What is the pathophysiology of hypoparathyroidism?
Insufficient parathyroid hormone (PTH) production leading to decreased blood calcium levels.
How does negative feedback regulation work in the parathyroid glands?
Parathyroid glands produce PTH when calcium is low; PTH mobilizes calcium; when calcium rises, hormone production stops.
What happens when parathyroid function is impaired?
Decreased PTH → decreased calcium levels in the blood.
What are the main causes of hypoparathyroidism?
How does low magnesium affect hypoparathyroidism?
Magnesium is required for PTH secretion; low Mg impairs PTH release, worsening hypocalcemia.
What are the clinical manifestations of hypoparathyroidism related to low calcium?
Hair dryness/loss, nail ridges/breakage, dry skin, bone loss, tingling in extremities, visual changes, muscle cramps, seizures, fatigue, positive Chvostek’s sign.
What does a positive Chvostek’s sign indicate?
Neuromuscular irritability due to hypocalcemia.
How is hypoparathyroidism diagnosed?
Based on medical/surgical history, physical examination, and lab tests.
What might be observed during a physical exam for hypoparathyroidism?
Brittle nails, dry skin, and other visible calcium deficiency signs.
What lab findings are seen in hypoparathyroidism?
Low PTH, low calcium, high phosphorus, low or normal magnesium, and low urinary calcium.
What does low magnesium in hypoparathyroidism suggest?
That magnesium deficiency may be the cause of the disorder or contributing to symptoms.
What are the treatments for hypoparathyroidism?
Calcium supplementation (carbonate or citrate), Vitamin D (enhances calcium absorption), Calcitriol, and recombinant/synthetic parathyroid hormone.
What is the role of Vitamin D in hypoparathyroidism treatment?
Enhances calcium absorption from the GI tract.
What is the pathophysiology of Cushing Syndrome?
Excess glucocorticoid (cortisol) secretion from the adrenal cortex affecting metabolism, stress response, and immune/inflammatory function.
What are the four major causes of Cushing Syndrome?
What happens when corticosteroids like prednisone are taken long-term?
Exogenous Cushing’s develops, leading to moon face, trunk obesity, and buffalo hump.
What are the metabolic alterations in Cushing Syndrome?
Excess circulating glucose, glucose intolerance, suppressed immune/inflammatory response, behavioral changes, and impaired stress response.
What is the typical body appearance in Cushing Syndrome?
Truncal obesity, moon face, and buffalo hump.
Why do patients with Cushing Syndrome have glucose intolerance?
Excess cortisol promotes gluconeogenesis and decreases insulin sensitivity.
Why is inflammation and immunity suppressed in Cushing Syndrome?
Cortisol suppresses immune and inflammatory responses, making patients more prone to infections.
What behavioral changes occur in Cushing Syndrome?
Mood swings, irritability, insomnia, and sometimes depression.
What happens to the stress response in Cushing Syndrome?
It becomes impaired; the body remains in a constant “fight or flight” state.
How is Cushing Syndrome diagnosed?
Elevated cortisol in 24-hour urine, low-dose dexamethasone suppression test (no suppression = high cortisol), and imaging for tumors.
How is a 24-hour urine collection for cortisol performed?
Patient voids and discards first urine; collection starts after that and continues for 24 hours; urine is stored in a jug on ice or in a refrigerator.