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PARATHYROID GLAND DISEASES

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Title: PARATHYROID GLAND DISEASES


1
PARATHYROID GLAND DISEASES
  • Primary hyperparathyroidism
  • Hypoparathyroidism

2
Disorders of the Parathyroid Glands
  • Maintenance of calcium, phosphate and magnesium
    homeostasis is under the influence of two
    polypeptide hormones
  • parathyroid hormone(PTH)
  • and calcitonin (CT)
  • as well as a sterol hormone
  • -1,25 dihydroxy cholecalciferol (1,25 (OH)2D3 ).

3
Disorders of the Parathyroid Glands
  • These hormones regulate the flow of minerals in
    and out of the extracellular fluid compartments
    through their actions on intestine, kidneys, and
    bones.

4
Disorders of the Parathyroid Glands
  • The PTH acts directly on the bones and kidneys
    and indirectly on the intestine through its
    effect on the synthesis of 1,25 (OH)2D3. Its
    production is regulated by the concentration of
    serum ionized calcium.
  • Lowering of the serum calcium levels will
    induce an increased rate of parathyroid hormone
    secretion

5
Disorders of the Parathyroid Glands
  • Calcitonin is released by the C cells
    (parafollicular cells in the thyroid gland) in
    response to small increases in plasma ionic
    calcium. It acts on the kidney and bones to
    restore the level of calcium to just below a
    normal set point which in turn inhibits secretion
    of the hormone.

6
Disorders of the Parathyroid Glands
  • Calcitonin is therefore the physiological
    antagonist of PTH. The two hormones act in
    concert to maintain normal concentration of
    calcium ion in the extracellular fluid.

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8
Disorders of the Parathyroid Function
Hyperparathyroidism
  • Primary hyperparathyroidismis due to excessive
    production of PTH by one or more of
    hyperfunctioning parathyroid glands. This leads
    to hypercalcemia which fails to inhibit the gland
    activity in the normal manner.

9
P-HPTH
  • Common, usually asymptomatic disorder
  • The incidence of the disease increases after the
    age of 50
  • 2-4 fold commoner in females than in males
  • Incidence approx. 42 per 100,000 inhibitants/year
  • Single parathyroid adenoma 80,
  • parathyroid hyperplasia 15
  • parathyroid carcinoma 1-2

10
Hyperparathyroid bone disease
  • Osteitis fibrosa cystica (lt 10 of patients)
  • Pain , pathologic fractures
  • Cystic lesions containing fibrous tissue (brown
    tumours) or cyst fluid
  • Subperiosteal resorption of cortical bone,
    salt-and-pepper appearance of the skull
  • Secondary osteoporosis (loss of cortical bone)

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Hyperparathyroid kidney disease
  • Kidney stones (lt 15 of patients)
  • Nephrocalcinosis
  • Polidypsia, poliuria (loss of renal concentration
    ability)
  • Gradual loss of renal function

14
Other features of P-HPTH
  • Lethargy, fatigue, depression, difficulty in
    concentrating, personality changes
  • Frank psychosis
  • Muscle weakness
  • Hypertension
  • Dyspepsia, nausea, constipation
  • Chondrocalcinosis (pseudogout), gouty arthritis

15
Stones Renal stones Nephrocalcinosis
Polyuria Polydipsia Uraemia
Bones Osteitis fibrosa
subperiosteal resorption
osteoclastomas bone cysts Radiologic
osteoporosis Osteomalacia or rickets Arthrithis
Abdominal groans Constipation
Indigestion, nausea, vomiting
Peptic ulcer Pancreatitis
Psychic moans Lethargy, fatigue
Depression Memory loss
Psychoses paranoia Personality
change, neuroses Confusion, stupor,
coma
P-HPTH signs symptoms
Other Proximal muscle weakness Keratitis,
conjunctivitis Hypertension anemia
Itching
16
Disorders of the Parathyroid Function
Clinical Features
  • Now a days almost 90 of diagnosed cases in the
    developed countries are picked up by routine
    screening for calcium level using the new
    automated machines
  • asymptomatic

17
Laboratory findings in P-HPTH
  • ? total Cas (may be intermittent), ? Cau, ? Ps, ?
    Pu
  • ? intactPTH (may be upper normal)
  • hyperchloremic acidosis
  • ? GFR

18
Treatment of P-HPTH
  • The adenoma may be located throughout the neck or
    upper mediastinum
  • The only localization study needed in a patients
    with hyperparathyroidism is to locate an
    experienced parathyroid surgeon
  • Surgical parathyroidectomy ? cure rate over 95
    (adenoma excellent surgeon)
  • Localization studies are very useful in
    reoperative parathyroid surgery neck ultrasound,
    99mTc-sestamibi scanning, CT, MRI (rarely
    angiography, venous sampling)

19
Surgery
  • Surgical treatment should be considered after
    diagnosis of primary hyperparthyroidism.
  • During surgery the surgeon identifies all four
    parathyroid glands (using biopsy if necessary)
    followed by the removal of enlarged parathyroid
    or 3 ½ glands in multiple glandular disease.

20
  • Surgery should be recommended if
  • serum Ca is markedly elevated (above 2.8 mmol/l)
  • if there has been a previous episode of
    life-threatening hypercalcemia
  • if creatinine clearance is reduced below 70 of
    normal
  • if a kidney stone is present
  • if urinary calcium is markedly elevated (gt 400
    mg/24 h)
  • if bone mass is substantially reduced (less than
    2 SD below normal for age, sex, and race)
  • if the patient is young (under 50 years of age,
    particularly premenopausal women)

21
Treatment of P-HPTH (II)
  • Calcitonin
  • Also inhibit osteoclast activity and prevent bone
    resorption
  • Bisphosphonates
  • They are given intravenously or orally to prevent
    bone resorption.

22
Treatment of P-HPTH (II)
  • Phosphate
  • Oral phosphate can be used as an
    antihypercalcaemic agent and is commonly used as
    a temporary measure during diagnostic workup.
  • Estrogen
  • It also decrease bone resorption and can be given
    to postmenopausal women with primary
    hyperparathyroidism using medical therapy

23
Treatment of P-HPTH (II)
  • Management of hypercalcaemia rehydrating with
    saline, furosemide, calcitonin s.c. (4-8 IU/kg
    every 12 hrs.), bisphosponates (etidronate
    disodium, pamidronate disodium), glucocorticoids
    p.o. (in multiple myeloma, sarcoidosis,
    intoxication with vitamin D or A).

24
Differential diagnosis
  • Causes of hypercalcemia
  • Primary hyperparathyroidism sporadic, associated
    with MEN 1 or MEN 2a, familial, after renal
    transplantation
  • Secondary, tertiary hyperparathyroidism

25
Causes of hypercalcemia
  • Malignancies humoral hypercalcemia (caused by
    PTHrP, 1,25(OH)2D3, PTH), local osteolytic
    hypercalcemia
  • Sarcoidosis
  • Endocrinopathies thyrotoxicosis, adrenal
    insufficiency, pheochromocytoma, acromegaly
  • Drug induced vitamin A, D intoxication,
    thiazides, lithium,milk-alkali syndrome,
    estrogens, androgens, tamoxifen
  • Immobilization
  • Acute renal failure

26
Causes of Hypercalcemia
Parathyroid - related
Vitamin D related
  • Primary hyperparathyroidism
  • Solitary adenomas
  • Multiple endocrine neoplasia
  • Lithium therapy
  • Familial hypocalciuric hypercalcemia
  1. Vitamin D intoxication
  2. 1,25(OH)2D sarcoidosis and other granulomatous
    diseases
  3. Idiopathic hypercalcemia or infancy

27
Differential Diagnosis
Causes of Hypercalcemia
Associated with high bone turnover
Malignancy - related
  1. Solid tumor with metastases(breast)
  2. Solid tumor with humoral mediation of
    hypercalcemia (lung kidney)
  3. Hematologic malignancies (multiple myeloma,
    lymphoma, leukemia)
  • Hyperthyroidism
  • Immobilization
  • Thiazides
  • Vitamin A intoxication
  • Assocated with Renal Failure
  • Severe secondary hyperparathyroidism
  • Aluminum intoxication
  • Milk alkali syndrome

28
hypoparathyroidism
29
Clinical features of hypoparathyroidism (of
hypocalcemia)
  • Neuromuscular manifestations
  • overt tetany carpopedal spasm, painful
    laryngospasmus, blepharospasmus
  • latent tetany Chvosteks sign, Trousseaus
    sign
  • focal or generalized seizures, papilledema,
    confusion, organic brain syndrome, mental
    retardation in children,
  • calcification of basal ganglia (skull X-ray, CT)

30
Clinical features of hypoparathyroidism (of
hypocalcemia)
  • Cardiac effects prolongation of QT interval,
    congestive heart failure
  • Ophtalmologic effects subcapsular cataract
  • Dermatologic effects dry and flaky skin, brittle
    nails, impetigo herpetiformis, pustular psoriasis

31
Trousseau's sign
the induction of carpopedal spasm by inflation of
a sphygmomanometer above systolic blood pressure
for 3 minutes adduction of the thumb, flexion of
the metacarpophalangeal joints, extension of the
interphalangeal joints, and flexion of the
wrist.
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33
Chvostek's sign
  • Chvostek's sign is contraction of the ipsilateral
    facial muscles elicited by tapping the facial
    nerve just anterior to the ear
  • The response ranges from twitching of the lip to
    spasm of all facial muscles and depends upon the
    severity of the hypocalcemia
  • occurs in about 10 percent of normal subjects
  • Although Trousseau's sign is more specific than
    Chvostek's sign, both may be negative in patients
    with hypocalcemia

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35
diagnosis
  • low Calcium
  • high Phosphate
  • low or undetectable intact PTH level

36
Hypoparathyroidism causes
  • Surgical, autoimmune, idiopathic, neonatal,
    familial, postradiation, infiltrative
  • Surgical ensues 1-2 days postoperatively,
    transient in 50 of cases
  • Autoimmune most commonly associated with
    Addisons disease and mucocutaneous candidiasis
    (type I polyglandular autoimmune syndrome)
  • Idiopathic an isolated form, age of onset 2-10
    years, commoner in females
  • Familial due to activating mutation of the
    parathyroid calcium receptor gene

37
Differential diagnosis
38
Pseudohypoparathyroidism (PHP)
  • Resistance to PTH action
  • A heritable disorder of target-organ
    unresponsineness to PTH (Ellsworth-Howard test
    lack of an increase in urinary cAMP after
    administration of exogenous PTH)
  • Hypocalcemia and hyperphosphatemia, but elevated
    PTH level and a markedly blunted response to PTH
    administration
  • 2 distinct forms
  • PHP 1A characteristic somatic phenotype, i.e.
    Albrights hereditary osteodystrophy (short
    stature, a round face, short neck, brachydactyly,
    subcutaneous ossifications)
  • PHP 1B no characteristic somatic phenotype

39
Causes of hypocalcemia
  • Failure to produce 1,25(OH)2D3 vitamin D
    deficiency, hereditary vitamin D-dependent
    rickets, type 1 (1?-hydroxylase deficiency)
  • Resistance to produce 1,25(OH)2D3 hereditary
    vitamin D-dependent rickets, type 2 (defective
    VDR)
  • Acute complexation or deposition of calcium
    acute hyperphosphatemia (crush injury, rapid
    tumour lysis, excessive enteral and parenteral
    phosphate administration), acute pancreatitis,
    citrated blood transfusion, hungry bones syndrome

40
  • Dietary deficiency of vitamin D or calcium
  • Decreased intestinal absorption of vitamin D or
    calcium due to primary small bowel disease, short
    bowel syndrome, and post-gastrectomy syndrome.
  • Drugs that cause rickets or osteomalacia such as
    phenytoin, phenobarbital, cholestyramine, and
    laxative.
  • Severe hypomagnesemia
  • Chronic renal failure

41
Treatment of hypocalcemia
  • Acute hypocalcemia calcium chloride or gluconate
    i.v. (up to 400-1000 mg/24 h), oral calcium and
    vitamin D should be started (caution digitalis
    treatment, stridor)
  • Chronic hypocalcemia objective normalisation of
    serum calcium and phospate
  • 1.0-2.0 g of elemental calcium p.o. per day,
    vitamin D3, active metabolites alfacalcidol
    (1?OHD3), calcitriol (1?,25OH2D3), low
    phosphate diet (no milk)

42
IV calcium
  • Symptomatic patients
  • Ca lt 2 mmol/L
  • 10 ml of 10 calcium gluconate in 50 ml of normal
    saline given over 10 min with ECG monitoring
  • Repeat above treatment until symptoms free
  • Treat hypomagnessemia if present with IV
    magnesium sulfate

43
IV calcium
  • Start IV infusion of 100 ml (10 ampoules) of 10
    calcium gluconate in 1L of NS 0.9 or D5 at a
    rate of 50 to 100 ml/hr
  • Adjust the rate to normalize calcium
  • Start oral calcium and potent vitamin D
  • Treatment with PTH?
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