magnesium is required for PTH secretion and for PTH action

• Serum Ca and Serum Mg level always go parallel in the body.
• The notable exceptions
• CRF (Hypocalcemia and Hypermagnesemia),
• Gitelman syndome (Normocalcemia and hypomagnesemia)

• Causes of hypomagnesemia
• 1. Reduce intake especially common in alcoholic patient and on TPN
• 2. GI losses - chronic diarrhea
• 3. Kidney loss – diuretics, Gitelman syndrome.
• 4. Acute pancreatitis
• 5. Drugs - Foscarnet (It is an anti herpes group of drug used generall in zoster
ophthalmitis).

Rx
• Magnesium supplement

Hypermagnesemia

Causes
• 1. ARF, CRF
• 2. Addison disease
• 3. Magnesium containing drugs.
• 4. Hemolysis

CF
• Occur due to vasodilatation and neuromuscular blockage.
• There is paradoxical Bradycardia, Hypotension, Altered sensorium,
respiratory depression

• Treatment:
• 1. Injection calcium gluconate for heart
• 2. Diuretics (Frusemide)
• 3. Dialysis

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