PARATHYROID GLANDS

Hyperparathyroidism

Secondary

primary

tertiary

  • PTH overproduction induced by hypocalcemia.
  • PTH serum H, Ca serum L, P serum H-renal /L-vit.D, ALP serum H Ca urine L
  • Caused by chronic renal failure (most common cause), as well as vitamin D de ciency and renal hypercalciuria.
  • secondary to long standing secondary hyperparathyroidism, characterised by development autonomous hypersecretion of PTH causing hypercalcemia.
  • PTH serum H, Ca serum H, P serum H, ALP serum H, Ca urine various
  • group of sings and symptoms related to overproduction of PTH not caused by impaired mineral imbalance ( ca & p) resulting in abnormal ca & p homeostasis.
  • PTH serum H, Ca serum H, P serum L, ALP serum H, Ca urine H
  • classification: sporadic (90 %), hereditary (10 %).
  • aetiology:
    85 % - parathyroid adenoma,
    15 %- parathyroid hyperplasia of all 4 glands,
    < ,5 % - parathyroid carcinoma.
  • symptoms:
    80% asymptomatic,
    20% systemic: classical ( related to hypercalcemia, urinary [ nephrolithiasis { recurrent, bilateral, calcium oxalate}, polyuria, polydipsia, chronic renal failure due to cacinosis], osseous system [subperiosteal resorption, osteoporosis, osteopenia, soul 'salt and pepper', brown bone, pathologic fracture, phalangeal tuff resorption, osteitis fibrous cystica (“brown tumors”)]), GI [peptic ulcer, pancreatitis, constipation, vomiting, loss of appetite] , CVS [tachycardia, arrhythmia, short qt interval, hypertension], CNS [ headache, sleepless, psychosis, confusion], anaemia, glucose intolerance, ca in tissue, band keratopathy- ca in horizontal band in the cornea.

diagnosis

  • DD:
    -neurofibromatosis type 1 (NF1);
    criteria ( 2 or more): 6 or more cafe au lait spots, 2 or more neurofibromas, freckling in axilla or groin, optic glioma, 2 or are lisch nodule (iris hamartomas), bony lesion (dysplasia of the sphenoid bone or dysplasia or thinking of long bone cortex),
    -osteitis deformano ( paget's disease),
    -bone neoplasms
  • lab: UP.
  • imaging: Tc 99- gold standard, MRI, ct, hires ultrasund.mipi

treatment

non-surgical:

  • observation:
    ca <12 mg%,
    diet should have 800-100 mg of calcium per day,
    avoid thiazides
  • pharmacological: sever hyperca. - Ca > 14 mg% or > 12 mg% + symptoms:
    increase calciuresis: .9 nacl iv.- 2-4 l/d, furosemide 10-20 mg
    decrease bone resorption: pamidronic acid, zoledronic acid, klodronic acid, calcitonin 400-8-- iu iv.
    decrease vit.d activation: hydrocortisone.

surgical:

  • absolute:
    "classical" symptoms,
    ca serum > 12, ca urne >400 mg/24h, bmd score <-2.0 sd,
    pancreatitis, neuromuscular disorder.
  • relative: age <50, progressive renal damage, progressive meant disturbances.
  • Most common cause of hypercalcemia,
  • can occur as part of MEN,

Hypoparathyroidism

  • primary: low PTH activity that cause low ionised ca in extracellular fluid.
  • secondary: low PTH in response to a primary process that causes hypercalcemia
  • primary: low PTH, low ca. / secondary: low PTH, HIGH ca
  • aetiology:
  • absolute lack PTH: iatrogenic, mutation in PTH genome, autoimmune disease.
  • PTH resistance: PTH receptor defect ( blomastrand's chondrodysplasy), pseudohypoparathyroidism 1a, 1c
  • hyper function of ca sensing receptors: familial hypercalciuric hypocalcemia
  • causes:
    -acquired:
    iatrogenic: excision of all parathyroid glands-surgery (common), extensive irradiation, hungry bone syndrome-after parathyroidectomy for hpyperparathyroidism; bones retail ca under influence of osteoblasts.
    autoimmune: type 1 autoimmune polyglandular syndrome (APS1, APCED, HAM syndrome): at least 2 of 3 criteria: chronic mucoctaneous candidiasis, hypoparathyroidism, autoimmune adrenal insufficiency., isolated autoimmune hypoparathyroidism ( common in 7 y.o).
    infiltration: hemochrombtosis, wilson disease, metastatic, amyloidosis, progressive systemic sclerosis.
    metal overload: hypomagnesemia (causes primary hypoparathyroidism), hypermagnesemia (decrease PTH release).
    -congenital:
    branchial dysgenesis (digeorge syndrome).
    HDR syndrome- barakat syndrome (primary Hypoparathyroidism, nerve Deafness, steroid resistant nephrosis (Renal dysplasia)).
    PTH receptor defect ( blomastrand's chondrodysplasy)

symptoms

  • muscles:
    -cramps of lower half of the body.
    -increased neuromuscular irritability - spasmophilia:
    chvostek sign: facial twitching, induced by tapping ipsilateral facial nerve.
    trousseau sign: carpal spasm induced by inflating a blood pressure cuff around the arm.
    -smooth mm. cramp:
    bronchospasm - wheezing
    laryngospasm- hoarseness
    **coronary artery-angina
    peripheral artery-raynaulds syndrome
    cerebral - migraine **
  • neurological: parenthesis , seizures, personality disturbance

complication

cataract, calcifications in soft tissue, especially in basal ganglia (Fahr's syndrome)

treatment

  • tetany onset:
    ca i.v., 1-2 g/day ca orally
    ACTIVE metabolites of vit.d3: calcitriol, alphacalcidol
  • chronic hypoparathyroidism:
    milk-free diet ,
    calcium 1-2 g/d orally, vit. d.
    thiazides
    active metabolites of vit.d3: calcitriol, alphacalcidol

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