Causes and mechanisms of development
The disease occurs due to hyperfunction of the parathyroid glands. In the vast majority of cases, the cause is the formation of an adenoma, while diffuse hyperplasia of the glandular tissue is less common. Women who have reached the age of fifty are traditionally in the risk group.
Excess parathyroid hormone triggers a cascade of reactions leading to a pathological increase in blood calcium levels (hypercalcemia). This process is mediated through three main mechanisms:
- Bone resorption: calcium is intensively leached from the bone tissue.
- Intestinal absorption: calcium absorption in the gastrointestinal tract increases manifold.
- Renal retention: renal excretion of the element decreases due to enhanced reabsorption in the renal tubules.
General clinical picture
Symptoms in hyperparathyroidism develop extremely slowly, which is why patients do not seek medical help for a long time. Nonspecific manifestations often come to the fore:
- Dyspeptic syndrome: patients complain of nausea, episodes of vomiting, loss of appetite, and noticeable weight loss.
- Psychoneurological and muscular disorders: deep depression, general lethargy, cramps, and progressive muscle weakness up to muscular atrophy are characteristic.
Bone and visceral forms
Excess parathyroid hormone affects specific target organs, producing two classic clinical variants of the disease.
The bone form is caused by total demineralization of the skeleton, which inevitably leads to systemic osteoporosis. The main danger of this condition is pathological fractures. X-rays reveal localized destructive lesions in the form of cysts. Typical sites of involvement include the spine, pelvic bones, ribs, wrists, and long tubular bones.
The visceropathic form manifests as damage to internal organs:
- Kidneys: affected in the majority of patients. Urolithiasis (nephrolithiasis) and deposition of calcium salts directly in the renal parenchyma (nephrocalcinosis) develop.
- GI tract: peptic ulcer disease of the stomach or duodenum is found in every fifth patient, and the risk of pancreatitis is also high.
Rare manifestations include myocardial involvement (calcification), joint syndrome (chondrocalcinosis), and inflammation of the salivary glands (parotitis).
Diagnostics and differential search
The key laboratory sign of hyperparathyroidism is hypercalcemia. An important diagnostic detail: calcium levels may further increase after taking bendroflumethiazide (or hydrochlorothiazide).
Since hypercalcemia occurs in numerous other diseases, the physician must perform a thorough differential diagnosis. First of all, the following are excluded:
- Oncological pathology: multiple myeloma and malignant tumors producing osteolytic metastases.
- Other endocrinopathies: acromegaly, thyrotoxicosis, adrenal insufficiency.
- Alimentary and iatrogenic factors: vitamin A and D overdose, as well as milk-alkali syndrome (occurring during ulcer treatment with large amounts of milk and alkalis).
Principles of treatment
The main goal of therapy is the most rapid possible reduction of plasma calcium concentration. Treatment is divided into conservative and surgical.
Conservative therapy includes a comprehensive set of measures:
- Forced diuresis: administration of diuretics (e.g., furosemide) to accelerate renal calcium excretion.
- Rehydration: intravenous administration of sodium chloride, which is especially critical in untamable vomiting.
- Calcium binding in the blood: use of chelating agents (Na-EDTA).
- Phosphorus replenishment: infusions of phosphate solutions.
- Hormonal correction: glucocorticoids (prednisolone) are prescribed for life-threatening hypercalcemia.
Surgical treatment is a radical method and is strictly indicated in cases where computed tomography (CT) reliably confirms the presence of a parathyroid tumor.
Briefly: answers to topical questions
What are the normal values of total and ionized calcium in the blood?
The sources do not provide normal values for ionized calcium in the blood. For total calcium, it is indicated that hypercalcemia is an increase in the total serum calcium content above the normal range; a value of > 2.57 mmol/L (or 10.3 mg%) is cited.
What ECG changes are characteristic of severe hypercalcemia?
Hypercalcemia is characterized by changes in time intervals, in particular, shortening of the Q-T interval.
What specific laboratory urine markers are used to diagnose hyperparathyroidism?
The sources do not specify laboratory urine markers for the diagnosis of hyperparathyroidism. It is only mentioned that excess parathyroid hormone (PTH) leads to hypercalciuria (increased urinary calcium excretion) and phosphaturia.
To remember the main target organs in hyperparathyroidism, use the rule "BPT" (Bones, Kidneys, Tummy): Bones — osteoporosis and fractures; Kidneys — stones and nephrocalcinosis; Tummy — nausea, ulcers, and pancreatitis.
Class and exam questions
Why does hypercalcemia develop in hyperparathyroidism?
Excess parathyroid hormone forces bone tissue to release calcium into the blood (resorption), while simultaneously forcing the intestine to absorb it in large volumes and the kidneys to retain it by reducing urinary excretion.
What radiological changes are characteristic of this disease?
Radiographs of long tubular bones, the spine, ribs, and pelvis visualize signs of systemic osteoporosis and specific destructive lesions resembling cysts.
Which iatrogenic conditions must hyperparathyroidism be differentiated from?
First of all, with vitamin D and A overdose, as well as with milk-alkali syndrome, which can develop against the background of irrational treatment of peptic ulcer disease.
In which cases is surgical intervention indicated?
Surgery is indicated if CT results visualize and prove a parathyroid tumor (adenoma).
What else to study on this topic
- Pathogenesis of GI ulcer formation in hypercalcemia
- Mechanism of action of Na-EDTA in relieving hypercalcemic crisis
- Features of milk-alkali syndrome in differential diagnosis
- Mechanisms of chondrocalcinosis formation in hyperparathyroidism
- The role of glucocorticoids in emergency therapy of hypercalcemia
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