SEMINAR ON: DISEASES OF PARATHYROD
 MULTIPLE ENDOCRINE NEOPLASIAS
 APUDOMAS
SUBMITTED BY:TANVI OHRI
ROLL NO. 16941
BDS THIRD YEAR.
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increasing osteoclastic resorption of bone
increasing intestinal absorption of calcium
increasing synthesis of 1,25-(OH)2D3
increasing renal tubular reabsorption of
calcium
increasing excretion of phosphate.
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A clinical condition chracterised by exessive
secretion of parathyroid harmone
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Primary hyperparathyroidism results from a hyper
function of the parathyroid glands themselves.
There is over secretion of PTH due
to adenoma, hyperplasia or, rarely, carcinoma of
the parathyroid
Secondary hyperparathyroidism:-IT is the reaction
of the parathyroid glands to a hypocalcemia
caused by something other than a parathyroid
pathology, e.g. chronic renal failure.
Tertiary hyperparathyroidism result from
hyperplasia of the parathyroid glands and a loss of
response to serum calcium levels. This disorder is
most often seen in patients with chronic renal
failure and is an autonomous activity
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GENERAL:-weight loss,tiredness,lassitude
GI TRACT:-nausea,
vomiting,anorexia,constipation,peptic
ulceration
CNS:-drowsiness ,lack of
concentration,depression,loss of
memory,myopathy
RENAL:-polyurea,polydipsia,stones
formation,nephrocalcinocis,may be
precipitation of gout and uraemia
BONE:-bone pain,tenderness,
fractures,deformities,osteitis fibrosa cystica
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CARTILAGE:-chondrocalcinosis
CADIOVASCULAR:-hypertension
SKIN:-pruritus
EYE:-corneal calcification
SOFT TISSUE:-ectopic calcification of soft
tissue of hands and feet
FOR DIAGNOSIS:
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BIOCHEMICAL:SERUM CALCIUM:-raised
SERUM PHOSPHATE:-decreased
SERUM PTH:-raised
SERUM ALKALINE PHOSPHATE:-raised
RADIOLOGICAL:X_RAY OF PHALANGES SHOW
SUBPERIOSTEAL EROSIONS
LATERAL X-RAY OF SKULL SHOW “PEPPER
POT” APPEARANCE
X-RAY OF KIDNEY SHOW SCATTERED
OPACITIES DUE TO NEPHROCALCINOSIS
SOFT TISSUE CALCIFICATION
FOR LOCALISATION OF
TUMOUR:
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Ultrasonography of pararhyroid
Selective neck vein catheterisation and pth
measurements
Ct scan
Substraction imaging by radionuclide studies
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Asymptomatic old patients with serum calcium
level less than 3.0mmol/L do not require
treatment.
Surgical removal of adenoma.
If there is hyperplasia of all the 4 parathyroid
glands, then treatment is to remove them &
transplant some of the parathyroid tissue in the
fore arm
If hypercalcaemia retuns after transplantation, a part
of tissue can be removed under local anaesthesia
 Hypocalcaemia , after surgery is beter treated by
calcium:-1-alpha hydroxicholecalciferol(alphacalcidol)
2.0microgm DAILY FOR 48hrs BEFORE SURGERY &
CONTINUE FOR 1-2 WEEKS AFTER SURGERY
-Calcium gluconate (i.V.) AS 10ml 10% SOLUTION
3-4hrs DURING POSTOPERATIVE PERIOD
-Oral calcium supplements used
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Hypercalcaemia is an elevated calcium level in
the blood.[1] (Normal range: 9–10.5 mg/dL or
2.2–2.6 mmol/L)
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Nousea
Vomitting
Pain in abdomen
Dehydration
Hypotension followed by different stages of
unconciousness
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hypoparathyroidism is decreased function of
the parathyroid glands, leading to decreased
levels of parathyroid hormone
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Tetany
Cataract
Psychosis
Basal ganlia calcification
Epilepsy
Papilloedema
Candidiasis of nails, skin & mucous membrane
 True hypoparathyroidism:Deficient production of pth due to heritable or
acquired causes
 Pseudo hypoparathyroidism:A Heritable or congenital disorder in which
there is tissue resistance to the effects of pth.
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POSTOPERATIVE:-due to complication of
thyroid surgery , damage to parathyroid
glands or their blood supply &surgery of
graves disease
IDIOPATHIC HYPOPARATHYROID:-it is
either due to autoimmune destruction of
parathyroid glands or is associated with
mucocutanious canadiasis
INFANTILE HYPOPARATHYROIDISM:it may be transient or persistent. Transient
occurs in infants born to mother who were
suffering. Persistent is seen due to thymic
aplasia
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PSEUDOHYPOPARATHYROIDISM:-This is a
congenital variety in which parathroidharmone
production is normal, but there is resistence to
its effect.in this mental retardation ,skeletal or
osseous abnormalties i.e.short 4th &5th
metacarpals & metatarsals with short
stature.Serum PTH level elevated.
PSEUDOPSEUDOHYPOPARATHYROIDISM:-ossious
menifestations are present without any clinical
symptoms & signs.
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Parathroid harmone substitution threpy
Ca OR vitd ANALOGUE(1ALPHA
CALCIDOL)
In acute condition, calcium gluconate(i.V) 10ml
10% solution 3-4 hrs INTERVAL BY ALPHA
CALCIDOL OR CALCITROL IN DOSES OF 13 microgm DAILY
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It is chracterised by low levels of ionised
calcium leading to increased neuromascular
excitability. Ca LEVEL MAY REMAIN
NORMAL.
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Neuromuscular function, calcium, potassium &
magnesium’s low levels
Hypocalcaemia:Malabsorption
Osteomalacia
Hypoparathyroidism
Chronic renal failure
Acute pancreatitis
Anticonvulsans (dilantin)
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Hypomagnesaemia
Alkalosis or hypokalaemia:Repeated vomiting
Excessive intake of alkalies
Hysterical-hyperventilation leading to alkolosis
Primary hyperaldosteronism
ACUTE ANION LOAD (CITRATE,LACTATE
,hco3etc)
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It may be latent or menifest.
IN CHILDREN:-triad of carpopedal spasm,
stridor, convulsions may occurred in various
combinations
IN ADULT:-tingling sensatins in peripheral
parts of limbs or around the mouth. Less
often,painfull carpopedal spasms may occur.
Stridor & convulsions are rare.
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Absence of signs
Signs can be indused by provocative tests:TROUSSEAU’S SIGN:-raising of blood
pressure above systolic level by inflation of cuff
produce chracterstic carpal spasm within 3-5
minutes
CHVOSTEK’S SIGN:-a tap at facial nerve at
angle of jaw produses twitching of facial
muscles
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TREAMENT OF HYPOCALCAEMIA:-Injetion of
20ml of 10% calcium gluconate may be given to
correct hypocalcaemia & relieve tatany. An
intrammuscular injection of 10ml may be used for
prolonged effect.
TREATMENT OF ALKALOSIS:-Isotonic solution
(i.V.) For vomiting.
-Withdrawl of alkalies. If not relieved, ammonium
chloride 2.0g ORALY AFTER EVERY 4hrs
-Hyperventilation:-inhalation of 5% co2 in oxygen
may be prescrived or ask for rebreath the expired air
from asuitable bag.
-Treated bypsycothrepy.
In
which more than one endocrine
glands become the site of neoplasia.
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It is an autosomal dominant disorder associated
with mutation of MEN-1 tumor suppressor gene
on chromosome 11.
In this group the parathyroid glands are most
frequently involved(chief cell hyperplasia-90%)
producing hyperparathyroidism which is often
mild.
There is often multiple pancreaticoduodenal
neuroendocrine tumors causing Zollinger-Ellison
syndrome
The anterior pituitary is involved next (65%)
causing acromegaly or cushings syndrome or there
may be hyperplasia of adrenal cortex and carcinoid
tumor.
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Duodenal ulceration is a common feature of this
syndrome.
It may be related to hyperparathyroidism as
hypercalcaemia promotes the secretion of gastrin.
Prathyroidectomy often reduces the secretion of
the acid and sometimes cures duodenal ulceration.
In fact operation for duodenal ulcer should be
postponed untill all endocrine lisions have been
treated.unless the patient has pancreatic
gastrinoma , for which total gastrectomy should be
performed.
Other associated disorders include thyroid
neoplasms(adenoma or differentiated thyroid
carcinoma) , adrenal neoplasms and lipomas.
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In this case tere is medullary carcinoma of
thyroid with pheochromocytoma and
hyperparathyroidism.
It is further divided into 2a and 2b.
In type 2a hyperparathyroidism is seen in 25%
of patients whereas in 2b there are additional
neurofibromas affecting lips,eyelids and face
producing swellings in these regions,
megacolon and ganglioneuromatosa.
Hyperparathyroidism is rarely seen with this
syndrome.
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APUDOMAS are endocrine tumors which arise
from apud cells.
The ‘APUD’ cells are widely distributed in the
body and have common cytochemical
characteristics related to synthesis of
polypeptides and amines.
The name APUD was first proposed by Pearse
in 1968 and is derived from initial letters of
main properties of these cells--High content of amine.
The capacity for amine precursor uptake from
the environment.
Presence of amino acid decarboxylase for
conversion of amino acid into amines.
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The average diameter of these apud cells is 100200 micrometers and contain dense storage
granules of their polypeptide products.
Majority of gastrointestinal apud cells possess
long apical processes which reach the
glandular lumen ending in tufts of microvilli.
Pearse suggested that neural crest cells should
be considered as ancestors of these apud cells.It
is well accepted fact that the apud cells, be it in
the carotid body, the thyroid, anterior
pituitary,elimentary tract and even parathyroid
arise from neural crest or neuroectoderm.
APUDOMAS can be conveniently classified into the
following groups:A. ORTHOENDOCRINE.
1.Tumors secreting normal polypeptides of their cells of
origin eg. Insulinoma,gastrinoma, pancreatic
glucogonoma, calcitoninoma.
2.Tumors secreting normal amines of their cells of origin
eg. Phoechromocytoma, neuroblastoma and
ganglioneuroma(all from adrenal medulla) and
carcinoid tumor.
B. PARAENDOCRINE APUDOMA SYNDROME(PES)
1.Tumors of endocrine glands secreting hormones
characteristic of other glands.
2.Tumors of organs, not usually regarded as endocrine in
nature, secreting hormones eg.oat cell carcinoma of
bronchus producing ectopic ACTH & WDHA
syndrome which is non- beta-islet cell tumor of
pancreas presenting with water diarrhoea,
hypocalcaemia and hypo or achlorhydria.