Endocrinology fourth

• Growth hormone deficiency in childhood results in pituitary dwarfism, characterized by a proportionally small adult with features like a large head on a proportionally small body.
• Growth hormone excess in childhood causes gigantism, leading to an individual that is proportionally larger in all aspects.

Acromegaly

• Acromegaly usually occurs in adulthood and stems from growth hormone excess, often due to a benign anterior pituitary acidophil adenoma.
• Most growth plates are fused in adults, but any residual growth plates expand.

Clinical Features of Acromegaly

• Enlarging head, hands, and feet necessitate larger hats, gloves, and shoes.
• Chin enlargement causes dentures to become too small, leading to malocclusion and orthodontic changes.
• Cranial nerves can be pinched in bony foramina, resulting in focal neurology.

Visual Field Defects in Acromegaly

• Adenomas can press on the optic chiasm, causing bitemporal hemianopia.

Diagnosing Acromegaly

• A glucose tolerance test can indicate acromegaly if there is a failure of normal GH suppression.
• Elevated serum GH and insulin-dependent GF-1 levels are indicative of acromegaly.
• Lateral skull radiographs may show an enlarged pituitary fossa and erosion of the sella cortex in 90% of cases.
• CT/MRI scans help define tumors in the sella turcica.
• Visual field defects, such as bitemporal hemianopia, may be present.
• Hyperprolactinemia is found in 30% of acromegaly cases.

Managing Acromegaly

• Surgery: Trans-sphenoidal or occlusal trans-frontal pituitary tumor excision may be performed.
• Radiotherapy: It may take 1-10 years to become effective when administered alone.
• Drugs:
  • Octreotide: This long-acting somatostatin analogue controls difficult cases and can shrink inoperable tumors for resection.
  • Bromocriptine: It is prescribed for elderly and frail patients.

Thyroid Mechanism

• The thyroid is controlled by the hypothalamus via TRF.
• The anterior pituitary releases TSH, which stimulates the production of T4 and T3 (more active) in the circulation.
• Most circulating T3 is produced through the peripheral conversion of T4.

Hypothyroidism

• Hypothyroidism is typically a primary disease of the thyroid tissue, resulting in low T3/T4 levels and elevated TSH.
• In rare cases, it results from hypothalamic-pituitary axis disease, leading to low T3/T4 levels and low TSH.

Variations of Hypothyroidism

• Atrophic autoimmune hypothyroidism: The most common cause involves anti-microsomal antibodies and lymphoid infiltrate of the gland, leading to fibrosis and atrophy, often associated with other autoimmune diseases.
• Hashimoto’s thyroiditis: Anti-microsomal antibodies cause atrophic changes with regeneration, resulting in a goiter.
• Iatrogenic hypothyroidism: About 40% of cases become hypothyroid after surgery or radioiodine therapy for hyperthyroidism.
• Iodine deficiency (Goitre): Diets lacking iodine can cause goiters.
• Dyshormonogenesis: Rare inherited conditions caused by genetic enzyme-encoding errors produce defective and ineffective thyroxine.

Clinical Features of Hypothyroidism

• Slower movement
• Coldness
• Macroglossia
• Normocytic/macrocytic anemia
• Hypercholesterolemia
• Hyponatremia

Managing Hypothyroidism

• Lifelong replacement therapy with thyroxine (50-200mcg daily), which supplies T4.
• TSH tests are conducted to ensure the correct dosage.

Severe Hypothyroidism Symptoms

• Hypothermia
• Hypoventilation
• Cardiac failure

Hyperthyroidism

• Grave’s disease: It is the most common cause of hyperthyroidism, resulting from LATS (long-acting thyroid stimulant), which releases IgG molecules. IgG autoantibodies act against TSH receptors, stimulating thyroxine production.
• Solitary toxic nodules: They account for 5% of cases and rarely achieve prolonged remission with drug therapy.
• Toxic multinodular goitre: It primarily affects older women and is rarely successfully treated with drug therapy.
• De Quervian’s Thyroiditis: It causes transient hyperthyroidism secondary to inflammation.

Clinical Features of Hyperthyroidism

• Hot sensation
• Frustration and agitation
• Weight loss

Eye Signs in Grave’s Disease

• Exophthalmos is caused by antibody-mediated retro-orbital inflammation and edema.
• Proptosis limits eye movements, causing lid lag and corneal scarring due to the inability to close eyelids properly.
• Eye signs do not always parallel the course of thyroid disease.

Graves Disease

• A CT scan is needed to exclude a retro-orbital tumor.

Diagnosing Hyperthyroidism

• Thyroid function test: T4 and T3 are elevated, and TSH is suppressed.

Managing Hyperthyroidism

• Drugs:
  • Carbimazole: It inhibits the formation of thyroid hormones while having mild immunosuppressive powers; the dose is gradually reduced after 2-3 weeks.
  • Beta blockers: Used to quickly control sympathetic symptoms.
• Radioiodine I131: Concentrates in the glands, providing localized radiotherapy, and is typically used for women beyond childbearing years or as a salvage after failed surgery or relapse after drug treatment.
• Surgery: Anti-thyroid drugs are discontinued two weeks before resection and replaced with potassium iodide.

Goitre

• Goitre is more common in women.
• It can cause dysphagia or stridor due to pressure on the larynx.
• A bruit in a goitre may reflect increased vascularity.

Physiological Causes of Goitre

• Puberty
• Pregnancy

Pathological Causes of Goitre

• Graves/Hashimoto’s disease
• Iodine deficient endemic goitre
• Benign cyst/lymphoma/carcinoma

Diagnosing Goitre

• Thyroid function tests (TSH/T3/T4) help define hyper/hypo or euthyroid status.
• Radiographic thoracic inlet is studied.

Parathyroid Hormone

• PTH works with Vitamin D to defend serum ionized calcium.
• Its activity is controlled by a direct negative feedback loop where serum Ca affects the four parathyroid glands.
• The upper two parathyroid glands lie behind the thyroid level at the level of the superior thyroid artery, and the lower pair usually lies below the uppers.

Hyperparathyroidism

• Hyperparathyroidism: Increased secretion of parathyroid hormone (PTH).
• Primary hyperparathyroidism: Unstimulated PTH excess by adenoma inappropriate to serum Ca level.
• Approximately 50% of patients with primary hyperparathyroidism present with renal stones, bone disease, or peptic ulcers.
• On an X-ray, there is general porosis of bone with loss of cortex and trabecular pattern and pepper pot skull.
• Osteoclast masses can erode dental roots.

Biochemical Features of Primary Hyperparathyroidism

• Serum Ca is elevated, and phosphate levels are decreased.
• Serum PTH is elevated despite high Ca levels.
• Increased alkaline phosphatase indicates bone resorption.
• Hypercalciuria is present (24-hour collection).

Treating Primary Hyperparathyroidism

• Resect adenoma, located via CT/MRI, neck ultrasound, selective venous sampling, and a Thallium-Technetium subtraction scan.
• All four glands must be identified since adenomas can arise in any, and Calcium and Vitamin D are given to avoid tetany from hypocalcemia.

Secondary Hyperparathyroidism

• PTH hypersecretion develops in response to gut malabsorption of Ca or chronic renal failure Ca losses.
• All glands are hyperplastic as they work to defend serum calcium.

Tertiary Hyperparathyroidism

• Develops when a secondary hyperplastic parathyroidism gland develops autonomy, resulting in an adenoma and the gland not compensating for Ca losses; it is treated as for primary.