CLASSES Parathyroid

HYPERPARATHYROIDISM
HYPOPARATHYROIDISM
HYPERPARATHYROIDISM
 HYPERPARATHYROIDISM
• Hyperparathyroidism is over activity of
parathyroid gland.
• It is a condition in which one or more of the
parathyroid glands become overactive and
secrete too much parathyroid hormone (PTH).
TYPES OF HYPERPARATHYROIDISM
• Primary hyperparathyroidism
• Secondary hyperparathyroidism
• Tertiary hyperparathyroidism
PRIMARY HYPERPARATHYROIDISM
• Is due to an idiopathic primary disorder of the
gland and is unassociated with any recognized
previous disturbance of calcium metabolism.
 PRIMARY HYPERPARATHYROIDISM
EPIDEMIOLOGY
• Incidence is from 34 to 120 per 100,000
person-years (mean 66) among women, and
from 13 to 36 (mean 25) among men.
Commonly reported prevalence is 1: 1000
population.
• More common in females. 1: 500 in females;
1:2000 in males
 PRIMARY HYPERPARATHYROIDISM
ETIOLOGY
• Parathyroid adenoma: most cases of primary
hyperparathyroidism (85%) are caused by a
solitary adenoma. Adenoma is multiple in 6%.
• Hyperplasia of parathyroid gland
• Parathyroid carcinoma
• Hereditary hyperparathyroidism in the context
of MEN (Multiple Endocrine Neoplasia)
syndrome
 PATHOPHYSIOLOGY OF PRIMARY
HYPERPARATHYROIDISM
• Increased serum parathyroid hormone (PTH)
levels result in increased bone resorption and
increased calcium absorption from intestines
and kidney, causing HYPERCALCAEMIA.
• Calcium is mobilized from bone by stimulating
osteoclastic activity.
• Calcium levels are also elevated by increased
vitamin D production by parathyroid hormone.
 PATHOPHYSIOLOGY OF PRIMARY
HYPERPARATHYROIDISM
• Increased PTH level causes decreased tubular reabsorption of
phosphate, causing HYPOPHOSPHATEMIA.
• PTH decreases proximal tubular reabsorption of bicarbonate,
resulting in bicarbonate wasting and consequently a LOW
SERUM BICARBONATE level and reciprocally a INCREASED
SERUM CHLORIDE LEVEL.
• With the tendency for hyperchloremia and hypophosphatemia,
most patients have MILD RENAL TUBULAR ACIDOSIS and a
SERUM CHLORIDE/PHOSPHATE RATIO OF 33 OR GREATER.
• This SERUM CHLORIDE/PHOSPHATE ratio can help distinguish
between primary hyperparathyroidism and other causes of
hypercalcaemia.
 PATHOPHYSIOLOGY OF PRIMARY
HYPERPARATHYROIDISM
• The serum alkaline phosphate level is elevated in about
15% of patients with primary hyperparathyroidism, and
these patients have increased bone turn over.
• Sub periosteal resorption of bone; osteitis fibrosa
cystica is frequently observed in patients with primary
hyperparathyroidism and increased serum alkaline
phosphate level, but rarely evident when the serum
alkaline phosphate level is normal.
• Bone biopsy reveals increased osteoclastic activity in
almost all patients
 PATHOPHYSIOLOGY OF PRIMARY
HYPERPARATHYROIDISM
• HYPERURICEMIA is a common abnormal
laboratory finding in 25% of patients, due to
impaired excretion of uric acid.
• NEPHTOLITHIASIS is more common.
• Metastatic calcification that is deposition of
calcium in normal tissue may occur. Kidney
arteries may be involved; so also sympathetic
ganglion.
 BONE LESIONS
Great effect of hyperparathyroidism is decalcification. This happens when oral intake
of calcium is insufficient to compensate for urinary loss of bony calcium
Following are the stages of bone involvement
STAGE-1 STAGE-2 STAGE-3 STAGE-4 STAGE-5 STAGE-6

There is first This is Coinciden Thin but bone Cysts may

halisteresis, a followed t with the trabeculae destruction develop in the
removal of lime by removal of new predominat newly formed
salts due to osteopo of bone bone are es, so that fibtous tissue
some changes rosis, there is formed in bones often giving rise
in the removal formation the fibrous become to fractures
relationship of of fibrous foci. pliable and (osteitis fibrosa;
between decalcifi tissue There is marked osteitis fibrosa
plasma bathing ed between thus a deformities cystica).
the bone and material the bony continuous develop Pseudotumors
the bone itself. by trabecula process of (Von refer to cysts
Excessive osteocla e bone Recklinghau lined by giant
amounts of sts, the destruction sen’s cell derived from
calcium into the phagocy and disease of osteoclast may
blood stream te of formation, bone) develop esp., in
bone. the jaw bones
 METASTATIC CALCIFICATION
• Is a natural accompaniment of extensive
decalcification of the skeleton. Calcium is
deposited particularly in the arteries, renal
pelvis and the renal tubules.
 RENAL LESIONS
• Elevated calcium leads to renal calculi formation.
• A fine deposit of calcium occur in the renal tubules and
interstitial tissue of pyramids. There may be
calcification of tubular epithelium and the tubular
basement membrane compromising renal function and
also stone formation.
• When disease proves fatal, death is due to renal failure.
• Renal insufficiency itself may give rise to secondary
hyperparathyroidism, which in turn may be responsible
for further renal damage
 GASTROINTESTINAL LESIONS
• Increased calcium ionic concentration in
sympathetic ganglion impedes transmission of
afferent stimuli and diminish efferent
discharges. This results in gastric atony leading
to dyspepsia, nausea and vomitting. Peptic
ulcer develops in 8% of patients.
• Intestinal atony leads to marked constipation.
 CARDIOVASCULAR LESIONS
• High levels of calcium can increase blood
pressure and lead to electrical abnormalities that
change the heart’s rhythm, adding strain.
• The heart beats when electrical impulses move
through it and cause it to contract. Calcium plays a
role in regulating this process, and too much
calcium can lead to an irregular heartbeat.
• Arterial stiffness and endothelial dysfunction have
been observed in patients with primary
hyperparathyroidism
 NEUROLOGIC (BRAIN) LESIONS
• Abnormal parathyroid hormone (PTH) levels play a
role in neuronal calcium dysregulation,
hypoperfusion and disrupted neuronal signaling.
Too much calcium in the blood can affect the
performance of the brain.
• It is hypothesized that calcium ions cross the blood-
brain barrier which may result in calcium overload,
neuronal signaling disruption or atrophy in
hippocampus. Calcium deposits in the brain have
also been related to frontal-subcortical dementia.
 PRIMARY HYPERPARATHYROIDISM
CLINICAL FEATURES
• Now a days majority of patients with this condition
are diagnosed by chance finding of increased
calcium and low phosphate levels in routine test, or
in the course of investigation for some unrelated
condition.
• Isolated system involvement and manifestation is the
current common method of clinical manifestation
• Only very few patients have the classic
manifestations of combination of renal stones,
painful bones, abdominal groans and psychic moans.
Isolated system involvement and manifestation
is the common method of clinical manifestation
• 1) commonest mode of clinical presentation is
a renal disorder due to calculus disease.
2) second mode of
presentation is with features related to
hypercalcaemia
3) least common mode
of presentation is metabolic bone disease
Primary hyperparathyroidism has
many SYMPTOMS but no SIGN
CLINICAL FEATURES OF PRIMARY
HYPERPARATHYROIDISM
SYMPTOMS DUE TO RENAL INVOLVEMENT
• Polyuria: Excessive thirst and frequent urination. Too much
calcium means that the kidneys have to work harder. As a result,
a person may urinate more often, leading to dehydration and
increased thirst.
• Nocturia
• Renal colic
• Hematuria
• Many have recurrent renal calculi, the calculi forming rapidly
after removal

• Investigations reveal features of renal insufficiency: raised blood

urea, raised serum creatinine
 SYMPTOMS DUE TO HYPERCALCEMIA
• Signs and symptoms of hypercalcemia range from nonexistent to
mild to severe.
• Mild hypercalcemia (serum calcium up to 11.5mg): Asymptomatic
or nonspecific symptoms, such as constipation, fatigue, and
depression
• Moderate hypercalcemia (up to 13mg): polyuria, polydipsia,
dehydration, anorexia, nausea, muscle weakness, and changes in
sensorium (confusion, lethargy, fatigue, anxiety and depression).
• Severe hypercalcemia (more than 13mg): progression of these
symptoms. High blood pressure and abnormal heart rhythms.
• The mnemonic "stones, bones, abdominal moans, and psychic
groans" describes the constellation of symptoms and signs of severe
hypercalcemia.
SYMPTOMS DUE TO BONY INVOLVEMENT

• Bone pain. Many patients presenting with vague pains in

bones and joints are mistakenly diagnosed as rheumatic.
Fractures are one of the causes of bone pain.
• Significant disability
• Loss of independence
• Prolonged immobility
• Curvature of the spine
• Becoming shorter over time
• Many patients presenting with vague pains in bones and
joints are mistakenly diagnosed as rheumatic.
INVOLVEMENT OF OTHER ORGANS/TISSUES

• Skin: pruritis, brittle nails

• Ophthalmic findings may include band
keratopathy, which is calcium precipitation in a
horizontal band across the cornea in the
palpebral aperture.
 CLASSICAL PRESENTATION IN THE PAST

Classic manifestations of combination of renal stones, painful

bones, abdominal groans and psychic moans is rare now.
Moans Stones (kidney- Groans Bones (bone pain
(gastrointestinal related (psychological and bone-related
conditions) conditions) conditions) conditions)
Constipation Kidney stones Confusion Bone aches and
Nausea Flank pain Dementia pains
Decreased Frequent Memory loss Fractures
appetite urination Depression Curving of the
Abdominal pain spine and loss of
Peptic height
ulcer disease
 PRIMARY HYPERPARATHYROIDISM
PHYSICAL EXAMINATION
• Physical examination is almost always
negative
 PARATHYROID HORMONE (PTH)
RADIOIMMUNO ASSAY
• Where facilities for radioimmuno assay for PTH are
available diagnosis of parathyroidism in a
hypercalcemic patient is actually straight forward
and no longer a diagnosis of exclusion. Normal
values are 10-55 pg/dL.
• An elevated serum PTH level in the presence of
hypercalemia makes diagnosis of
hyperparathyroidism almost certain.
• In primary hyperparathyroidism, both serum
calcium and PTH are raised.
 PRIMARY HYPERPARATHYROIDISM
BIOCHEMICAL FINDINGS
In centers where there are no facilities for PTH assay
diagnosis of hyperparathyroidism rests on certain
biochemical findings, and exclusion of other causes of
hypercalcaemia.
• Elevated serum calcium level
• Low serum phosphate level
• Elevated chloride/phosphate ratio
• In some cases increased serum alkaline phosphatase level
• Increased urinary excretion of calcium and phosphate as a
result of increased bone turn over
 IMAGING STUDIES
RADIOGRAPHY PARATHYROID SCANNING
BONE RENAL Using sestambi: Sestamibi is a small
Early X-ray Nephrocalcinosis protein which is labeled with the
changes first (diffusely radio-pharmaceutical technetium99.
appear in the scattered foci of Scanning done to localize diseased
skull and in the calcium salt parathyroid glands prior to a minimal
phalanges with deposition - invasive operation.
loss of density calcification -in
and sub the renal
periosteal erosion parenchyma.
Renal stones
 PRIMARY HYPERPARATHYROIDISM
DIAGNOSIS
• Diagnosis is by
1)clinical features (symptoms),
2)blood tests and
3)findings in the operating room.
• Parathyroid scanning is undertaken only if a
minimal invasive operation is planned.
 PRIMARY HYPERPARATHYROIDISM
DIFFERENTIAL DIAGNOSIS
• Bony metastasis: due to increased osteoclastic activity.
• Carcinoma with endocrine secretion (carcinoma of
bronchus, kidney, ovary): secrete PTH like substance
• Multiple myeloma: due to increased osteoclastic
activity.
• Vitamin D intoxication
• Sarcoidosis

• PARATHYROID HORMONE IS NOT ELEVATED IN THE

ABOVE CONDITIONS
 TREATMENT OF PRIMARY
HYPERPARATHYROIDISM
• The only corrective treatment is surgical removal
of the overactive parathyroid gland or glands.
• In symptomatic patients, indications for
operations are clear cut.
• In asymptomatic and mildly symptomatic
patients indication for operation is less clear. A
balance needs to struck up between symptomatic
relief after surgery and complications of surgery.
 SURGERY FOR PRIMARY HYPERPARATHYROIDISM
PREOPERATIVE LOCALIZATION OF PARATHYROID GLAND
• An experienced surgeon can • Less experienced surgeons may
successfully localize the take the help of localization tests
parathyroid gland and tumor on in the initial phase.
the operation table – for him • U/S scanning
pre operative localization tests • CT scan is valuable for detecting
are not indicated. For him parathyroid gland in the
localization tests are required in mediastinum
case re-exploration surgery is • Sestambi scan; Thallium-
required or in recurrent technetium subtraction scan.
hyperparathyroidism • Invasive technique- selective
• However if a minimally invasive angiography; selective venous
surgery if planned then sampling
preoperative localization is • Intra-operative PTH
indicated. determination
 PARATHYROID SURGERY
• Parathyroid adenoma: Excision of parathyroid adenomatous gland only
• Parathyroid hyperplasia:Subtotal parathyroidectomy: removal of 3
and a half gland. This operation is indicated in hyperplasia in which all 4
glands are involved. 50% of one gland with an intact blood supply is spared
and not removed or Total parathyroidectomy with autotransplantation of
some parathyroid tissue in the muscles of the forearm. In selected cases
Total parathyroidectomy with thymectomy and
autotransplantation(sometimes the 5th parathyroid gland is situated in the
region of thymus.
• Parathyroid carcinoma: Excision of the tumor, adjacent muscle,
ipsilateral thyroidectomy (thyroid lobectomy) and regional
lymphadenectomy. Cancer is suspected if a palpable lump is present in the
neck in patients with elevated serum calcium and elevated serum PTH
 TWO FOLD JOB OF THE SURGEON AT
OPERATION IN PARATHYROID SURGERY
• The surgeon at operation must identify all 4 glands, study
each gland carefully both grossly and, if required, by
frozen section biopsy (if no pre-operative undertaken).
• Thus the surgeon must do both functions during the
operation-
1)diagnose the pathology and then
2)treat (operate) accordingly.
• In 90% hyperparathyroidism is due to a single gland
disease (adenoma); in 10% of cases are associated with
multiple gland disease either hyperplasia or more than
one adenoma
 OTHER OPERATIVE AND TREATMENT OPTIONS
IN PRIMARY HYPERPARATHYROIDISM
• PEA (Percutaneous parathyroid Ethanol
Ablation)
• Minimally invasive parathyroidectomy –
endoscopic/radioguided.
• Calcimimetices (e.g., cinacalcet), a class of
calcium receptor agonists can be used to
reduce PTH release by parathyroid cells. Not
recommended as first line of treatment.
 PROGNOSIS AFTER SURGERY
• Most patients improve.
• Bones recalcify and pseudo tumor resolve.
• Deterioration in renal function is prevented.
• Psychiatric patients show early recovery.
• Sense of well being is restored.
 MEDICAL TREATMENT OF
HYPERPARATHYROIDISM
INDICATIONS TREATMENT
• Mild hyperparathyroidism • Raloxifene (it is both
• Asymptomatic oestrogen agonist and
hyperparathyroidism antagonist)
• Where surgery cannot be • Alendronate (belongs to
undertaken because of co- bisphonates class of drugs
morbidities, prior used for treating
osteoporosis)
unsuccessful exploration or
those who refuse surgery • Cinacalcet (mimics calcium
circulating in blood thus
reducing serum
concentration of calcium)
ACUTE PRIMARY HYPERPARATHYROIDISM

DIAGNOSIS TREATMENT
• Characterized by life-threatening • First Restore Hydration: volume
hypercalcemia (>14mg/dL) along expansion with isotonic saline solution
with rapid deterioration of • Diuretics like frusemide to induce
central nervous system, cardiac, calciuresis
• Infuse dilute phosphate solution
gastrointestinal, and renal
• Alternatively hypercalcemia can be
functions
reduced by chelation with sobium
• Diagnosis is difficult and only too EDTA (Ethylene Diamine Tetra Acetic
often made after death. acid)
• Nausea and abdominal pain • Calcitonin is also of valve in this
followed by severe vomiting, situation
dehydration, oliguria and finally • This is followed by semi-urgent
coma parathyroidectomy
 Primary hyperparathyroidism
Secondary hyperparathyroidism
Tertiary hyperparathyroidism

SECONDARY HYPERPARATHYROIDISM
 SECONDARY (RENAL)
HYPERPARATHYROIDISM
• Secondary hyperparathyroidism is the result of
another condition that lowers calcium levels.
This causes parathyroid glands to produce
extra PTH to compensate for the calcium loss.
• Commonly occurs in patients with chronic
renal failure. May also occur in patients with
hypocalcemia secondary to inadequate
calcium or vitamin D intake or malabsorption.
 PREVALENCE
• The international burden of secondary hyperparathyroidism
(SHPT) is unknown, but it may be estimable through the
available chronic kidney disease (CKD) literature. The
prevalence in Europe of renal secondary
hyperparathyroidism is predicted at around 8.5%
• Hyperparathyroidism is a common complication of stage 3
and 4 chronic kidney disease which is not associated to
detectable changes in serum calcium and phosphate levels.
It is therefore advisable to measure PTH levels in all patients
with decreased glomerular filtration rate. It has been
reported that 30-50% of patients with stage 5 CKD have high
PTH levels.
 SECONDARY (RENAL)
HYPERPARATHYROIDISM
CLINICAL FEATURES DIAGNOSIS
• Most of the symptoms of • Secondary
secondary hyperparathyroidism can be
hyperparathyroidism are due diagnosed with simple
to the underlying cause. People
blood tests and these will
with vitamin D deficiency may
notice muscle aching and
reveal low or normal blood
weakness, or aching bones. In calcium and raised
severe cases they can develop parathyroid hormone. Bone
osteomalacia (soft bones) density scans (DXA) and X-
which can cause fractures and rays may be used to look for
bone deformity (in children osteomalacia.
- rickets).
 TREATMENT OF SECONDARY
HYPERPARATHYROIDISM
• Management is medical and includes appropriate
treatment of the underlying cause, low phosphate diet,
phosphate binders, and calcium and vitamin D
supplementation
• If the problem elsewhere in the body can be corrected,
the parathyroid glands go back to functioning normally.
• Surgery is rarely required. When patients have been on
dialysis for many years or cincalcet is unable to control
PTH production; the PTH levels can be extremely high and
may require parathyroid surgery. All four parathyroid
glands are involved in this disease process.
 Primary hyperparathyroidism
Secondary hyperparathyroidism
Tertiary hyperparathyroidism

TERTIARY HYPERPARATHYROIDISM
TERTIARY HYPERPARATHYROIDISM
• In many patients who have undergone kidney transplants,
parathyroid function returns to normal.
• In some patients, the parathyroid glands have functioned
abnormally for so long while patients have kidney failure and
are on dialysis that the abnormal parathyroid gland become
autonomous, and parathyroid function never returns to
normal.
• The incidence in patients in whom the disease appears or
progresses after kidney transplantation (tertiary
hyperparathyroidism) is 6% to 7%.
• Tertiary hyperparathyroidism causes problems similar to
primary hyperparathyroidism.
 TREATMENT OF TERTIARY
HYPERPARATHYROIDISM
• Observation only: in majority of patients there
is spontaneous correction
• Oral phosphates to lower the serum calcium till
elevated secretion of PTH ceases on its own. It is
important to protect the transplanted kidney
from any negative effects excess parathyroid
hormone (high calcium)may have on the kidney
• If symptomatic disease persists for more than
one year then parathyroid surgery is undertaken.
 COMPARISON OF TREATMENT OF 3 TYPES
OF HYPERPARATHYROIDISM
PRIMARY SECONDARY TERTIARY

First line of SURGERY MEDICAL OBSERVATION ONLY

treatment (NO TREATMENT)
 PRIMARY PREVENTION OF
HYPERPARATHROIDISM
• There are no established measures for the primary
prevention of primary hyperparathyroidism and
tertiary hyperparathyroidism
• Effective measures for the primary prevention of
secondary hyperparathyroidism in chronic kidney
disease include:
– Aggressive management of hyperphosphatemia in
early stages of chronic kidney disease.
– Prevention and treatment of vitamin D deficiency in
late stages of chronic kidney disease.
HYPOPARATHYROIDISM
 HYPOPARATHYROIDISM
• Hypoparathyroidism is the state of decreased secretion
or activity of parathyroid hormone (PTH). This leads to
decreased blood levels of calcium (hypocalcemia) and
increased levels of blood phosphorus
(hyperphosphatemia), decreased levels of vitamin D,
and clinical signs primarily involving neuromuscular
disturbances
• Low calcium is the key to the clinical picture, for it
facilitates the transmission of nervous impulses across
the myo-neural junction, resulting in increased neuro
muscular excitability.
 INCIDENCE
• The prevalence of hypoparathyroidism is
estimated to be 37 per 100 000 person-years
in the United States
 ETIOLOGY
• Commonest cause is Surgery: 75% of all cases of hypoparathyroidism.
After Total Thyroidectomy; after Parathyroidectomy.
• The first (and by far most common) cause of inadequate parathyroid
hormone production is the accidental removal of parathyroid glands
during thyroid surgery. Because of the close relationship that the
thyroid and parathyroid have to one another (including sharing the
same blood supply), the parathyroid glands can be injured or
removed accidentally when the much larger thyroid is removed. This
complication can occur in about 1% to 3% of cases following a total
thyroidectomy
• The second operation associated with post-operative
hypoparathyroidism is parathyroid surgery, or “parathyroidectomy.”
 ETIOLOGY
Other causes of hypoparathyroidism
• Neonatal
• Familial
• Heavy metal deposition
• Magnesium depletion
• Congenitally absent gland
• Autoimmune
• Idiopathic
 PATHOPHYSIOLOGY
• Hypoparathyroidism is a rare hormone-deficiency syndrome
in which the body lacks parathyroid hormone (PTH).
• Regardless of the underlying cause, the absence of PTH in
patients with hypoparathyroidism results in hypocalcemia
secondary to increased urinary loss (i.e., hypercalciuria),
decreased bone mobilization, and decreased intestinal
absorption of calcium. Hypocalcemia causes tetany.
• The primary symptoms of hypoparathyroidism are due to low
serum calcium (hypocalcemia). Tetany is a symptom. Tetany is
a disorder of increased neuronal excitability usually associated
with hypocalcemia/alkalosis (alkalosis results in decrease in
the ionized calcium level), and includes enhanced
neuromuscular activity and associated sensory disturbance.
 PATHOPHYSIOLOGY (continued)
• Hyperphosphatemia occurs from decreased urinary loss, which
overcomes decreased bone mobilization and decreased
intestinal absorption of phosphorus.
• PTH is a potent stimulator and phosphorus a potent inhibitor of
the 25(OH)-cholecalciferol-1a-hydroxylase system in the renal
tubules; consequently, the absence of PTH and the presence of
hyperphosphatemia work together to decrease renal synthesis
of calcitriol. Decreased levels of calcitriol contribute to
hypocalcemia through decreased intestinal calcium absorption
• Long standing hypoparathyroidism results in ectodermal tissue
changes - cataracts may develop, skin becomes coarse and dry,
scalp hair falls out, nails brittle and deformed.
 PATHOPHYSIOLOGY (continued)
• When the extracellular concentration of calcium ions
declines to subnormal levels, the nervous system
becomes progressively more excitable because of
increased neuronal membrane permeability. This
increase in excitability occurs in both the peripheral
system and central nervous system (CNS), although
most clinical signs are manifested peripherally.
• Nerve fibers may become so excitable that they begin to
discharge spontaneously, initiating impulses to
peripheral skeletal muscles, where they elicit tetanic
contraction.
 CLINICAL FEATURES
• Symptoms can range from quite mild (tingling in
the hands, fingers, and around the mouth) to
more severe forms of muscle cramps. The most
severe symptoms are tetany (severe muscle
cramping of the entire body) and convulsions (this
is very rare).
• The duration and magnitude of the calcium
depression as well as the rate of calcium decline
interact to determine the severity of clinical signs.
 CLINICAL SIGNS
• The signs of hypocalcemia are similar regardless of the
cause. Signs vary from hardly discernible to severe
generalized seizures, and can be abrupt or gradual in onset.
• The nursing staff may be the first to notice that the patient
is unexpectedly anxious or irritable.
• Patients initially develop circumoral and finger tip
numbness and tingling. At this stage latent tetany is
revealed by Chvostek sign and Trousseau sign.
• As the condition progresses (severe cases) overt tetany is
manifested by carpopedal spasm, painful cramps, spasm of
facial and massetter muscle causing risus sardonicus
 LATENT TETANUS SIGNS
Chvostek sign Trousseau sign
• Chvostek sign is contraction • The hand adopts a characteristic posture
when the sphygmomanometer cuff
of facial muscles provoked placed around the arm is inflated above
by lightly tapping over the the systolic blood pressure, around
200mmHg (within 3-5 minutes)
facial nerve anterior to the • The metacarpophalangeal joints are
ear as it crosses the flexed, the interphalangeal joints of the
zygomatic arch. This induces fingers and thumb are extended and the
thumb is strongly adducted
twitching of the facial (obstetrician hand; d’accoucheur hand).
muscles on the same side • Trousseau sign is more specific than
Chvostek sign for latent tetany, which
due to hyperexcitability of can be caused by hypocalcemia,
the nerve hypomagnesemia and metabolic
alkalosis
 OVERT TETANUS SIGNS
Carpopedal spasm Risus sardonicus
• Spasmodic contraction of the • Painful smiling appearance.
muscles of the hands, feet, and
• Sustained contraction of
especially the wrists and ankles
• Flexion of the hands at the
facial musculature produces
wrists and of the fingers at the m a sneering grin expression
etacarpophalangeal joints • Characterized by raised
and extension of the fingers at th eyebrows and grinning
e phalangeal joints; the feet are distortion of the face
dorsiflexed at the ankles
and the toes plantar flexed.
resulting from spasm of
• Spasms are usually brief, but
facial muscles
they can be severe and painful
 OTHER CLINICAL SIGNS
• Blurring of vision due to spasm of intraocular muscles.
• Cataract in prolonged unrectified hypocalcemia
• Occasionally, spasm of laryngeal muscles and muscles
of respiration occur, culminating in severe dyspnoea,
and the patient is not only in great pain but in mortal
dread of suffocation.
• In later stages generalized epileptic convulsions may
occur. Unlike classic grand mal convulsions, however,
hypocalcemic seizures are not associated with loss of
consciousness or incontinence
 DENTAL CHANGES IN
HYPOPARATHYROIDISM
• Cemental hyperplasia
• Hypoplastic enamel
• Short rounded roots
• Hypodontia and delay or lack of tooth
eruption
• Widening of the periodontal ligaments
 DIAGNOSIS
• Diagnosis is made based on
1)hypocalcemia and hyperphosphatemia,
2)low PTH, and
3)exclusion of other causes of
hypocalcemia.
 DIFFERENTIAL DIAGNOSIS
{OTHER CAUSES OF TETANY (HYPOCALCEMIA)}
• Renal failure leading to reduced absorption of
calcium in the tubules
• Alkali tetany: alkalosis occurring in hyperventilation,
gastric tetany (pyloric stenosis)
• Malabsorption
• Vitamin D deficiency: in children rickets; in adults
osteomalacia
• Calcium deficiency may also result from increased
loss during pregnancy and lactation, and this may
lead to tetany.
 HYPOPARATHYROIDISM TREATMENT
• Calcium supplements and vitamin D are the
primary treatments for hypoparathyroidism,
regardless of the cause. The majority of
patients need to take calcium several times
per day along with high-dose vitamin D once
per day.
 HYPOPARATHYROIDISM TREATMENT
• Calcium supplementation: 2 grams thrice daily and dietary
advice. Calcium citrate or calcium gluconate or calcium
lactate (13% elemental calcium). All varieties of calcium
supplements are better absorbed at mealtimes. Calcium
citrate is absorbed equally well with or without food. Calcium
phosphate salts should be avoided.
• Vitamin D: calcitriol has a rapid action (hours) and is
frequently used as the initial vitamin therapy. As prolonged
hypercalcemia remains a serious risk with all vitamin D
derivatives, the rapid reversal of hypercalcemia after calcitriol
treatment discontinuation makes this agent preferable to
ergocalciferol and alphacalcidol.
 HYPOPARATHYROIDISM TREATMENT
• Thiazide diuretics when hypercalciuria is
present
• Phosphate binders when hyperphosphatemia
is more than 6.5mg.
• PTH: recombinant human parathyroid
hormone introduced in 2015
 PTH THERAPY IN HYPOPARATHYROIDISM

• Hypoparathyroidism represents one of the few

remaining hormone deficiencies for which an
approved replacement therapy did not exist till
recently but now teriparatide [PTH (1–34)] and the
full-length natural secretory product of the
parathyroid glands, PTH (1–84), have ushered a
new era in the management of this disease
 SEQUELAE OF HYPOPARATHYROIDISM
TREATMENT
• Insufficient PTH causes a range of symptoms, which must be
managed in part through lifelong, high-dose supplements of calcium
and vitamin D. Hospital and emergency room visits are common, and
the high-dose supplements can cause kidney damage.
• Overall, hypoparathyroidism and its long-term classical treatment
(with oral calcium, calcitriol or other active vitamin D analogues)
increases the risk of renal stone formation and nephrocalcinosis, and
ultimately, decreased glomerular filtration rate (GFR), especially in
those with episodes of treatment-induced hypercalcemia. These
renal complications are the most serious long-term risks for patients
with hypoparathyroidism. Patients with activating CaSR (Calcium
Sensing Receptor) mutations are even at higher risk
 TREATMENT OF ACUTE
HYPOPARATHYROIDISM
• Although hypoparathyroidism is a chronic disorder, patients can
present with acute hypocalcemia in settings that reflect the early
consequences of anterior neck surgery, unanticipated changes in
requirements for calcium and vitamin D, or in patients who
become noncompliant or poorly compliant.
• Signs of acute hypocalcemia range from mild paresthesia to
carpal or pedal spasm and, in the extreme, laryngospasm or
seizures.
• Urgent management of symptomatic hypocalcemia requires iv
Ca2+ salts in two steps: one or two ampules of a 10% solution of
calcium gluconate, containing 90–180 mg elemental calcium in
50 mL of 5% dextrose, over 10 to 20 minutes followed by a
slower infusion of calcium gluconate, 0.5 to 1.5 mg/kg/h over an
8- to 10-hour period. The experience with the use of PTH in this
acute setting is too limited to make any specific
recommendations
PSEUDO HYPOPARATHYROIDISM
 PSEUDO HYPOPARATHYROIDISM
(Resistance to Parathyroid Hormone)

• Genetic disease. This condition is usually inherited from the mother.

Pseudohypoparathyroidism is characterized by an inadequate response to
the parathyroid hormone, although the hormone is present in normal
amounts. It is a very rare disorder, with estimated prevalence between 0.3
and 1.1 cases per 100000 population depending on geographic location.
• The inadequate response to PTH affects bone growth in individuals with
Pseudohypoparathyroidism, and is characterized by short stature, a round
face, short neck, and shortened bones in the hands and feet. Intelligence
usually ranges from low normal to mentally retarded. Headaches,
weakness, tiring easily, lethargy, cataracts and blurred vision or
hypersensitivity to light may also be present. During childhood, seizures
may occur. Teeth with underdeveloped enamel tend to erupt later than
normal during infancy. Levels of calcium in the blood are usually low, while
phosphate and the parathyroid hormone are elevated. Patients with
Pseudohypoparathyroidism can lead a normal life.
 PSEUDO HYPOPARATHYROIDISM
(Resistance to Parathyroid Hormone)

• If the levels of parathyroid hormone and phosphorous are

high and if the levels of calcium or low, this indicates the
possibility of pseudohypoparathyroidism. So diagnosis is by
the coexistence of hypocalcemia and hyperphosphatemia with
elevated PTH levels in the presence of normal vitamin D values
and normal renal function and the absence of hypercalciuria.
• Treatment same as for hypoparathyroidism. The goals of
therapy are to maintain serum total and ionized calcium levels
within the reference range to avoid hypercalciuria and to
suppress PTH levels to normal. This is important because
elevated PTH levels in patients with PHP can cause increased
bone remodeling and lead to hyperparathyroid bone disease.
 PSEUDO PSEUDO
HYPOPARATHYROIDISM
 PSEUDOPSEUDO HYPOPARATHYROIDISM
(Albright hereditary osteodystrophy)
• Also a genetic disease. This condition is usually
inherited from the father.
• The disease causes short stature , round face, and
short hand bones.
• It differs from pseudohypoparathyroidism in that
metabolic abnormalities of raised phosphate and low
calcium do not exist, but physical features remain the
same as pseudo hypoparathyroidism
• No specific treatment. Treatment focuses on
symptoms, with genetic counseling recommended