Parathyroid Gland

Hikmat Permana

Sub Div Endocrinology and metabolism

Internal Medicine Hasan Sadikin Hospital
Medicine Faculty Padjadjaran University
Anatomy of Parathyroid gland

2 pair parathyroid gland

Located on :
the posterior aspect the thyroid gland

Each : about 0.5 cm diameters

weight 75 mg
Function of Parathyroid gland :
Secretion of Parathyroid Hormone
(PTH)

Calcium and phosphate homeostasis

Calcitonin
Vitamin D
 Synthesis, processing and secretion of
parathyroid hormone

BLOOD

PARATHYROID PTH NH2

NH2 NH2
Pro-PTH NH2
PTH
COOH COOH COOH
Pro-pro PTH C-AMP
ENDOPLASMIC RETICULUM COOH LIVER

COOH

COOH

KIDNEY
Biologic effect of PTH on calcium concentration

Hypocalcemia hypercalcemia

Stimulate PTH Suppresses PTH

effect of PTH on calcium concentatrion

3 Mechanism :

Stimulation of renal synthesis D, 1,25-(OH)2 D

Stimulation of calsium resorption from bone
Stimulation of Ca resorption in distal tubulus
effect of PTH on phosphate concentatrion

Block renal tubular resorption

Increase urinary phosphate excretion

Decrease serum phosphate concentration

DIETARY CALCIUM
ICF
CALSIUM BALANCE
1000 mg
Ca
12 gm

BONE
Formation
Secretion Ca
300 mg ECF 300 mg
Absorption Ca 1300 mg
Resorption
500 mg 900 mg
300 mg/day

Glomerular Resorbed
Filtrate From Filtrate
10,000 mg Ca 9800 mg Ca

INTESTINE

FECAL CALSIUM
Urine Ca
800 mg
200 mg
factor to contribute calsium metabolism

Calcitonin
Vitamin D
dietary sources
intestinal absorption
Binding protein for vitamin D metabolisms.
RELATIONSHIP PLASMA PTH WITH Ca CONSENTRATION

PLASMA
PTH

NORMAL HIGH

HYPOCALCEMIC HYPOPARATHYROIDISM HYPOPARATHYROIDISM

Decreases PTH tissue response

Secondary
NORMOCALCEMIC NORMAL HYPERPARATHYROIDSM

Other Primary
HYPERCALCEMIC
Hypercalcemia State HYPERPARATHYROIDSM
Primary Hyperparathyroidsm
Etiology :

Single Parathyroid Adenoma 90 %

Multiple Parathyroid Adenoma 2%
Hyperplasia of parathyroid gland 8 %

Chronic hypersecretion of PTH

clinical feature
Asymptomatic
Symptomatic :
weakness
anorexia
nause
Manifestation of disease :
nephrolithiasis
Peptic ulcer disease
acut pancreatitis
bone disease
Elderly : a hypercalcemic syndrome :
confusion
dehydration
Diagnosis

Laboratory finding

Elevated serum PTH

Hypercalcemia
Hypophosphatemia
causing of hypercalcemia
Primary hyperparathyroidism
Malignancy-associate hypercalcemia :
Multiple Myeloma
Leukemia
lymphoma
Endocrinopathies : Thyrotoxycosis
Adrenal Insufficiensy
Pheochromacytoma
Drug Induced : Thiazide diuretics
Vitamin D intoxication
Vitamin A intoxication
Milk alkali syndrome
clinical feature :
CNS : Lethargy, depression,
psychosis, ataxia, stupor,
coma
Neuromuscular : weakness,
Proximal myopathy
Hypertonia
Cardiovascular : Hypertension, Shortened QT interval

Renal : decreased GFP, Polyuria, Nephrolithiasis

GI : nausea, vomitus, constipation, anorexia
 Causing of hypocalcemia

Decreased PTH secretion Decreased PTH action

Primary hyporathyroidism Pseudohypoparathyroidism

Transient Ineffective PTH
Parathyroid immaturity in new born Hypomagnesemia
Hypomagnesemia Vitamin D Deficiency
Treatment of Leukemia Gastrectomy
Permanent Resection of smmal bowel
Parathyroid aplasia Steatorhea
Kenny’s Syndrome Therapy with anticonvulsant agent
Surgical parathyroid gland
Irradiation
Idiopathic ( Autoimmune )
clinical feature :
• Maybe Asymptomatic
• Symptomatic :
Increased neuromuscular irritability
Tetany
Growth or mental retardation or bone
deformities
Psychiatry manifestation
Weakness
Two sign : Chvostek’s and Trousseau’s (+)
Secondary Hyperparathyroidism
Cause
1. Vitamin D defisiensi
Nutritional
Malnutrition
Postgastrectomy
Fat malabsorption states
2. Defective Vitamin D metabolisme
Anticonvulsant grud therapy
Severe liver disease
Chronic renal disease
3. Primary Decrease Calcium absorption in elderly
4. Increased Urinary Calcium Loss
Renal tubular acidosis
Renal leak type idiopathic hypercalciuria
5. Hypocalcemia Due to increased serum phosphate
Acute and chronic renal failure
6. Target Organ Resistance Psudohypoparathyrodism
Osteoporosis

Loss of bone mass

microarchitecture of matrix disorder
risk of fracture

Cause : bone turnover decrease

Occuring with aging
Female > Male : menopause
loss bone mass >>
Osteoporosis
In the world : Problem ( Global Issue )
Develompment country :
incidence rate increased
Geriatic group increased

Degenerative disease and metabolic :

Coronary artery disease
Diabetes Mellitus
Hipertension
Obesity
Dislipidemia
Osteoporosis
Site of Fracture

All of Bone
Common :
Compressi fracture vetebrae
Colles Fracture
Femur fracture
Differences between :

Normal Osteoporosis Osteomalacia

 function and structure of bone
Bone :
 cel : osteoblast formating
Osteoclast resorption
extraceluller matrixs :
anorganic matrixs Inorganic matrix
30-40 % 60-70 %
type 1 colagen mineral : calsium
Phosphate
Magnesium
Citrate
Chloride
Carbonate
MOVEMENT OF Ca TO AND FROM BONE

ECF Ca Osteoclast

Osteoblast
Ca

Ca
Ca
Ca MINERALIZED
BONE
Newly Synthesized
Matrix Ca Osteocyte
BONE
Bone Modeling

Formating resorption
Growth

Bone remodeling
Formating resorption
Occurs throughout life
Bone Mass
Growth Phase Epyphiseal Plate Clossure

Consolidation Phase 10 – 15 years

Increased Bone mAss
Peak Bone Mass
30 old years

Involution Phase Loss Trabecular Cortical

Female : 35 – 50 25 –30 %
Male : 15 – 45 5 – 15 %
40 old years :
function of Osteoblast
decreased
Activity of Bone Remodeling :

Systemic Factors Hormonal :

PTH
1,25 (OH)2 Vit D
Calcitonin
Insulin
Estrogen
Androgen
GH
Thyroid Hormone

Local Factors Cytokine

Growth factors
 Factors favoring net Increased Factors favoring net Decreased
in Bone mass in bone mass

Stimulation of formating: Stimulation of resorption

1. Compressive stressed 1. PTH
of gravity and muscle 2. Osteoclast activiting factor
use 3. Prostaglandins
2. Thyroid hormone 4. Thyroid hormone excess
3. Growth hormone 5. Glucocortikoid excess
4. Insulin 6. Increased bone blood flow
5. Fluoride 7. Local inflamation
8. Heparin
9. Acidosis

Suppression of formating
Suppression of resorption 1. Immobilization
1. Estrogen 2. Glucocarticoid
2. Androgen 3. Malnutrition
3. Fluoride 4. Chronic disease
4. High ECF calsium
5. High ECF Phosphate
PTH : Stimulate to product osteoclast
Role of product 1,25 (OH)2 vit D in Renal

Vitamin D : Skin and intesinal

Liver
25 hydroxycholecalcipherol
Renal
1.25 hydroxycholecalcipherol
increased absorption Ca / P intestine
Stimulate to product osteoclast
Calcitonin : parafolikuler- C Thyroid Gland
to prevent activity osteoclast
Estrogen :
Supressed Resorption premenopause
 bone loss associated With
older ages

Bone acquisition is almost complete

girl : 17 years
boy : 20 years
to contribute :
body size
hormonal responsiveness
bone-spesific protein
gonadal steroid
physical activity
nutrient intake
Once peak bone mass
stable about age 50

maintenance of bone :
diet
physical activity
reproduktive status
smoking
alcohol excess
many medication
 bone loss associated with
Estrogen deficiency

Deprivation estrogen :
Post Menopause
constrain on osteoblastic production
stimulated proliferasi of osteoclast precrussor

osteoporosis
bone loss associated Excess of
corticosteroid agent
patient with :
asthma bronkhiale
Cushing’s disease
drug abuse of steroid
Glucocorticoid Supression :
Oscteoblast function
Intestinal Ca absorption

Osteoporosis
 clinical feature of Osteoporosis
Asymptomatic

Symptomatic :
Severe body pain
Skeletal deformity
Frakture
Neurologis symptoms
Loss of height

Female > male

 diagnosis of Osteoporosis

Bone mineral density (BMD) :

predictor of fracture risk
diagnostic :
< - - 2,5 SD : Osteoporosis
-1 - - 2,5 SD : Osteopenia
Radiology of Bone
principles management of osteoporosis

Spesific Antiresorptive Agents

Calsium,
Vitamin D
calcitriol
Estrogen
Selective estrogen response modulators (SERMs)
Calsitonin
Biphosphonate
Bone formating agent :
Fluoride
Androgen
Parathyroid hormone