The document discusses the benefits of exercise for mental health. Regular physical activity can help reduce anxiety and depression and improve mood and cognitive functioning. Exercise causes chemical changes in the brain that may help protect against mental illness and improve symptoms.

1. HARMANDEEP KAUR
Roll No.-18/2011

2. •The parathyroid glands are two pairs of glands
positioned behind the outer wings of
the thyroid I.e posterolateral aspect.
•There are typically four parathyroid glands.
• The two parathyroid glands on each side
which are positioned higher are called the
superior parathyroid glands, while the lower
two are called the inferior parathyroid glands.
•The parathyroid glands usually weigh between
25 mg and 40 mg in humans.

4.  The blood supply, drainage, and lymphatic
drainage of the parathyroid glands are
equivalent to the thyroid gland.
 The superior parathyroid glands receive their
blood from the superior thyroid arteries, which
are direct branches from the common carotid
arteries.
 The inferior parathyroid glands receive a variable
blood supply, from either the ascending branch
of the inferior thyroid arteries or the thyroid ima
artery. The inferior thyroid artery arises from
the subclavian arteries.

5.  The parathyroid artery drains into the
superior and, middle and inferior thyroid
veins.
 The superior and middle veins drain into
thejugular vein and the inferior thyroid
vein drains into the brachiocephalic
veins.

7.  The major function of the parathyroid glands
is to maintain the
body's calcium and phosphate levels within a
very narrow range, so that
the nervous and muscular system can function
properly. The parathyroid glands do this by
secreting parathyroid hormone.
 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.

8.  Calcium- 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.
 Phosphate - PTH is the major regulator of
serum phosphate concentrations via
actions on the kidney. It is an inhibitor of
proximal tubular reabsorption of
phosphorus. Through activation of Vitamin
D the absorption of Phosphate is increased.

9.  Regulation of serum calcium
 Parathyroid hormone regulates serum
calcium through its effects on the following
tissues.

11.  Regulation of serum phosphate PTH
reduces the reabsorption
of phosphate from the proximal tubule of
the kidney, which means more phosphate
is excreted through the urine.
 However, PTH enhances the uptake of
phosphate from the intestine and bones
into the blood.
 In the bone, slightly more calcium than
phosphate is released from the
breakdown of bone.

12.  In the intestines, absorption of both
calcium and phosphate is mediated by an
increase in activated vitamin D. The
absorption of phosphate is not as
dependent on vitamin D as is that of
calcium. The end result of PTH release is a
small net drop in the serum concentration
of phosphate.
 Vitamin D synthesis
 PTH increases the activity of 1-α-
hydroxylase enzyme, which converts 25-
hydroxycholecalciferol to 1,25-
dihydroxycholecalciferol, the active form
of vitamin D.

14.  Parathyroid disease is conventionally
divided into states where the
parathyroid is over active
(hyperparathyroidism), and states where
the parathyroid is underactive
(hypoparathyroidism).
 Both states are characterised by their
symptoms, which relate to the excess or
deficiency of parathyroid hormone

15.  Excessive PTH secretion may be due to
problems in the glands themselves, in
which case it is referred to
as primary hyperparathyroidism and which
leads to hypercalcaemia (raised calcium
levels).
 It may also occur in response to low
calcium levels, as encountered in various
situations such as vitamin D
deficiency or chronic kidney disease; this is
referred to
as secondary hyperparathyroidism. In all
cases, the raised PTH levels are harmful
to bone,

16.  Primary
hyperparathyroidism causes hypercalce
mia
(elevated blood calcium levels) through
the excessive secretion of parathyroid
hormone (PTH), usually by
an adenoma (benign tumors) of
the parathyroid glands.

17. I. Parathyroid-related
 Primary hyperparathyroidism Adenoma(s) Multiple
endocrine neoplasia Carcinoma
 Lithium therapy
 Familial hypocalciuric hypercalcemia
II. Malignancy-related
 Solid tumor with metastases (breast)
 Solid tumor with humoral mediation of hypercalcemia
(lung, kidney)
 Hematologicmalignancies (multiple myeloma,
lymphoma, leukemia)
III. Vitamin D—related
 Vitamin D intoxication
 1,25(OH)2D; sarcoidosis and other granulomatous
diseases
 Idiopathic hypercalcemia of infancy

18. IV. Associated with high bone turnover
 Hyperthyroidism
 Immobilization
 Thiazides
 Vitamin Aintoxication
V. Associated with renal failure
 Severe secondary hyperparathyroidism
 Aluminum intoxication
 Milk-alkali syndrome

19.  The signs and symptoms of primary
hyperparathyroidism are those of
hypercalcemia. They are classically
summarized by the mnemonic "stones,
bones, abdominal groans and psychiatric
moans".
 "Stones" refers to kidney
stones, nephrocalcinosis, and diabetes
insipidus (polyuria and polydipsia). These
can ultimately lead to renal failure.

20.  "Bones" refers to bone-related
complications. The classic bone disease in
hyperparathyroidism is osteitis fibrosa
cystica, which results in pain and sometimes
pathological fractures. Other bone diseases
associated with hyperparathyroidism
are osteoporosis, osteomalacia, and arthritis.
 "Abdominal groans" refers to
gastrointestinal symptoms
of constipation, indigestion, nausea and vomiti
ng.
 Hypercalcemia can lead to peptic
ulcers and acute pancreatitis. The peptic
ulcers can be an effect of increased gastric
acid secretion by hypercalcemia,[4] but may
also be part of a multiple endocrine neoplasia
type 1 syndrome of both hyperparathyroid
neoplasia and a gastrinoma.

21.  "Psychiatric moans" refers to effects on
the central nervous system. Symptoms
include lethargy, fatigue,
depression, memory loss, psychosis, ataxia,
delirium, and coma.
 "Thrones" refers to polyuria and
constipation.
 Left ventricular hypertrophy.
 Increased all-cause mortality
 Other signs include proximal muscle
weakness, itching, and band keratopathy of
the eyes.

22.  The diagnosis of primary
hyperparathyroidism is made by blood
tests.
 Serum calcium levels are elevated,
and the parathyroid hormone level is
abnormally high compared with an
expected low level in response to the
high calcium.

23.  Complications
 The classic bone disease in
hyperparathyroidism is osteitis fibrosa
cystica, which results in pain and
sometimes pathological fractures. Other
bone diseases associated with
hyperparathyroidism
are osteoporosis, osteomalacia,
and arthritis.

26. 
Treatment is usually surgical removal of
the gland(s) containing adenomas.

27. Guidelines for Surgery in Asymptomatic Primary
Hyperparathyroidism
Parameter Guideline
Serum calcium (above normal) >1 mg/dL
24-h urinary Ca No indication
Creatinine clearance
(calculated)
If <60 mL/min
Bone density T score <–2.5 at Any of 3 sitesb
Age <50

28. Guidelines for Monitoring in Asymptomatic Primary
Hyperparathyroidism
Parameter Guideline
Serum calcium Annually
24-h urinary calcium Not recommended
Creatinine clearance Not recommended
Serum creatinine Annually
Bone density Annually (3 sites)

29.  MEN I: parathyroid, pancreatic (Zollinger
Ellison), pituitary (prolactinoma)
tumor suppressor MENI gene, autosomal
dominant inheritance
 MEN 2A: parathyroid, pheochromocytoma,
medullary thyroid cancer
RET proto-oncogene, autosomal dominant
inheritance
 Familial Hypocalciuric Hypercalcemia:
autosomal dominant, surgery not indicated,
PTH normal
 Neonatal Severe Hyperparathyroidism
 Hyperparathyroidism- Jaw Tumor Syndrome

30.  Secondary hyperparathyroidism refers
to the excessive secretion
of parathyroid hormone (PTH) by
the parathyroid glands in response
to hypocalcemia (low blood calcium leve
ls) and associated hypertrophy of the
glands. This disorder is especially seen
in patients with chronic renal failure.

31.  Chronic renal failure is the most common
cause of secondary hyperparathyroidism.
 Failing kidneys do not convert
enough vitamin D to its active form, and
they do not adequately
excrete phosphate.
 When this happens, insoluble calcium
phosphate forms in the body and removes
calcium from the circulation.
 Both processes lead to hypocalcemia and
hence secondary hyperparathyroidism.

32.  Secondary hyperparathyroidism can
also result from malabsorption (chronic
pancreatitis, small bowel disease,
malabsorption) in that the fat soluble
vitamin D can not get reabsorbed.
 This leads to hypocalcemia and a
subsequent increase in parathyroid
hormone secretion in an attempt to
increase the serum calcium levels

34.  Bone and joint pain are common, as are limb
deformities.
 The elevated PTH has also pleiotropic effects
on blood, immune system and neurological
system

35.  The PTH is elevated due to decreased levels
of calcium or 1,25-dihydroxy-vitamin D3.
 It is usually seen in cases of chronic renal
disease or defective calcium receptors on the
surface of parathyroid glands.

36.  If the underlying cause of the hypocalcemia
can be addressed, the hyperparathyroidism
will resolve.
 In patients with chronic renal failure,
treatment consists of dietary restriction of
phosphorus, supplements with an active form
of vitamin D such as calcitriol,etc.
 and phosphate binders which can be divided
into calcium-based and non-calcium based.

37.  Most patients with hyperparathyroidism
secondary to chronic kidney disease will
improve after renal transplantation, but many
will continue to have a degree of residual
hyperparathyroidism (tertiary
hyperparathyroidism) post-transplant with
associated risk of bone loss, etc.

38.  If left untreated, the disease will progress
to tertiary hyperparathyroidism, where
correction of the underlying cause will not
stop excess PTH secretion, i.e. parathyroid
gland hypertrophy becomes irreversible.

39.  is a state of excessive secretion of parathyroid
hormone (PTH) after a long period of secondary
hyperparathyroidism and resulting in hypercalcemia.
It reflects development of autonomous (unregulated)
parathyroid function following a period of persistent
parathyroid stimulation.
 The basis of treatment is still prevention in
chronic renal failure, starting medication and dietary
restrictions long before dialysistreatment is initiated.
 Cinacalcet has greatly reduced the number of
patients who ultimately require surgery for secondary
hyperparathyroidism; however, approximately 5% of
patients do not respond to medical therapy.

40.  When secondary hyperparathyroidism is
corrected and the parathyroid glands remain
hyperfunctioning, it becomes tertiary
hyperparathyroidism. The treatment of choice
is surgical removal of three and one
half parathyroid glands.

41.  Hypoparathyroidism is decreased function of
the parathyroid glands with underproduction
of parathyroid hormone.
 Causes
 Hypoparathyroidism can have a following
causes:
 Removal of or trauma to the parathyroid glands
due to thyroid surgery (thyroidectomy) or other
surgical interventions to the neck is a
recognized cause.
 It is now uncommon, as surgeons generally can
spare them during procedures after identifying
them.
 In a small percentage of cases, however, they
can become traumatized during surgery and/or
their blood supply can be compromised. When
this happens the parathyroids may cease
functioning for a while or stop altogether.

42.  Autoimmune invasion and destruction is the
most common non-surgical cause. It can
occur as part of autoimmune polyendocrine
syndromes.
 Hemochromatosis can lead to iron
accumulation and consequent dysfunction of
a number of endocrine organs, including the
parathyroids.

43.  Absence or dysfunction of the parathyroid
glands is one of the components
of chromosome 22q11 microdeletion
syndrome (other names: DiGeorge syndrome,
Schprintzen syndrome, velocardiofacial
syndrome).
 Magnesium deficiency

44.  The main symptoms of hypoparathyroidism are
the result of the low blood calcium level, which
interferes with normal muscle
contraction and nerve conduction.
 As a result, people with hypoparathyroidism can
experience paresthesia, an unpleasant tingling
sensation around the mouth and in the hands
and feet, as well as muscle cramps and severe
spasms known as "tetany" that affect the hands
and feet.
 Many also report a number of subjective
symptoms such as fatigue, headaches, bone
pain and insomnia.[
 Crampy abdominal pain may occur.

45.  Physical examination of someone
with hypocalcemia may show tetany, but it is also
possible to provoke tetany of the facial muscles by
tapping on the facial nerve (a phenomenon known
as Chvostek's sign) or by using the cuff of
a sphygmomanometer to temporarily obstruct the
blood flow to the arm (a phenomenon known
asTrousseau's sign of latent tetany).
 A number of medical emergencies can arise in people
with low calcium levels. These are seizures, severe
irregularities in the normal heart beat, as well as
spasm of the upper part of the airways or the smaller
airways known as the bronchi (both potentially
causing respiratory failure).[1]

46.  Diagnosis is by measurement
of calcium, serum albumin (for correction)
and PTH in blood.
 If necessary, measuring cAMP (cyclic AMP) in
the urine after an intravenous dose of PTH
can help in the distinction between
hypoparathyroidism and other causes.

47.  Severe hypocalcemia, a potentially life-threatening
condition, is treated as soon as possible
with intravenous calcium (e.g. as calcium gluconate).
 Generally, a central venous catheter is recommended,
as the calcium can irritate peripheral veins and
cause phlebitis.
 In the event of a life-threatening attack of low
calcium levels or tetany (prolonged muscle
contractions), calcium is administered by intravenous
(IV) infusion.
 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 as often as
four times a day.

48.  Long-term treatment of hypoparathyroidism is
with vitamin D analogs and calcium
supplementation may be ineffective in some due
to potential renal damage.
 The use of pump delivery of synthetic PTH 1-34
provides the closest approach to physiologic
PTHreplacement therapy.
 Teriparatide, a recombinant form of PTH
(presently registered for osteoporosis) might
become the treatment of choice for PTH
supplementation.