Chap 18, Endocrine System, Pathology Flashcards Preview

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Flashcards in Chap 18, Endocrine System, Pathology Deck (30)


Enlargement of the thyroid gland. Low iodine levels in diet lead to low T3 and T4 levels. This causes feedback to the hypothalamus and adenohypophysis, stimulating them to secrete releasing factors and TSH. TSH then promotes the thyroid gland to secrete T3 and T4, but because there is no iodine available, the only effect is to increase the size of the gland (goiter). Prevention includes increasing the supply of iodine (as iodized salt) in the diet.


endemic goiter

Enlargement of the thyroid gland. Occurs in certain regions where there is a lack of iodine in the diet. Low iodine levels in diet lead to low T3 and T4 levels.


nodular or adenomatous goiter

Hyperplasia occurs as well as formation of nodules and adenomas. Some patients with nodular goiter develop hyperthyroidism with clinical signs and symptoms such as rapid pulse, tremors, nervousness, and excessive sweating. Treatment is with thyroid-blocking drugs or radioactive iodine to suppress thyroid functioning.



Overactivity of the thyroid gland; thyrotoxicosis.

The most common form of this condition is Graves disease (resulting from autoimmune processes). Because metabolism is faster, the condition is marked by an increase in heart rate (with irregular beats), higher body temperature, hyperactivity, weight loss, and increased peristalsis (diarrhea occurs). In addition, exophthalmos (protrusion of the eyballs, or proptosis) occurs as a result of swelling of tissue behind the eyball, pushing it forward. Treatment of Graves disease includes management with antithyroid drugs to reduce the amount of thyroid hormone produced by the gland and administration of radioactive iodine, which destroys the overactive glandular tissue.



Underactivity of the thyroid gland.

Any of several conditions can produce hypothyroidism (thyroidectomy, thyroiditis, endemic goiter, destruction of the gland by irradiation), but all have similar physiologic effects. These include fatigue, muscular and mental sluggishness, weight gain, fluid retention, slow heart rate, low body temperature, and constipation. Two examples of hypothyroid disorders are myxedema and cretinism.



Advanced hypothyroidism in adulthood. Atrophy of the thyroid gland occurs, and practically no hormone is produced. The skin becomes dry and puffy (edema) because of the collection of mucus-like (myx/o = mucus) material under the skin. Many patients also develop atherosclerosis because lack of thyroid hormone increases the quantity of blood lipids (fats). Recovery may be complete if thyroid hormone is given soon after symptoms appear.



Extreme hypothyroidism during infancy and childhood leads to a lack of normal physical and mental growth. Skeletal growth is more inhibited than soft tissue growth, so the affected person has the appearance of an obese, short, and stocky child. Treatment consists of administration of thyroid hormone, which may be able to reverse some of the hypothyroid effects.


thyroid carcinoma

Cancer of the thyroid gland.



Excessive production of parathormone. Hypercalcemia occurs as calcium leaves the bones and enters the bloodstream, where it can produce damage to the kidneys and heart. Bones become decalcified with generalized loss of bone density (osteoporosis) and susceptibility to fractures and formation of cysts. Kidney stones can occur as a result of hypercalcemia and hypercalciuria. The cause is parathyroid hyperplasia or a parathyroid tumor. Treatment is resection of the overactive tissue. Medical therapy is another option for the patient who is not a surgical candidate. Bisphosphonates, such as alendronate (Fosamax), decrease bone turnover and decrease hypercalcemia.



Deficient production of parathyroid hormone. Hypocalcemia results as calcium remains in bones and is unable to enter the bloodstream. This leads to muscle and nerve weakness with spasms of muscles, a condition called tetany (constant muscle contraction). Administration of calcium plus large quantities of vitamin D (to promote absorption of calcium) can control the calcium level in the bloodstream.


adrenal virilism

Excessive secretion of adrenal androgens. Adrenal hyperplasia or more commonly adrenal adenomas or carcinomas can cause virilization in adult women. Signs and symptoms include amenorrhea, hirsutism (excessive hair on the face and body), acne, and deepening of the voice. Drug therapy to suppress androgen production and adrenalectomy are possible treatments.


Cushing syndrome

Group of signs and symptoms produced by excess cortisol from the adrenal cortex. A number of signs and symptoms occur as a result of increased cortisol secretion, including obesity, moon-like fullness of the face, excess deposition of fat in the thoracic region of the back (so-called buffalo hump), hyperglycemia, hypernatremia, hypokalemia, steoporosis, virilization, and hypertension. The cause may be excess ACTH secretion or tumor of the adrenal cortex. Tumors and disseminated cancers can be associated with extopic sectretion of hormone, such as extopic ACTH produced by nonendocrine neoplasms (lung and thyroid tumors).

In clinical practice, most cases of Cushing syndrome result from chronic use of cortisone-like drugs, such as steroids. Examples are the cases in young athletes seeking to improve their performance and in patients treated for autoimmune disorders, asthma, kidney, and skin conditions. Steroids (prednisone is an example) are never discontinued abruptly because the adrenal cortex and pituitary gland (ACTH producer) need time to "restart" after long periods of prescribed cortisol use (the adrenal gland stops producing cortisol when cortisol is given as therapy).


Addison disease

Hypofunctioning of the adrenal cortex. The adrenal cortex is essential to life. When aldosterone and cortisol blood levels are low, the patient experiences generalized malaise, weakness, muscle atrophy, and severe loss of fluids and electrolytes (with hypoglycemia, low blood pressure, and hyponatremia). An insufficient supply of cortisol signals the pituitary to secrete more ACTH, which increases pigmentation of scars, skin folds, and breast nipples (hyperpigmentation).

Primary insufficiency is believed to be due to autoimmune adrenalitis. Treatment consists of daily cortisone administration and intake of salts or administration of a synthetic form of aldosterone.



Benign tumor of the adrenal medulla; tumor cells stain a dark or dusky (phe/o) color (chrom/o).

The tumor cells produce excess secretion of epinephrine and norepinephrine. Signs and symptoms are hypertension, tachycardia, palpitations, severe headaches, sweating, flushing of the face, and muscle spasms. Surgery to remove the tumor and administration of antihypertensive drugs are possible treatments.



Excess secretion of insulin causing hypoglycemia. The cause may be a tumor of the pancreas (benign adenoma or carcinoma) or an overdose of insulin. Hypoglycemia occurs as insulin draws sugar out of the bloodstream. Fainting spells, convulsions, and loss of consciousness are common because a minimal level of blood sugar is necessary for proper mental functioning.


diabetes mellitus (DM)

Lack of insulin secretion or resistence of insulin in promoting sugar, starch, and fat metabolism in cells. In diabetes mellitus (mellitus means sweet or sugary), insulin insufficiency or ineffectiveness prevents sugar from leaving the blood and entering the body cells, where it is used to produce energy. There are two types of diabetes mellitus. Type 1 diabetes and Type 2 diabetes.


Type 1 diabetes

Autoimmune disease. Autoantibodies against normal pancreatic islet cells are present. Onset is usually in early childhood but can occur in adulthood, and the etiology involves destruction of the beta islet cells producing complete deficiency of insulin in the body. Patients usually are thin and require frequent injections of insulin to maintain a normal level of glucose in the blood. Type 1 requires patients to monitor their blood glucose levels several times a day using a glucometer.


Type 2 diabetes

Separate disease from type 1. Patients often are older, and usually there is a family history of type 2 diabetes. Obesity is very common. The islet cells are not initially destroyed, and there is a relative deficiency of insulin secretion with a resistance by target tissues to insulin. Insulin resistance usually develops 5 to 10 years before type 2 diabetes is diabnosed, and is associated with an increased risk of cardiovascular disease. Often, high blood pressure, high cholesterol, and central abdominal obesity are seen in people who have insulin resistance.

Treatment of type 2 diabetes is with diet, weight reduction, exercise, and, if necessary, insulin or oral hypoglycemic agents. Oral hypoglycemic agents stimulate the release of insulin from the pancreas and improve the body's sensitivity to insulin.


Complications of diabetes

Both type 1 and type 2 diabetes are associated with primary and secondary complications.


Primary complication of type 1 diabetes

Hyperglycemia. This can lead to ketoacidosis (fats are improperly burned, leading to an accumulation of ketones and acids in the body). Ketoacidosis can also result from illness or infection, and initial symptoms may be upset stomach and vomiting.


Complications from Hypoglycemia

Hypoglycemia occurs when too much insulin is taken by the patient. Insulin shock is severe hypoglycemia caused by an overdose of insulin, decreased intake of food, or excessive exercise. Signs and symptoms are sweating, hunger, confusion, trembling, nervousness, and numbness.

Treatment of severe hypoglycemia is with either a shot of glucagon or intravenous glucose to restore normal blood glucose levels. Convulsions, coma, and loss of consciousness can result if treatment is not given.


Secondary (long-term) Complications from diabetes

Secondary (long-term) complicatons may appear many years after the patient develops diabetes. These include destruction of retinal blood vessels (diabetes retinopathy), causing visual loss and blindness; destruction of the kidneys (diabetic nephropathy), causing renal insufficiency and often requiring hemodialysis or renal transplantation; destruction of blood vessels, with atherosclerosis leading to stroke, heart disease, and peripherovascular ischemia (gangrene, infection, and loss of limbs); and destruction of nerves (diabetic neuropathy) involving pain or loss of sensation, most commonly in the extremities. Loss of gastric motility (gastroparesis) also occurs.


Gestational diabetes

Gestational diabetes can occur in women with a predisposition to diabetes during the second or third trimester of pregnancy. After delivery, blood glucose usually returns to normal. Type 2 diabetes may develop in these women later in life.



Hypersecretion of growth Hormone from the anterior pituitary (adenohypophysis) after puberty, leading to enlargement of extremities.

An excess of growth hormone (GH) is produced by adenomas of the pituitary gland (hypophysis) that occur during adulthood. This excess GH stimulates the liver to secrete a hormone (somatomedin C, or insulin-like growth factor (IGF) that causes the clinical manifestations of acromegaly (acr/o in this term means+ extremities). Bones in the hands, feet, face, and jaw grow abnormally large, producing a characteristic "Frankenstein" -type facial appearance.

Treatment: The pituitary adenoma can be irradiated or surgically removed.



Hypersecretion of growth hormone from the anterior pituitary (adenohypophysis), leading to abnormal overgrowth of body tissues.

Benign adenomas of the pituitary gland that occur before a child reaches puberty produce an excess of growth hormone.

Treatment: Gigantism can be corrected by early diagnosis in childhood, followed by resection of the tumor or irradiation of the pituitary.


Dwarfism; hypopituitary dwarfism

Congenital hyposecretion of growth hormone

Children who are affected are normal mentally, but their bones remain small.

Treatment: consists of administration of growth hormone. Achondroplastic dwarfs differ from hypopituitary dwarfs in that they have a genetic defect in cartilage formation that limits the growth of long bones.



Deficiency of all pituitary hormones.

Tumors of the sella turcica as well as arterial aneurysms may be etiologic factors causing a failure of the pituitary to secrete hormones that stimulate major glands in the body.


Syndrome of inappropriate ADH (SIADH)

Excessive secretion of antidiuretic hormone.

Hypersecretion of ADH produces excess water retention in the body.

Treatment consists of dietary water restriction. Tumor, drug reactions, and head injury are some of the possible causes.


Diabetes insipidus (DI)

Insufficient secretion of antidiuretic hormone (vasopressin).

Deficiency of antidiuretic hormone causes the kidney tubules to fail to hold back (reabsorb) needed water and salts. Clinical manifestations include polyuria and polydipsia.

Treatment: Synthetic preparations of ADH are administered with nasal sprays or intramuscularly.

Insipidus means tasteless, reflecting the condition of dilute urine, as opposed to mellitus, meaning sweet or like honey, reflecting the sugar content of urine in diabetes mellitus.

Both diabetes insipidus and mellitus are characterized by polyuria.


Comparison of Type 1 and Type 2 Diabetes Mellitus


Type 1: Usually occurs before age 30. Abrupt, rapid onset of symptoms. Little or no insulin production. Thin or normal body weight at onset. Ketoacidosis often occurs.

Type 2: Usually occurs after age 30. Gradual onset; asymptomatic. Insulin usually present. 85% are obese. Ketoacidosis seldom occurs.


Type 1: Polyuria (glycosuria promotes loss of water). Polydipsia (dehydration causes thirst). Polyphagia (tissue breakdown causes hunger).

Type 2: Polyuria sometimes seen. Polydipsia sometimes seen. Polyphagia sometimes seen.


Type 1: Insulin

Type 2: Diet (weight loss); oral hypoglycemics or insulin.

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