flowchart TD
A(Gland)
B(Too little)
C(Too much)
B1(Hormone Therapy)
C1(Counteracting Medication)
C2(Surgery)
A-->B
A-->C
B-->B1
C-->C1
C-->C2
C2-->B1
- Growth Hormone:
- Achondroplasia and Primordial Dwarfism: resultant of hyposecretion of GH. The method of treatment involves:
- Management:
- Hormone Therapy: Growth Hormone and/or Thyroid Hormone.
- Distraction Osteogenesis and Metal Rod use can allow a patient with dwarfism to become taller.
- Management:
- Gigantism and Acromegaly: resultant of hypersecretion of GH. The difference between gigantism and acromegaly is whether the onset of hypersecretion precedes or succeeds the closure of the epiphyseal plates. The most common cause of this disorder is a secretory pituitary tumor. This appears as large extremities, organs (organomegaly), joint pains, hyperglycemia, prognathism (underbite due to bone deformity), hypertension, dysphagia, and a deep voice.
- Management:
- Medication: Bromocriptine Mesylate (Parlodel) can act as a growth hormone suppressant. It can produce orthostatic hypotension, and must be administered with meals.
- Surgery: Transphenoidal Hypophysectomy to remove the pituitary gland or tumor.
- Post-operative:
- Elevate the head of bed for two weeks.
- Nasal packing to compress the incision site.
- Instruct the patient to NOT BLOW their nose, as this can damage the surgical site.
- Assess for nasal drainage, taking note of the halo sign, a sign of CSF leakage. Drainage is placed on a clean dressing, then allowed to dry. In a few minutes, CSF would try and produce a “halo” appearance. This is an indication of CSF leakage and is a danger sign.
- Management:
- Achondroplasia and Primordial Dwarfism: resultant of hyposecretion of GH. The method of treatment involves:
- Antidiuretic Hormone:
- Syndrome of Inappropriate Antidiuretic Hormone (SIADH): resultant of hypersecretion of ADH. This may be caused by trauma, cerebrovascular disease, or a tumor. The inhibition of fluid excretion (i.e., excessive fluid retention) results in edema (and weight gain), hypertension, and dilutional hyponatremia.
- Management:
- Medication: Diuretics, hypertonic IV (reduce edema)
- Fluid restriction through education (“hidden fluids”) and by avoiding stimuli that enhance thirst or hunger.
- Safe environment is required; hyponatremia can alter the level of consciousness.
- Management:
- Diabetes Insipidus (DI): resultant of hyposecretion of ADH (Central DI). This may also be due to an inability of the kidneys to recognize and respond to ADH (Nephrogenic DI). The kidneys will then excrete dilute (low specific gravity) urine excessively, producing dehydration that triggers excessive thirst. The lack of fluids also produces constipation as stool becomes dry. The reduction in blood fluid volume will produce hemoconcentration— concentration hypernatremia
- Management:
- Hormone Therapy: Desmopressin/Vasopressin via transmucosal spray or nasal spray. Side effects include stomatitis, allergies, and chest tightness. An alternative for this can be used as subcutaneous medication.
- Management:
- Syndrome of Inappropriate Antidiuretic Hormone (SIADH): resultant of hypersecretion of ADH. This may be caused by trauma, cerebrovascular disease, or a tumor. The inhibition of fluid excretion (i.e., excessive fluid retention) results in edema (and weight gain), hypertension, and dilutional hyponatremia.
- Thyroid Hormones: triiodothyronine (T3), thyroxine (T4), calcitonin, parathyroid hormone (parathormone)
- Hypothyroidism: a deficiency of T3 and T4. This may be due to exposure to drugs that inhibit the thyroid, following a thyroidectomy, or autoimmune (Hashimoto’s Thyroiditis). A reduction of these hormones will cause a depression in metabolic processes, resulting in an intolerance to cold (decreased heat production), weight gain (unused calories), dry skin, constipation, bradycardia, bradypnea, apathy, slow speech, dull expressions, extreme fatigue, anorexia, etc. All of these signs are “low”, except for weight gain and menstrual disturbances (menorrhagia, polymenorrhea).
- Management:
- Hormone Therapy: Levothyroxine Sodium (Synthroid), (Levothyroid, Cytomel, Thyrolar, Thycar). These are taken without food.
- Diet: low calorie, low cholesterol, low fat (reduce intake to match reduced metabolism), and high fiber (counteract constipation)
- Management:
- Hyperthyroidism: an excess of T3 and T4. This may due to emotional stress, autoimmune (Graves’ disease), or tumors. These mirror the effects of hypothyroidism; all of the signs are “high”, except for weight loss and menstrual disturbances (amenorrhea). Another classical sign of this disease is exophthalmos.
- Management:
- Diet: high calorie diet to supply the high metabolic rate of the individual
- Rest: the patient is easily fatigued; a non-stimulating, safe environment must be provided for safety.
- Artificial Tears are given to prevent corneal ulceration due to exophthalmos.
- Avoid Stimulants, as these further amplify the effect of the disorder.
- Medications:
- Tapazole, an anti-thyroid medication.
- Beta-blockers and Calcium channel blockers
- Oral radioactive iodine (131I) uptaken by the thyroid, which is then inhibited. This takes six to eight weeks to take effect, and is contraindicated in pregnancy.
- Surgery: Thyroidectomy, either total or subtotal.
- Post-operative:
- Monitor for hypocalcemia (Chvostek/Trousseau’s Sign) from the removal of the parathyroid glands. These also produce paresthesias and tetany. Patients are given calcium supplements as maintenance, and given calcium gluconate IV in cases of emergency.
- Management:
- Hypothyroidism: a deficiency of T3 and T4. This may be due to exposure to drugs that inhibit the thyroid, following a thyroidectomy, or autoimmune (Hashimoto’s Thyroiditis). A reduction of these hormones will cause a depression in metabolic processes, resulting in an intolerance to cold (decreased heat production), weight gain (unused calories), dry skin, constipation, bradycardia, bradypnea, apathy, slow speech, dull expressions, extreme fatigue, anorexia, etc. All of these signs are “low”, except for weight gain and menstrual disturbances (menorrhagia, polymenorrhea).
- Adrenal Hormones: adrenal cortex (glucocorticoids, sex hormones, mineralocorticoids), and adrenal medulla (epinephrine, norepinephrine)
- Addison’s Disease: an insufficiency of the hormones of the adrenal cortex. This may be the result of an autoimmune process. Altered levels of cortex hormones results in hypoglycemia, weight loss, hypotension, changes in body hair distribution (sex hormones), GI disturbances, and weakness.
- A bronze skin appearance (hyperpigmentation) occurs in Addison’s as the efforts of the body to increase ACTH also stimulates the production of melanocyte-stimulating hormone (MSH) through the production of the requisite proopiomelanocortin protein. This also affects other parts of the body and mucosa that are pigmented.
- In an Addisonian crisis (extremely low levels of adrenal hormones), profound fatigue, dehydration, vascular collapse, renal shut down, decreased sodium, and increased potassium can occur.
- Management:
- Hormone Therapy: glucocorticoids, mineralocorticoids, hydrocortisone
- Monitoring: vital signs, weight, glucose, potassium levels (observe for potential crisis)
- Diet: high calorie, low-potassium, high-sodium diet to counteract electrolyte imbalances and weight loss.
- Cushing’s Disease: hypercortisolism, often caused by steroid medications. Normally, cortisol will increase blood sugar, increase memory and attention, increase blood pressure, suppress the immune system, decrease sensitivity to pain, and decrease serotonin. In hypercortisolism, hyperglycemia, hypotension, inattention, immunosuppression, increased sensitivity to pain, and depression may occur. This is the opposite of Addison’s, producing hypokalemia and increasing the level and effect of adrenal hormones.
- A Cushingoid appearance is unique; truncal obesity, moon face, and a buffalo hump are all classic characteristics of a patient with Cushing’s. Additionally, reddish-purple striae (like stretch marks) on the trunk, hirsutism, and acne can appear.
- Hypertension, hyperglycemia, hypokalemia, and immunosuppression.
- Management:
- Medication: Mitotane (Lysodren) is a cortisol-reduction drug used for patients with Cushing’s disease.
- Monitoring: weight, vital signs, serum sodium, and serum potassium.
- Surgery: removal of the pituitary (hypophysectomy) or a tumor if ACTH is the cause of excessive cortisol, or removal of the adrenal glands themselves (bilateral or unilateral adrenalectomy)
- After removal of an adrenal gland, the remaining adrenal gland may be able to return the body to normal functioning in two years, and hormone replacement therapy will end then. If both adrenal glands are removed, hormone replacement therapy after adrenalectomy is continued life-long.
- Pheochromocytoma: a secretory tumor of the adrenal medulla that produces catecholamines (epinephrine, norepinephrine). Its cause is unknown. There are five general manifestations (mn. 5 H’s): hypertension (hallmark), headache, hyperhidrosis, hypermetabolism, and hyperglycemia. These are all effects of catecholamines.
- Management:
- Do not palpate the abdomen in the presence of a tumor. This can cause a sudden excretion of its catecholamine contents, or a rupture of the tumor.
- Monitoring: vital signs and blood glucose.
- Position the patient with the head of the bed elevated.
- An adrenalectomy may be performed to remove the tumor. Adrenal hormone replacement therapy will be required for two years following a unilateral adrenalectomy.
- Management:
- Addison’s Disease: an insufficiency of the hormones of the adrenal cortex. This may be the result of an autoimmune process. Altered levels of cortex hormones results in hypoglycemia, weight loss, hypotension, changes in body hair distribution (sex hormones), GI disturbances, and weakness.
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