Chapter 20: Alterations of Hormonal Regulation

SIADH

Excessive secretion (hypersecretion) or action of ADH (antidiuretic hormone) despite normal or low plasma osmolality.

SIADH Causative Factors

CNS Disorders (strokes, tumors, trauma, surgery), malignancy (small cell lung cancer), SSRIs, carbamazepine.

SIADH Pathophysiology

Excess ADH -> acts on the renal collecting ducts -> increases permeability to water -> Water reabsorption -> Dilutional Hyponatremia.

Hyponatremia

More water than sodium in the body.

SIADH Clinical Manifestations

Hypoosmolality (<280 mOsm/kg), Urine is hyperosmolality, Cerebral edema, Hyponatremia, Weight Gain.

Hypoosmolality

Measures the concentration of fluid in the blood.

SIADH Treatments

Fluid restriction (too much fluid in body), ADH receptor antagonists; Vaptans or Demeclocycline (help block ADH at kidneys), Loop diuretics and sodium supplements (helps with Hyponatremia).

SIADH Prognosis

Depends on cause and sodium correction.

Diabetes Insipidus

Insufficient/hyposecretion of ADH or renal insensitivity (nephrogenic DI).

Diabetes Insipidus Causative Factors

Head trauma, pituitary surgery, lithium toxicity, renal damage.

Diabetes Insipidus Neurogenic

Central Diabetes Insipidus, insufficient ADH, idiopathic, CNS (injury, surgery, trauma).

Diabetes Insipidus Nephrogenic

Insensitivity to or inadequate response to ADH. This increases permeability of the membrane.

Diabetes Insipidus Pathophysiology

Acts on collecting ducts & distal tubules -> increasing membrane permeability to & reabsorption of water -> hypernatremia.

Diabetes Insipidus Clinical Manifestations

Polyuria, polydipsia, nocturia, voluminous & diluted urine, hyperosmolality (>300 mOsm/kg), Hypernatremia (not enough fluid in blood).

Diabetes Insipidus Neurogenic Treatment

Fluid replacement, desmopressin (helps kidneys retain water).

Diabetes Insipidus Nephrogenic Treatment

Treating underlying cause & discontinuing medication and precautions when traveling.

Diabetes Insipidus Prognosis

Good with treatment; depends on etiology.

Hyperthyroidism

Results from excess T3/T4 which increases metabolism.

Graves' Disease

Autoimmune disorder that results in the overproduction of thyroid hormones and typically women 20-40 years of age.

Hyperthyroidism + Graves' Disease

It causes antibodies to stimulate TSH receptors leading to goiter and exophthalmos. High T3/T4 & Low TSH.

Thyroid storm

Life-threatening hypermetabolic crisis.

Graves Disease Clinical Manifestations

Tachycardia (increased BP) or Arrhythmias, Diaphoresis, Tremors, Loose Stools, Thin but Increased Appetite, Flushed & Warm, Heat Intolerance.

Hyperthyroidism + Graves Disease Treatment

Antithyroid drugs (propylthiouracil), beta blockers, radioactive iodine, surgery.

Hyperthyroidism + Graves Disease Complications

Tachyarrhythmias, High-output Heart Failure, Hypertension, Hyperglycemia, Osteoporosis.

Hypothyroidism

Deficient production of thyroid hormones (T3 & T4) or impaired action of these hormones, resulting in slowed metabolism in virtually all body systems. Low T3/T4 & High TSH.

Hypothyroidism Causes

Hashimoto's Thyroiditis, Iodine Deficiency, Thyroidectomy, Radiation or Drug induced.

Hypothyroidism Symptoms

Pale cool skin with edema, Cold intolerance, fatigue, Bradycardia, Weight increase with decreased appetite.

Hypothyroidism Treatment

Lifelong Levothyroxine replacement, make sure to start low & go slow in older adults. Myxedema coma, Thyroid hormone combined with circulatory & ventilatory support.

Type 1 Diabetes Mellitus Onset

Childhood/Adolescence.

Type 1 Diabetes Mellitus Etiology

Autoimmune beta cell destruction -> absolute insulin deficiency, Idiopathic, Genetic, Environmental (viral, cow milk).

Type 1 Diabetes Mellitus Pathophysiology

Cell-mediated destruction of beta cells. No insulin -> ketone production.

Type 1 Diabetes Signs & Symptoms

Polyphagia, weight loss, blurry vision, polyuria and polydipsia.

Type 1 Diabetes Mellitus Treatment

Insulin Therapy.

Type 1 Diabetes Mellitus Complications

Diabetic Ketoacidosis (DKA), Hypoglycemia (Insulin Shock); lowered plasma glucose level.

Type 2 Diabetes Mellitus Onset

Adulthood (>45 years).

Type 2 Diabetes Mellitus Etiology

Family history, hypertension, dyslipidemia. Insulin resistance + beta cell dysfunction.

Type 2 Diabetes Mellitus Pathophysiology

Insulin resistance in peripheral tissues, failure of compensation by beta cells. Insulin is present but ineffective.

Type 2 Diabetes Mellitus Signs & Symptoms

Hyperglycemia, Glucosuria, Polyuria, Polydipsia, Polyphagia, Unexplained weight loss, blurred vision, lower extremity paresthesia, yeast infections.

Type 2 Diabetes Mellitus Treatment

Lifestyle modification, oral agents and insulin if needed.

Diabetes Ketoacidosis (Type 1)

An absolute or relative deficiency of insulin.

Diabetes Ketoacidosis Pathophysiology

Insufficient insulin in blood -> hyperglycemia. Mobilization of lipids -> production of ketones -> acidosis.

Diabetes Ketoacidosis Clinical Manifestations

Polyuria, dehydration, Kussmaul's respirations, acetone breath.

Diabetes Ketoacidosis Factors

Infection, trauma, surgery, diet, alcohol.

Diabetes Ketoacidosis Treatment

Insulin + IV Fluids + bicarbonate. Replacement of electrolytes & Monitor potassium K+ level.

Hyperosmolar Hyperglycemic Syndrome (Type 2)

Extreme hyperglycemia, dehydration, and no ketosis. Life threatening emergency.

Hyperosmolar Hyperglycemic Syndrome Factors

Infections, Medications, Noncompliance, Coexisting Disease.

Hyperosmolar Hyperglycemic Syndrome Treatment

Treat with fluids, insulin.

Hypoglycemia

Confusion, sweating, tremors.

Microvascular Complications of Diabetes

Retinopathy, nephropathy, neuropathy.

Macrovascular Complications of Diabetes

CAD, Stroke, PVD.

Diabetes Mellitus Prevention

Glucose control, BP, Lipid management, Screenings.

Hypercortisolism (Cushing Disease)

Excessive anterior pituitary secretion of adrenocorticotropic hormone (ACTH).

Hypercortisolism Causative Factors

Pituitary adenoma/adrenal tumor, steroids.

Hypercortisolism Pathophysiology

Excess cortisol -> protein breakdown.

Hypercortisolism Clinical Manifestations

Moon face, buffalo hump, obese trunk, bruising of skin, fatigue, weakness, delayed healing.

Hypercortisolism Treatment

Remove tumor, taper steroids.

Hypocortisolism (Addison's Disease)

Deficiency of adrenocorticoid secretions; aldosterone & cortisol.

Hypocortisolism Causative Factors

Autoimmune destruction. Infection.

Hypocortisolism Pathophysiology

Cortisol/aldosterone deficiency -> sodium loss.

Hypocortisolism Clinical Manifestations

Weight loss, fatigue, anorexia, nausea, diarrhea, hypotension, syncope, hyperpigmentation.

Hypocortisolism Treatment

Lifelong steroid replacement.

Addison's Disease Pathophysiology

There is a deficiency of cortisol (glucocorticoids) & aldosterone (mineralocorticoids). Deficiency of adrenocorticoid secretions from the dysfunction/destruction of the adrenal cortex.

Addison's Disease Evaluation

ACTH stimulation test (no cortisol rise), hyponatremia, hyperkalemia, low glucose.

Addison's Disease Treatment

Lifelong steroid replacement, glucocorticoid replacement. Stress management, emergency IM hydrocortisone for crisis.

What is hypersecretion in the context of growth disorders?

Hypersecretion refers to excess secretion of growth hormone (GH) and insulin-like growth factor 1 (IGF-1), leading to conditions like gigantism and acromegaly.

Hypersecretion Pathogenesis

Excess secretion of GF & IGF-1 insulin-like growth factor

What is gigantism and when does it occur?

Gigantism is characterized by excessive growth hormone secretion before the epiphyseal plate closes, resulting in tall statures.

What is acromegaly and when does it occur?

Acromegaly occurs when there is excess growth hormone secretion after the epiphyseal plate closes, leading to bone thickening and soft tissue growth.

What are some clinical manifestations of hypersecretion of growth hormone?

Clinical manifestations include transfrontal scar, frontal bossing, protruding jaw, enlarged tongue, and larger hands and feet.

What are the risks associated with gigantism and acromegaly?

Risks include hypertension, atherosclerosis, type 2 diabetes mellitus (DM), and coronary artery disease (CAD).

What are the treatment options for gigantism and acromegaly?

Treatment options include surgery, medication (for a short time), and radiation.