Pituitary Disorder Flashcards
What is hyperpituitarism and what causes it?
Hyperpituitarism is a condition characterized by the excessive secretion of trophic hormones from the anterior pituitary gland. The most common cause is a pituitary adenoma, a benign tumor. Other causes include hyperplasia (enlargement due to excessive stimulation by hypothalamic hormones), ectopic hormone production by tumors outside the pituitary, carcinoma of the anterior pituitary, and hypothalamic disorders.
What are the symptoms and signs of hyperpituitarism?
Symptoms depend on the hormone involved but can include:
- Prolactinoma (Prolactin-secreting adenoma): Amenorrhea, galactorrhea, loss of libido, infertility.
- Growth Hormone-secreting adenoma: Gigantism in children (generalized increase in body size with long limbs), acromegaly in adults (enlarged soft tissues, skin, internal organs, hands, feet, facial bones).
- ACTH-secreting adenoma: Cushing’s disease (weight gain, hypertension, glucose intolerance, muscle weakness).
What is hypopituitarism and what causes it?
Hypopituitarism is a condition characterized by a deficiency of one or more pituitary hormones due to damage to the pituitary gland. Causes include tumors and other mass lesions (especially nonfunctioning adenomas), Sheehan syndrome (ischemic necrosis post-partum), surgical or radiation ablation, inflammatory lesions (sarcoidosis or tuberculosis), trauma, and metastatic tumors.
What are the clinical features of hypopituitarism?
The clinical features depend on which hormones are deficient:
- ACTH deficiency: Adrenal insufficiency (fatigue, hypotension, weight loss).
- TSH deficiency: Hypothyroidism (fatigue, weight gain, cold intolerance).
- LH/FSH deficiency: Hypogonadism (amenorrhea, infertility, loss of secondary sexual characteristics).
- GH deficiency: Growth retardation in children, decreased muscle mass and strength in adults.
- Prolactin deficiency: Failure of lactation postpartum.
What are the local mass effects of pituitary tumors?
Local mass effects include:
- Compression of adjacent structures: Can lead to headaches, visual disturbances (e.g., bitemporal hemianopia due to optic chiasm compression), and cranial nerve abnormalities.
- Hypopituitarism: Tumor mass can impair normal pituitary tissue, leading to hormone deficiencies.
- Hypersecretion of hormones: Tumors can cause overproduction of pituitary hormones, leading to conditions like hyperprolactinemia.
- Compression of blood vessels: Can result in reduced blood flow, leading to ischemia or infarction.
- Skull base involvement: Tumor can extend beyond the pituitary, affecting nearby nerves and bones, leading to additional neurological symptoms.
What are lactotroph adenomas (prolactinomas) and their effects?
Lactotroph adenomas secrete prolactin and are the most common type of hyperfunctioning pituitary adenoma. They cause hyperprolactinemia, leading to symptoms such as amenorrhea, galactorrhea, loss of libido, and infertility. Other causes of hyperprolactinemia include pregnancy, high-dose estrogen therapy, renal failure, hypothyroidism, hypothalamic lesions, certain medications, and the stalk effect from masses in the suprasellar region.
What conditions are caused by somatotroph adenomas?
Somatotroph adenomas secrete excessive growth hormone, leading to:
- Gigantism (in children): Excessive growth before epiphyseal plate closure, resulting in a generalized increase in body size with disproportionately long limbs.
- Acromegaly (in adults): Growth hormone excess after epiphyseal plate closure, causing enlargement of soft tissues, internal organs, and certain bones (e.g., face, hands, feet). Metabolic effects include peripheral insulin resistance, gonadal dysfunction, muscle weakness, hypertension, arthritis, congestive heart failure, and increased risk of gastrointestinal cancers.
What is Cushing’s disease and its relation to corticotroph adenomas?
Cushing’s disease is caused by corticotroph adenomas that produce excessive amounts of ACTH, leading to increased cortisol secretion by the adrenal glands (hypercortisolism). It manifests as Cushing syndrome, which includes symptoms like weight gain, hypertension, glucose intolerance, muscle weakness.
What is Cushing’s disease and its relation to corticotroph adenomas?
Cushing’s disease is caused by corticotroph adenomas that produce excessive amounts of ACTH, leading to increased cortisol secretion by the adrenal glands (hypercortisolism). It manifests as Cushing syndrome, which includes symptoms like weight gain, hypertension, glucose intolerance, muscle weakness, and in some cases, hyperpigmented skin due to increased melanocyte-stimulating hormone (MSH) production.
Example symptoms: weight gain, hypertension, glucose intolerance, muscle weakness, hyperpigmented skin.
What is diabetes insipidus and its types?
Diabetes insipidus (DI) is a condition characterized by excessive thirst and the production of large volumes of dilute urine due to a deficiency or dysfunction of vasopressin (ADH). The two main types are:
- Central Diabetes Insipidus: Caused by defects in vasopressin production, release, or action, often due to idiopathic origins, trauma, infections, autoimmune disorders, or genetic mutations.
- Nephrogenic Diabetes Insipidus: Caused by the kidneys’ improper response to vasopressin, due to genetic mutations, chronic kidney disease, or electrolyte imbalances.
Example causes of central diabetes insipidus: idiopathic origins, trauma, infections, autoimmune disorders, genetic mutations.
What are the causes of central diabetes insipidus?
Causes include idiopathic origins, trauma (head injuries, neurosurgery, tumors), infections (encephalitis, meningitis, tuberculosis), autoimmune disorders (autoimmune hypophysitis), and genetic mutations.
Example causes: head injuries, neurosurgery, infections, autoimmune disorders.
What leads to nephrogenic diabetes insipidus?
Causes include inherited genetic mutations affecting kidney function, chronic kidney disease (e.g., polycystic kidney disease, chronic pyelonephritis), and electrolyte imbalances (hypokalemia, hypercalcemia).
Example causes: genetic mutations affecting kidney function, chronic kidney disease, electrolyte imbalances.
What is SIADH?
SIADH is a condition characterized by excessive release and action of antidiuretic hormone (ADH), leading to dilutional hyponatremia (low sodium levels) and the concentration of other solutes in the body.
Example consequence: dilutional hyponatremia.
What are the common causes of SIADH?
Causes include:
- Medications: Antidepressants (SSRIs), anticonvulsants (carbamazepine, oxcarbazepine), antipsychotics (haloperidol, risperidone), certain chemotherapeutic agents.
- Pulmonary Disorders: Lung diseases (pneumonia, COPD, lung cancer, tuberculosis, ARDS).
- CNS Disorders: Brain disorders or injuries (head trauma, brain tumors, infections, stroke, intracranial hemorrhage).
- Malignancies: Cancers (particularly small-cell carcinomas of the lung) producing ectopic ADH or ADH-like substances.
- Postoperative/Post-traumatic States: After major surgeries or severe physical trauma.
- Other Causes: Severe pain, infections (pneumonia, urinary tract infections), autoimmune disorders (systemic lupus erythematosus), endocrine disorders (hypothyroidism, adrenal insufficiency).
Example causes: medications, pulmonary disorders, CNS disorders, malignancies, postoperative/post-traumatic states, other causes.
What are the pathogenesis and clinical manifestations of SIADH?
Pathogenesis involves excessive water retention leading to dilutional hyponatremia. Clinical manifestations include:
- Hyponatremia: Low blood sodium levels.
- Hypoosmolality: Decreased serum osmolality due to dilution.
- Concentrated Urine: High urine osmolality despite low serum sodium.
- Normal Kidney Function: Normal kidney function tests despite impaired water excretion.
- Low BUN Levels: Decreased blood urea nitrogen due to dilution from excess water retention.
Example manifestations: hyponatremia, hypoosmolality, concentrated urine, normal kidney function, low BUN levels.
