Parathyroid gland
PTH - calcium in blood,phosphorus
1) stimulates osteoclasts
2) enhances reabsorption of Ca++ by kidneys
3) increases absorption of Ca++ by intestinal mucosal cells
hyperparathyroidism hypoparathyroidism
1) too much Ca++ drawn out of bone; 1)most often follow parathyroid gland
could be due to tumor trauma or after removal of thyroid---
2) due to tumor tetany, muscle twitches, convulsions; if
1) Bones soften and deform untreatedrespiratory paralysis and
2) Elevated Ca2+ depresses nervous death
system and contributes to
formation of kidney stones gland trauma or removal or dietary
magnesium deficiency
Results in tetany, respiratory
paralysis, and death
hiperparatiroidisme
Primary secondary tertiary Hypercalcemic
Crisis
E a solitary parathyroid adenoma(83%) Decreased GFR leads to long-standing (Ca. very high
t Multiple adenomas (6%) reduced inorganic secondary >12mg%
i Hyperplasia 10% phosphate excretion and hyperparathyr
o Carcinoma 1% consequent phosphate oidism, which +Acute:
l retention : stimulates the GIT symptoms
o Incidence increases above age 40 direct stimulatory growth of an
g effect on PTH autonomous
y Most patients with sporadic PHPT are synthesis and on adenoma. A
postmenopausal women with an cellular mass of clue to the
average age of 55 years the parathyroid diagnosis of
glands tertiary
excessive hyperparathyr
production and oidism is
secretion of PTH intractable
through lowering hypercalcemia
of ionized Ca2+ and/or an
and by inability to
suppression of control
calcitriol osteomalacia
production despite
Low calcitriol vitamin D
levels, in turn, therapy.
lead to
hyperparathyroid
ism
(Calcitriol is
known to have a
direct
suppressive
effect on PTH
transcription)
Reduced calcitriol
leads to impaired
Ca2+ absorption
from the GI tract
k • Symptomatic: Usually asymptomatic nausea, vomiting,
l • Classical pentad of severe hypercalcemia abd. pain,
i symptoms(Kid.stones, severe bone disease dehydration
n • painful bones,abdominal severe pruritis, NM ;fatigue,
i groans,psychic moans,& severe myopathy M weakness
s fatigue overtones) calciphylaxis, confusion , decreased
– Osteitis fibrosa cystica level of
– Nephrolithiasis consciousness
– Pathologic fractures
– Neuromuscular disease
– Life-threatening
hypercalcemia
– DU.pancreatitis
Asymptomatic:Hypercalmic
– Fatigue, muscle
weakness & ache
– Depression
– Polydipsia.Polyuria
– Anorexia,dyspepsiawt
loss.Constipation
– SOB.HT
l Elevated PTH in the (renal
a Serum tests Alteration setting of low or normal etiology)
b serum calcium is High calcium
Calcium Increased
diagnostic and
Intact PTH Increased(>0.5m phosphorus
g/L) If phosphorous is
elevated, cause is renal
Phosphate
P Chloride If phosphorous is low,
other causes of vit D
CL:PO4 (>33) deficiency should be
Alkaline N or (in the sought
phosphatase presence of
Uric acid bone disease)
N or
Acid-base Mild
status hyperchloremic
Ca- metabolic
:creatinine acidosis
clearance >0.02(vs<0.01 in
ratio BFHH)
Urine Test: N or
24h urinary (>250mg/24h)
Ca
c • Estrogen Prevention Surgical Foeced diuresis (N/S +
u – Dose required is high – Vit D Referral Lasix
r • SERMs replaceme - calcium-
e – Reduction in serum nt phosphate Mithramycin-
calcium and markers of – Phosphor product > 70 25µg/kg/day IV for 3-
bone turnover after 4 us binders 4 days- inhibits
weeks [Sevelame - severe bone osteoclast .rapid
• Bisphosphonates r] disease and onset in 12 h
– Studies have shown Treatment pain
increase in lumbar Calcimimetic agents - intractable Calcitonin 4 IU/kg
spine and femoral neck – pruritus SC/IM. Inhibits
mineral density Surgical osteoclast onset of
• Calcium/Vitamin D Considered in cases of - extensive soft action in hours , but
• Calcimimetic agents refractory tissue short –lived
(Cinacalcet) calcification
– Under investigation for with tumoral Biphosphonates(pami
primary HPT calcinosis dronate)- 60-90 mg IV
over 4-24h. Inhibits
- calciphylaxis osteoclast rapid
onset (2-3 days)
Gallium nitrate-
200mg/ m sq.BSA/d IV
for 5 days. increases
urinary
calcium.Delayed
onset of action(5-
7days)
Sterois
Hydrocortisone
100mg IV /8h.
Delayed onset (7-10
days) .useful for
hematologic malig.,
sarcoidosis, vit D
intoxication.
hyperthyroidism
hypoparathyroidism
etiology Surgical hypoparathyroidism
– It could be due to the removal of the parathyroid glands or due to
interruption of blood supply to the glands.
Idiopathic hypoparathyroidism
– A form occuring at an early age (genetic origin) with autosomal
recessive mode of transmission “multiple endocrine deficiency –
autoimmune-candidiasis (MEDAC) syndrome”
– “Juvenile familial endocrinopathy”
– “Hypoparathyroidism – Addisson’s disease – mucocutaneous
candidiasis (HAM) syndrome”
– Circulating antibodies for the parathyroid glands and the adrenals
are frequently present.
– Other associated disease:
– Pernicious anemia
– Ovarian failure
– Autoimmune thyroiditis
– Diabetes mellitus
Functional hypoparathyroidism
– In patients who has chronic hypomagesaemia of various causes.
– Magnesium is necessary for the PTH release from the glands and
also for the peripheral action of the PTH.
klinis – Neuromuscular
nerves are exposed to low levels of calcium they show abnormal neuronal
function which may include decrease threshold of excitation, repetitive response
to a single stimulus and rarely continuous activity.
– Parathesia
– Tetany
– Hyperventilation
– Adrenergic symptoms
– Convulsion (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
• Chvostek sign(penekanan ringan pada n.facialis
menyebabkan kontraksi otot wajah)
• Trousseau sign(sirkulasi darah ditahan dengan manset,
after 3min aka nada spasme carpopedal)
• Extrapyramidal signs (due to basal ganglia calcification)
– Other clinical manifestation
– Posterio-lenticular cataract
– Cardiac manifestation:
Prolonged QT interval in the ECG
Resistance to digitalis
Hypotension
Refractory heart failure with cardiomegally can occur.
– Dental Manifestation
Abnormal enamel formation with delayed or absent dental eruption and
defective dental root formation.
– Malabsorption syndrome
Presumably secondary to decreased calcium level and may lead to
steatorrhoea with long standing untreated disease.
lab absence of renal failure the presence of
calcimia, phosphatemia.
Undetectable serum iPTH confirms the diagnosis or it can be detectable if the
assay is very sensitive.
A) oral calcium pharmacological doses of vitamin D or its potent analogues.
cure
Phosphate restriction in diet may also be useful with or without aluminum
hydroxide gel to lower serum phosphate level.
Tetany& hungry bone syndrome
Calcium should be given parenterally till adequate serum calcium level is
obtained then give treatment A
Pseudohypoparathysoidism and Pseudopseudohypoparathyroidism
– A rare familial disorders with target tissue resistance to PTH
– calcimia, phosphatemia,thyroid gland function, with
increased serum iPTH(hormon yg dlpskan if calcium rendah
dalam darah)
– Short statue
– Short metacarpal and metatarsal bones
