Module 18 (Pathology)

Question 1

hyperthyroidism

Answer 1

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 eyeballs, or proptosis) occurs as a result of swelling of tissue behind the eyeball, 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. Exophthalmos, or thyroid eye disease (TED), can be treated with a new drug (Tepezza), which reduces eye pain and swelling)

Question 2

hypothyroidism

Answer 2

Under activity 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.
Myxedema is 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. Figure 18-15C shows a patient with myxedema.
In cretinism, 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.)

Question 3

thyroid carcinoma

Answer 3

Cancer of the thyroid gland

Question 4

hyperparathyroidism

Answer 4

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.)

Question 5

hypoparathyroidism

Answer 5

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.)

Question 6

adrenal virilism

Answer 6

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.)

Question 7

crushing syndrome

Answer 7

groups 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), diabetes, hypernatremia, hypokalemia, osteoporosis, virilization, and hypertension. The cause may be tumor of the adrenal cortex or excess ACTH secretion (Cushing disease) 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, colitis, and 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).)

Question 8

Addison disease

Answer 8

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 skin, scars, and breast nipples (hyperpigmentation) (Figure 18-17).
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.)

Question 9

pheochromocytoma

Answer 9

benign tumor of the adrenal medulla
(The tumor cells produce excess 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.)

Question 10

hyperinsulinism

Answer 10

excess secretion of insulin causing hypoglycemia
(The cause is 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.)

Question 11

diabetes mellitus (DM)

Answer 11

lack of insulin secretion or resistance 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 is an 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. To test sugar levels with this device, the user pricks a finger to draw blood. At a minimum, patients test before each meal and at bedtime, but many test up to 12 times a day. Patients must continually (every day) balance insulin levels with food and exercise (see In Person: Living with Diabetes, pages 730). In addition to injecting insulin into the body (buttocks, thighs, abdomen, and arms), it also is possible to administer insulin through a portable pump, which infuses the drug continuously through an indwelling needle. A continuous glucose monitor (CGM) can track glucose levels throughout the day and night and communicate with the insulin pump to deliver insulin as needed. See Figure 18-18A and B.
Type 2 diabetes is a separate disease from type 1. Patients often are older, but can be adolescents, and usually have a family history of type 2 diabetes (T2D). 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 diagnosed, 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.
Table 18-3 compares the clinical features, symptoms, and treatment of type 1 and type 2 diabetes.
Table Continued
Both type 1 and type 2 diabetes are associated with primary and secondary complications. The primary complication of type 1 is hyperglycemia. Hyperglycemia can lead to ketoacidosis (fats are improperly burned, leading to an accumulation of ketones and acids in the body). Ketoacidosis also can result from illness or infection, and initial symptoms may be upset stomach and vomiting. Hypoglycemia occurs when too much insulin is taken. 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 may appear many years after the patient develops diabetes. These include destruction of retinal blood vessels (diabetic 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. Figure 18-19 reviews the secondary complications of diabetes mellitus.
As a result of hormonal changes during pregnancy, 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.) *** CHECK TABLE FOR MORE INFO (Pg. 723)

Question 12

acromegaly

Answer 12

hypersecretion of growth hormone from the anterior pituitary after puberty, leading to enlargement of extremities.
(An excess of growth hormone (GH) is produced by adenomas of the pituitary gland 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 “coarsened” facial appearance. The pituitary adenoma can be irradiated or surgically removed. Figure 18-20 shows the features of a woman with acromegaly. Measurement of blood levels of somatomedin C as GH fluctuates is a test for acromegaly.)

Question 13

gigantism

Answer 13

hypersecretion of growth hormone from the anterior pituitary before puberty, 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. See Figure 18-21. The underlying hormonal problem caused by gigantism can be corrected by early diagnosis in childhood.)

Question 14

dwarfism

Answer 14

congenital hyposecretion of growth hormone; hypopituitary dwarfism
(Children who are affected are normal mentally, but their bones remain small. Treatment consists of administration of growth hormone. Patients with achondroplastic dwarfism differ from patients with hypopituitary dwarfism in that they have a genetic defect in cartilage formation that limits the growth of long bones.)

Question 15

panhypopituitarism

Answer 15

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.)

Question 16

syndrome of inappropriate ADH (SIADH)

Answer 16

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.)

Question 17

diabetes insipidus (DI)

Answer 17

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. Synthetic preparations of ADH are administered with nasal sprays or intramuscularly as treatment. 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. The term diabetes comes from the Greek diabainein, meaning to pass through. Both diabetes insipidus and diabetes mellitus are characterized by polyuria. See In Person: Diabetes Insipidus on page 731.
Table 18-4 reviews the abnormal conditions associated with hypersecretions and hyposecretions of the endocrine glands.)