Endocrinology Flashcards
Maintenance of calcium, phosphate and magnesium homeostasis is
under the influence of two polypeptide hormones;
• Parathyroid hormone(PTH), and
• Calcitonin (CT),
.1,25 dihydroxy cholecalciferol (sterol hormone)
The PTH acts directly on
And indirectly on
bones and kidneys
the intestine through its effect on the synthesis of 1,25 (OH) 2 D 3.
PTH production is regulated by
concentration of serum ionized
calcium.
Lowering of the serum calcium levels will induce
increased rate of
parathyroid hormone secretion
Primary hyperparathyroidism is due to
excessive production of PTH by
one or more of hyperfunctioning parathyroid glands.
excessive production of PTH leads to
hypercalcemia which fails to inhibit the gland activity in
the normal manner.
The two major sites of potential complications of primary hyper parathyroidism are the
Bones
Kidneys
The kidneys in primary hyper parathyroidism
may have renal stones (nephrolithiasis) or diffuse
deposition of calcium- phosphate complexes in the parachyma
(nephrocalcinosis)
Nowadays complications in kidney
are seen less commonly and around
20% of patients or less show such complications
Clinical Features of primary hyperthyroidism
• Muscle weakness • Easy fatigability • Peptic ulcer disease • Pancreatitis • Hypertension • Gout and pseudogout • Anemia • Depression
Diagnosis of primary hyperthyroidism
The presence of established hypercalcaemia in more than one serum
measurement accompanied by elevated immunoreactive PTH is
characteristic (iPTH)
Pre-operative localization of the abnormal parathyroid gland(s):
Ultrasonography • MRI • CT • Thallium 201 – Tehcnichum 99m scan (subtraction study)
Secondary hyperparathyroidism
An increase in PTH secretion which is adaptive and unrelated to
intrinsic disease of the parathyroid glands
Secondary hyperparathyroidism is due to
chronic stimulation of the parathyroid glands by a
chronic decrease in the ionic calcium level in the blood
Major causes of chronic hypocalcemia other than hypoparathyroidism
• Dietary deficiency of vitamin D or calcium
• Decreased intestinal absorption of vitamin D or calcium due to
primary small bowel disease,
• Short bowel syndrome, and
• Post-gastrectomy syndrome.
• Drugs that cause rickets or osteomalacia
• States of tissue resistance to vitamin D • Excessive intake of inorganic phosphate compunds • Pseudohypoparathyroidism • Severe hypomagnesemia • Chronic renal failure
Drugs that cause rickets or osteomalacia
such as phenytoin,
phenobarbital, cholestyramine, and laxative.
Hypoparathyroidism
Deficient secretion of PTH
Hypoparathyroidism manifests itself biochemically by
hypocalcemia, • Hyperphospatemia • Diminished or absent circulating iPTH and • Clinically the symptoms of neuromuscular hyperactivity.
Hypoparathyroidism
Causes:
Surgical hypoparathyroidism (most common)
Idiopathic hypoparathyroidism
Functional hypoparathyroidism
Surgical hypoparathyroidism
the removal of the parathyroid glands or due to
interruption of blood supply to the glands.
After anterior neck exploration (for thyroidectomy, abnormal parathyroid gland removal, excision of a neck lesion.)
Idiopathic hypoparathyroidism A form occuring at .. with … mode of transmission
early age (genetic origin) with autosomal
recessive mode of transmission
Examples of Idiopathic hypoparathyroidism
multiple endocrine deficiency –
autoimmune-candidiasis (MEDAC) syndrome” “Juvenile familial endocrinopathy” “Hypoparathyroidism – Addisson’s disease – mucocutaneous
candidiasis (HAM) syndrome”
In genetic origin Idiopathic hypoparathyroidism Circulating antibodies for … are
frequently present.
the parathyroid glands and the adrenals
Other associated diseases with genetic origin hypoparathyroidism
Pernicious anemia Ovarian failure Autoimmune thyroiditis Diabetes mellitus
The late onset form of Idiopathic hypoparathyroidism occurs
sporadically without circulating glandular
autoantibodies.
Functional hypoparathyroidism occurs in patients who
has chronic hypomagnesaemia of various causes.
Magnesium is necessary for
PTH release from the glands and also
for the peripheral action of the PTH.
Hypoparathyroidism Clinical Features
Neuromuscular
Other clinical manifestation
Neuromuscular clinical features
Parathesia
Tetany
Hyperventilation
Adrenergic symptoms
Convulsion
Signs of latent tetany
Convulsion تشنج
More common in
Takes the forms of
More common in young people and it can take the form of either
generalized tetany followed by prolonged tonic spasms or the typical epileptiform
seizures.
Signs of latent tetany
o Chvostek sign
o Trousseau sign
o Extrapyramidal signs (due to basal ganglia calcification)
B.Other clinical manifestation of hypoparathyroidism
• 1.Posterio lenticular cataract • 2.Cardiac manifestation 3.Dental Manifestation 4.Malabsorption syndrome
Cardiac manifestation of hypoparathyroidism
Prolonged QT interval in the ECG Resistance to digitalis Hypotension Refractory heart failure with cardiomegally can occur.
3.Dental Manifestation of hypoparathyroidism
Abnormal enamel formation with delayed or absent dental eruption
and defective dental root formation.
4.Malabsorption syndrome
Presumably secondary to decreased calcium level and may lead to
steatorrhoea with long standing untreated disease.
Diagnosis of hypoparathyroidism
In the absence of renal failure the presence of hypocalcaemia with
hyperphosphataemia is virtually diagnostic of hypoparathyroidism. •
… confirms the diagnosis or it can be
detectable if the assay is very sensitive.
Undetectable serum iPTH
Pseudohypoparathysoidism and Pseudopseudohypoparathyroidism rare familial disorders with target tissue resistance to
PTH
Pseudohypoparathysoidism and Pseudopseudohypoparathyroidism
hypocalcaemia, hyperphosphataemia, with increased
parathyroid gland function
Clinical symptoms of Pseudohypoparathysoidism and Pseudopseudohypoparathyroidism
variety of congenital defects in the growth and
development of skeleton
Ex: Albright Hereditary
Osteodystrophy):
Albright Hereditary
Osteodystrophy):
Short statue Short metacarpal and metatarsal bones
In pseudopseudohypoparathyroidism they have
developmental
defects without the biochemical abnormalities
The diagnosis is established when
low serum calcium level with
hyperphosphataemia is associated with increased serum iPTH
Diminished nephrogenous and • Phosphature response to PTH administration
