endocrine-parathyroid Flashcards
Location of parathyroid gland
variably located at the back of thyroid gland
Where do parathyroid glands come from?
pharyngeal pouch
Weight of each gland?
35-40mg
What does each gland comprise of?
chief cells-secrete PTH
oxyphil cells
What are the effects of PTH secretion?
Essentially decreased levels of calcium stimulate PTH hormone and cause
• Increase in renal tubular reabsorption of calcium
• Increase in urinary phosphate excretion, thereby lowering serum phosphate levels (since phosphate binds to ionized calcium)
• Increase in the conversion of vitamin D to its active dihydroxy form (1,25 dihydroxy vit D) in the kidneys, which in turn augments
gastrointestinal calcium absorption
• Enhancement of osteoclastic activity (i.e., bone resorption, thus releasing ionized calcium), mediated indirectly by promoting the differentiation of osteoclast
progenitor cells into mature osteoclasts
What is another name for 1,25 dihydroxyvitamin D?
calcitriol
What are the steps to make calcitriol?
Vitamin D is converted to calcidiol in the liver and then calcitriol in the kidney
Calcidiol acts on kidney and causes calcium reabsorption
Caltitriol acts on SI reabsorption of dietary calcium
Classify hyperparathyroidism
Primary
Secondary
Tertiary
Describe causes of primary hyperparathyroidism
•Primary (overproduction of PTH)
•Important cause of hypercalcaemia
1.Adenoma: 75-80%
Solitary, 0.5-5grm, well circumscribed, delicate capsule, other glands normal size / shrunken
2.Primary hyperplasia: 10-15%
Diffuse or nodular
Occur sporadically or as a component of MEN syndromes
3.Parathyroid carcinoma: <5%
Diagnosis made on invasion of surrounding tissue and metastasis
Describe secondary hyperparathyroidism
Any condition associated with a chronic decreased level of calcium leading to compensatory over activity of the parathyroid gland
Most common cause – renal failure
Chronic renal insufficiency -> ↓PO4 excretion -> hyperphosphataemia -> depress Ca levels -> stimulates parathyroid gland activity (hyperplasia of parathyroid glands) -> increased PTH secretion -> serum calcium remains near normal.
Another: Vit D deficiency
Describe tertiary hyperparathyroidism
In a minority of patients, parathyroid activity becomes autonomous and excessive with resultant hypercalcaemia. Hyperplasia of glands due to chronic secondary hyperparathyroidism
- Can be treated with parathyroidectomy.
What are the symptoms of hypercalcaemia?
painful bones, renal stones, abdominal groans, psychic moans
osteoporosis , osteitis fibrosis cystica
renal stones; renal insufficiency; polyuria
naseau,vomiting,constipation, PUD, pancreatitis, anorexia
weakness and fatigue
altered concentration, depression, confusion, seizures
mitral and aortic calcifications, heart block, hypertension ;
(Cardiac manifestations)
What treatment and investigation can be done for parathyroidism?
Lithium treatment, thiazide diuretics
imaging- U/S and sestamibi scan
Sestamibi allows intraop Gamma probe confirmation ; 91% specific
What is the epidemiology a/w hyperpaprathyroidism?
occurs in females more
1:1000 prevalence
What are the causes of hypoparathyroidism
•Surgical removal (inadvertently) during thyroidectomy – mistaken for lymph nodes
•Congenital absence (DiGeorge syndrome – along with thymic aplasia)
•Primary idiopathic atrophy (autoimmune) – antibodies against the Ca sensing receptors in parathyroid gland
•Familial hypoparathyroidism
–Condition presents in childhood
Signs of hypocalcaemia
–Numbness and tingling in the extremities and perioral region
–Muscle cramps
-Bronchospasm/laryngospasm/seizures
–Chvostek’s sign (muscle spasms of mouth/eye/nose with tapping of the facial nerve)
–Trousseau’s sign (carpal spasm with inflation of sphygmomanometer 20mmHg above systolic pressure)
–Cataract formation (calcification of lens)
–Intra-cranial manifestations (parkinsonian like movement)
–Cardiovascular manifestations – conduction defect with prolonged QT interval
Define MEN syndrome
familial diseases (AD) that are a/w hyperplasia and neoplasia of several endocrine organs
Type 1 (Werners syndrome) Type 2 A & 2 B
What is the most common manifestation for Werners syndrome?
What organs does it commonly affect?
primary hyperparathyroidism
3P’s
- pancreatic islet cells
- parathyroid gland
- pituitary
What is the genetic defect a/w Werners
TSG (MEN gene1) located chromosome 11q13
Explain type 2
two distinct groups (a&b) that have mutations in RET proto oncogenes located on chromosome 10q11.2
What is another name for type 2A and what is the outcome?
Sipple syndrome
medullary carcinoma
phaeochromocytoma
parathyroid hyperplasia
Explain what Type 2B is characterized by
medullary carcinoma phaeochromocytoma extraendocrine manifestations: -ganglioneuromas at mucosal sites -marfanoid habitus- long bones of axial skeleton
Is type 2B a/w primary hyperparathyroidism?
NO
General characteristics of MEN syndrome
- tumors occur at a younger age than compared w sporadic
- occurs in multiple endocrine organs
- multifocal
- tumors preceeded by an asymptomatic period of endocrine hyperplasia
- agressive and higher rate of recurrence than in sporadic tumors
