Endocrine

parathyroid glands are small endocrine glands in the neck that produce parathyroid hormone Humans usually have four parathyroid glands, which are usually located on the rear surface of the thyroid gland, or, in rare cases, within the thyroid gland itself or in the chest. Parathyroid glands control the amount of calcium in the blood and within the bones.
Anatomy
The parathyroid glands are four or more small glands, about the size of a grain of rice, located on the posterior surface (back side) of the thyroid gland. The parathyroid glands usually weigh between 25mg and 40mg in humans. There are typically two, one above the other, on the left lobe of the thyroid and similarly on the right. The two parathyroid glands on each side which are positioned higher (closer to the head) are called the superior parathyroid glands, while the lower two are called the inferior parathyroid glands. Occasionally, some individuals may have six, eight, or even more parathyroid glands.
The parathyroid glands are named for their proximity to the thyroid but serve a completely different role than the thyroid gland. The parathyroid glands are quite easily recognizable from the thyroid as they have densely packed cells, in contrast with the follicle structure of the thyroid However, at surgery, they are harder to differentiate from the thyroid or fat.
In the histological sense, they distinguish themselves from the thyroid gland, as they contain two types of cells:
History
The parathyroid glands were first discovered in the Indian Rhinoceros by Richard Owen in 1850. The glands were first discovered in humans by Ivar Viktor Sandström (1852-1889), a Swedish medical student, in 1880. It is the last major organ to be recognized in humans so far.
Physiology
The major function of the parathyroid glands is to maintain the body's calcium level within a very narrow range, so that the nervous and muscular systems can function properly.
When blood calcium levels drop below a certain point, calcium-sensing receptors in the parathyroid gland are activated to release hormone into the blood.
Parathyroid hormone (PTH, also known as parathormone) is a small protein that takes part in the control of calcium and phosphate homeostasis as well as bone physiology. Parathyroid hormone has effects antagonistic to those of calcitonin. PTH increases blood calcium levels by stimulating osteoclasts to break down bone and release calcium. PTH also increases gastrointestinal calcium absorption by activating vitamin D, and promotes calcium conservation (reabsorption) by the kidneys. PTH affects the perception of well being and absence of PTH can be associated with feeling of fatigue and anxiety.

Hypercalcemia

1. Parathyroid related :
a. primary hyperparathyroidism 1. solitary adenoma 2.MEN 1,2
b. lithium therapy
c. F.H.H & Jansen's disease
2. Malignancy related
a. solid tumor with bone metastasis (Ca.breast)
b. = = =out = = ( paraneoplastic) like CA.lung
c. haematolytic tumor leukemia
lymphoma
3. Vitamin D related
a. intoxication
b. increase 1 α 25(OH)2 c.c in sarcoidosis & other granulomatous dis.
c. idiopathic hypercalcaemia of infancy
4. Associated with bone-turn over
a. hyperthyroidism
b. immobilization
c. thiazides
d. vitamin A intoxication
5. Associated with renal-failure
a. sever 2ndry hyperparathroidism
b. aluminum intoxication
c. milk-alkali syndrome


Hyperparathyroidism
Hyperparathyroidism is excessive production of parathyroid hormone (PTH) by the parathyroid glands.
Causes, incidence, and risk factors
The parathyroid glands are located in the neck, near or attached to the back side of the thyroid gland. They produce parathyroid hormone, which controls calcium, phosphorus, and vitamin D levels within the blood and bone.
When calcium levels are too low, the body responds by increasing production of parathyroid hormone. This increase in parathyroid hormone causes more calcium to be taken from the bone and more calcium to be reabsorbed by the intestines and kidney. When the calcium level returns to normal, parathyroid hormone production slows down.
There are two main types of hyperparathyroidism.
Primary hyperparathyroidism is caused by enlargement of one or more of the parathyroid glands. This leads to too much parathyroid hormone, which raises the level of calcium in the blood. The term "hyperparathyroidism" generally refers to primary hyperparathyroidism.
Secondary hyperparathyroidism is when the body produces extra parathyroid hormone because the calcium levels are too low. This is seen when vitamin D levels are low or when calcium is not absorbed from the intestines. Correcting the calcium level and the underlying problem will bring the parathyroid levels in the normal range.
If the parathyroid glands continue to produce too much parathyroid hormone even though the calcium level is back to normal, the condition is called "tertiary hyperthyroidism." It occurs especially in patients with kidney problems.

Symptoms

Back pain
Blurred vision (because of cataracts)
Bone pain or tenderness
Decreased height
Depression
Fatigue
Fractures of long bones
Increased urine output
Increased thirst
Itchy skin
Joint pain
Loss of appetite
Nausea
Muscle weakness and pain
Personality changes
Stupor and possibly coma
Upper abdominal pain


Signs and tests
Blood tests will be done to check for increased levels of parathyroid hormone (PTH), calcium, and alkaline phosphatase, and lower levels of phosphorus. A 24-hour urine collection test can help determine how much calcium is being removed from the body.
Bone x-rays and bone mineral density test can help detect bone loss, fractures, or bone softening.
X-rays, ultrasound, or CT scans of the kidneys or urinary tract may show calcium deposits or a blockage.

Treatment : If you have mildly increased calcium levels due to primary hyperparathyroidism and no symptoms, you may just need regular checkups with your doctor.
However, you need treatment if:
Your kidneys do not work correctly
You have calcium loss from your bones
Kidney stones develop
If treatment is needed, it may include:
Drinking more fluids to prevent the formation of kidney stones
Movement and exercise
Avoiding thiazide-type diuretics ("water pills")
Using estrogen therapy (for postmenopausal women)
If symptoms are present or your calcium level is very high, surgery may be needed to remove the parathyroid gland that is overproducing the hormone. Surgery is also recommended for patients less than 50 years of age.
Treatment for severe symptoms may also include:
Fluids given through a vein (IV)
Medications such as bisphosphonates and calcitonin, which bring down calcium levels quickly

prognosis

The outlook is good for those with mild symptoms. Most cases of primary hyperparathyroidism are mild.


Complications
Bone damage
Increased risk of fractures
Pancreatitis
Pseudogout
Urinary tract infection due to kidney stones and blockage , nephrocarcinocis and chronic renal failure
Peptic ulcer disease
CNS ostentation (confusion, drowsiness)

Hypocalcaemia 1. PHT absent : a. hereditary hypoparathyroidism

b. acquired =
c. hypomagnecemia
2. PTH ineffective : a. chronic renal failure
b. active vitamin D lacking : decrease dietary intake or
sun light
defective metabolism:
anticonvulsant
therapy, vitamin D
dependent rickets
ineffective intestinal
malabsorbtion of vit.D
PHP
3. PTH overwhelmed : a. sever acute hyperphosphatemia : tumor lysis
A.R.F
rhabdomyolysis
b. osteitis fibrosa after parathyroidectomy


Hypoparathyroidism is is an endocrine disorder in which the parathyroid glands in the neck do not produce enough parathyroid hormone (PTH).
Causes, incidence, and risk factors
The parathyroid glands help control calcium use and removal by the body. They do this by producing parathyroid hormone, or PTH. PTH helps control calcium, phosphorus, and vitamin D levels within the blood and bone.
Hypoparathyroidism occurs when the glands produce too little PTH. Blood calcium levels fall, and phosphorus levels rise.
The most common cause of hypoparathyroidism is injury to the parathyroid glands during head and neck surgery. Rarely, hypoparathyroidism is a side effect of radioactive iodine treatment for hyperthyroidism.
Hypoparathyroidism may also be caused by
Low blood magnesium levels
Metabolic alkalosis
DiGeorge syndrome is a childhood disease in which hypoparathyroidism occurs because all the parathyroid glands are missing at birth. Familial hypoparathyroidism occurs with other endocrine diseases, such as adrenal insufficiency, in a syndrome called type I polyglandular autoimmune syndrome (PGA I).
The risk factors for hypoparathyroidism include recent thyroid or neck surgery, a family history of parathyroid disorder, or certain autoimmune diseases such as Addison's disease.

Symptoms

Abdominal pain
Brittle nails
Cataracts
Dry hair
Dry, scaly skin
Muscle cramps
Muscle spasms called tetany (can affect the larynx, causing breathing difficulties)
Pain in the face, legs, and feet
Seizures
Tingling lips, fingers, and toes
Weakened tooth enamel (in children)
Additional symptoms may include:
Decreased consciousness
Delayed or absent tooth formation
Hand or foot spasms
Painful menstruation


Signs and tests
Blood tests will be done to check calcium, phosphorus, magnesium, and PTH levels. An ECG may show abnormal heart rhythms.
A urine test may be done to determine how much calcium is being removed from the body.
Chvosteks sign
Trousseaus sign
QT interval is prolonged

Treatment

The goal of treatment is to restore the calcium and mineral balance in the body.
Treatment involves calcium carbonate and vitamin D supplements, which usually must be taken for life. Blood levels are measured regularly to make sure that the dose is correct. A high-calcium, low-phosphorous diet is recommended.
Persons who have life-threatening attacks of low calcium levels or prolonged muscle contractions are given calcium through a vein (IV). Precautions are taken to prevent seizures or larynx spasms. The heart is monitored for abnormal rhythms until the person is stable. When the life-threatening attack has been controlled, treatment continues with medicine taken by mouth.

prognosis

The outcome is likely to be good if the diagnosis is made early. However, changes in the teeth, the development of cataracts, and brain calcifications are irreversible.

Complications

Hypoparathyroidism in children may lead to stunted growth, malformed teeth, and slow mental development.
Overtreatment with vitamin D and calcium can cause hypercalcemia (high blood calcium) and may sometimes interfere with kidney function.
Hypoparathyroidism increases your risk of pernicious anemia, Addison's disease, cataracts, and Parkinson's disease.

Pseudohypoparathyroidism is a genetic disorder that is similar to hypoparathyroidism, but which results from the body's lack of response to parathyroid hormone rather than decreased production of the substance.
Causes, incidence, and risk factors
The parathyroid glands help control calcium use and removal by the body. They do this by producing parathyroid hormone, or PTH. PTH helps control calcium, phosphorus, and vitamin D levels within the blood and bone.
Persons with pseudohypoparathyroidism produce the right amount of PTH, but the body is "resistant" to its effect. This causes low blood calcium levels and high blood phosphate levels.
Pseudohypoparathyroidism is caused by abnormal genes. All forms of pseudohypoparathyroidism are very rare.
Type Ia is inherited in an autosomal dominant manner. That means only one parent needs to pass you the defective gene in order for you to develop the condition. The condition causes short stature, round face, and short hand bones, and is also called Albright's hereditary osteodystrophy.
Type Ib involves resistance to PTH only in the kidneys. Type Ib is less understood than type Ia. Type II is very similar to type I in its clinical features, but the events that take place in the kidneys are different.
Type II pseudohypoparathyroidism also involves low blood calcium and high blood phosphate levels, but persons with this form do not develop the physical characteristics seen in those with Type Ia.
All forms of pseudohypoparathyroidism are very rare.


Symptoms
Symptoms are related to low levels of calcium and include:
Cataracts
Dental problems
Numbness
Seizures
Tetany (a collection of symptoms including muscle twitches and hand and foot spasms)
Persons with Albright's hereditary osteodystrophy may have the following symptoms:
Calcium deposits under the skin
Dimples that can replace knuckles on affected fingers
Round face and short neck
Short hand bones, especially the bone below the 4th finger
Short stature

Signs and tests

Blood tests will be done to check calcium, phosphorus, and PTH levels. Urine tests may also be done.
Other tests may involve:
Genetic testing
Head MRI or CT scan of the brain

Treatment

Calcium and vitamin D supplements are prescribed to maintain proper calcium levels. If blood phosphate levels remain high, a low-phosphorus diet or medicines called phosphate binders (such as calcium carbonate or calcium acetate) may be necessary.


prognosis
Low blood calcium in pseudohypoparathyroidism is usually milder than in other forms of hypoparathyroidism.

Complications

Patients with type Ia pseudohypoparathyroidism have an increased rate of other endocrine abnormalities (such as hypothyroidism and hypogonadism.
Complications of hypocalcemia associated with pseudohypoparathyroidism may include seizures and other endocrine problems, leading to lowered sexual drive and lowered sexual development, lowered energy levels, and increased weight.

Pseudopseudohypoparathyroidism (pseudoPHP) is an inherited disorder, named for its similarity to pseudohypoparathyroidism in presentation. The term pseudopseudohypoparathyroidism is used to describe a condition where the individual has the phenotypic appearance of pseudohypoparathyroidism type 1a, but is biochemically normal.
presentation
Hormone resistance is not present in pseudopseudohypoparathyroidism. Short stature may be present. Obesity is less common in pseudopseudohypoparathyroidism than in pseudohypoparathyroidism. Osteoma cutis may be present.

Condition

Appearance
Calcium
PTH levels
Imprinting
Hypoparathyroidism
Skeletal defects
Low

Low

Not applicable
Pseudohypoparathyroidism 1A
• Skeletal defects


low
Normal
Gene defect from mother
Pseudopseudohypoparathyroidism
• Skeletal defects

Normal

Normal
Gene defect from father

Inheritance

A mother who has inherited pseudopseudohypoparathyroidism from her father may in turn pass along pseudohypoparathyroidism 1A to her children as the imprinting pattern on the inherited paternal chomosome will be changed to the maternal pattern in the mother's ovum during meiosis.
Pseudopseudohypoparathyroidism and pseudohypoparathyroidism both involve the same GNAS gene, but pseudopseudohypoparathyroidism has normal calcium homeostasis because of the normal maternal allele in the kidney.