Pathophysiology Chapter 16 Endocrine System Disorders

Hyperglycemia symptoms

Frequent Urination Blurred Vision Dry skin Drowsiness Extreme thirst Hunger Nausea

Endemic Goiter

Goiter refers to an enlargement of the thyroid gland, which is often visible on the anterior neck. Goiters are caused by various hypothyroid and hyperthyroid conditions. A goiter can become very large, compressing the esophagus and interfering with swallowing, or it can cause pressure on the trachea. It can also be of cosmetic concern

Chronic complications of DM

Vascular Problems. Changes occur in both the small and large arteries because of degeneration related to the metabolic abnormalities associated with diabetes (Table 16.4). Microangiopathy, in which the capillary basement membrane becomes thick and hard, causes obstruction or rupture of capillaries and small arteries, and it results in tissue necrosis and loss of function. Retinopathy is a leading cause of blindness (Fig. 16.5). Retinal changes can be observed through the pupil of the eye. Diabetic nephropathy, or vascular degeneration in the kidney glomeruli, eventually leads to chronic renal failure (Fig. 16.6). It is responsible for 40% of patients in end-stage renal failure. Macroangiopathy, like atherosclerosis, affects the large arteries (see Chapter 12), thus leading to a high incidence of heart attacks, strokes, and peripheral vascular disease in diabetics. Obstruction of the arteries in the legs frequently results in ulcers on the feet and legs that are slow to heal (Fig. 16.7). Ulcers are aggravated when peripheral neuropathy is present, reducing pain sensation. Peripheral vascular disease also causes intermittent claudication (pain with walking), which greatly impairs mobility. Decreased blood flow predisposes to frequent infection and gangrenous ulcers. In some cases, vascular problems necessitate amputation if gangrene develops. New surgical techniques allow for less invasive, less traumatic surgery to remove vascular obstructions, using angioscopic bypass surgery. This is very helpful to diabetics, who tend to have delayed healing. Neuropathy. Peripheral neuropathy is a common problem for diabetics. This leads to impaired sensation, numbness, tingling, weakness, and muscle wasting. It results from ischemia and altered metabolic processes. Degenerative changes occur in both unmyelinated and myelinated nerve fibers. The risks of tissue trauma and infection are greatly increased when vascular impairment and sensory impairment coexist. Autonomic nerve degeneration develops as well, leading to bladder incontinence, impotence, and diarrhea. Impaired vasomotor reflexes may cause dizziness when a person stands up. Infections. Infections are more common and tend to be more severe in diabetics, probably because of the vascular impairment, which decreases tissue resistance, the delay in healing because of insulin deficit, and the increased glucose levels in body fluids that support infection. Wound healing is slow, predisposing to infection in case of trauma or surgery. Diabetics are also susceptible to tuberculosis, which is increasing in incidence. Infections in the feet and legs tend to persist because of vascular impairment, and healing is slow, contributing to a high incidence of gangrene and resultant amputation. Fungal infections such as Candida occur frequently and persist on the skin in body folds (Fig. 16.8), in the oral cavity (see Fig. 17.5B), and vagina. The urinary tract is a common site of infection, particularly if bladder function is compromised, and predisposes the patient to cystitis and pyelonephritis. Periodontal disease (infection in the tissues around the teeth) (see Fig. 16.8) and dental caries (infection and decay in teeth) are much more common in diabetics Cataracts. Clouding of the lens of the eye is another degenerative process related to the abnormal metabolism of glucose, and it results in accumulated sorbitol and water in the lens, destroying the transparency. Cataracts may eventually lead to blindness and should be removed when they impair visual function (see Chapter 15). A summary of complications of diabetes may be found in Fig. 16.9. Pregnancy. Complications for both the mother and the fetus may occur during pregnancy. Maternal diabetes may become more severe, control is more difficult with the continual hormonal and metabolic changes, and there is an increased incidence of spontaneous abortions and abnormalities in infants born to diabetic mothers.

Pheochromocytoma

a benign tumor of the adrenal medulla that causes the gland to produce excess epinephrine

Hypoglycemic Shock

1. an excess of insulin in the blood, which causes a deficit of glucose in the blood (Fig. 16.3). It usually occurs in patients with type 1 diabetes, often quite suddenly, following strenuous exercise, an error in dosage, vomiting, or skipping a meal after taking insulin. Many individuals are able to recognize their own response. The lack of glucose quickly affects the nervous system, because neurons cannot use fats or protein as an energy source. 2. Increased transport of glucose into cells 3. HYpoglycemia; decreased CNS function 4. Stimulates SNS 5. Increased gluconeogensis 6. Excess insulin transports glucose into cells 7. Glucose intake can lead to normal state or 8. Blood glucose levels decrease further 9. Neurons cannot function 10. Coma and death SIGNS AND SYMPTOMS: The manifestations of hypoglycemia are related directly to the low blood glucose levels, not to the high insulin levels. One group of signs is related to impaired neurologic function resulting from the lack of glucose. These signs include the following: ~ Poor concentration ~ Slurred speech ~ Lack of coordination and staggering gait; persons with hypoglycemia are sometimes assumed to be intoxicated with alcohol The second group of signs is related to the hypoglycemic state stimulating the sympathetic nervous system, resulting in the following: ~ Increased pulse ~ Pale, moist skin ~ Anxiety ~ Tremors If hypoglycemia remains untreated, loss of consciousness, seizures, and death will follow. TREATMENT: consists of immediate administration of a concentrated carbohydrate, such as sweetened fruit juice or candy. If the person is unconscious, glucose or glucagon may be given parenterally (usually intravenously). Hypoglycemia can be life threatening or can cause brain damage if it is not treated promptly. It is wise to verify that patients who have come for other treatments have eaten and taken the appropriate medications before the appointment to minimize the risk of a hypoglycemic episode during the appointment. Appointments should be scheduled so that meals are not unduly delayed or missed

Addison's disease

Addison disease refers to a deficiency of adrenocortical secretions, the glucocorticoids, mineralocorticoids, and androgens. PATHO: An autoimmune reaction is the common cause. The gland may be destroyed by hemorrhage with meningococcal infection or by viral, tubercular, or histoplasmosis infections. Destructive tumors may also cause hypoactivity SIGNS: The major effects of these hormonal deficits include the following: ~ Decreased blood glucose levels ~ Poor stress response ~ Fatigue ~ Weight loss ~ Frequent infections Low serum sodium concentration, decreased blood volume, and hypotension, accompanied by high potassium levels, result from the mineralocorticoid (aldosterone) deficit and lead to cardiac arrhythmias and failure. Other manifestations include decreased body hair due to a lack of androgens and hyperpigmentation in the extremities, skin creases, buccal mucosa, and tongue, because of increased ACTH resulting from low cortisol secretion. TREATMENT: Replacement therapy with the necessary hormones controls the diseases. Increased doses may be required in times of stress.

Diabetic Ketoacidosis (DKA)

As indicated earlier, DKA results from insufficient insulin, which leads to high blood glucose levels and mobilization of lipids. It is more common in type 1 patients. PATHOPHYSIOLOGY: Ketoacidosis usually develops over a few days and may be initiated by an infection or stress, which increases the demand for insulin in the body. It may also result from an error in dosage or overindulgence in food or alcohol SIGNS AND SYMPTOMS: The signs and symptoms of diabetic ketoacidosis are related to dehydration, metabolic acidosis, and electrolyte imbalances DEHYDRATION: ~ Thirst ~ Dry, rough oral mucosa ~ Warm, dry skin ~ Pulse is rapid but weak and thready ~ Low blood pressure as the vascular volume decreases~ Oliguria (decreased urine output) indicates that compensation mechanisms to conserve fluid in the body are taking place Ketoacidosis leads to the following: ~ Rapid, deep respirations (Kussmaul respirations) ~ Acetone breath (a sweet, fruity smell) ~ Lethargy and decreased responsiveness, indicating depression of the central nervous system owing to acidosis and decreased blood flow Metabolic acidosis develops as ketoacids bind with bicarbonate ions in the buffer, leading to these reactions: ~ Decreased serum bicarbonate levels and decreased serum pH (see Chapter 2) ~ As dehydration progresses, renal compensation is reduced, acidosis becomes decompensated ~ A fall in serum pH ~ Loss of consciousness Electrolyte imbalances include imbalances of sodium, potassium, and chloride and have the following signs: ~ Primarily abdominal cramps ~ Nausea and vomiting ~ Lethargy and weakness Actual serum values of electrolytes may be misleading because the proportion of water lost can affect the serum level even though the electrolytes were lost in the urine. Serum sodium is often low, but the potassium concentration may be elevated because of acidosis (see Chapter 2). If the condition remains untreated, central nervous system depression develops owing to the acidosis and dehydration, leading to coma.

Cushing's Syndrome

Cushing syndrome is caused by an excess of glucocorticoids (eg, hydrocortisone or cortisol). The mechanism for the excess amount of hormone and the effect on related hormones depends on the cause. Excess glucocorticoids may result from various conditions: ~ Adrenal adenoma (Fig. 16.16) ~ Pituitary adenoma (Fig. 16.17) or Cushing disease ~ An ectopic carcinoma that causes paraneoplastic syndrome (see Fig. 16.17C and Chapter 20) ~ Iatrogenic conditions, such as the administration of large amounts of glucocorticoids for many chronic inflammatory conditions (see Fig. 16.17D and Chapter 5) Glucocorticoids are essential for the stress response and essential for life. They perform many important functions in the body. But in excess amounts, they produce many unfortunate effects. This is why prolonged treatment with these drugs is not recommended. Typical changes associated with Cushing syndrome include the following: ~ Characteristic change in the person's appearance; a moon face (round and puffy) and a heavy trunk with fat at the back of the neck (buffalo hump) and wasting of muscle in the limbs (Fig. 16.18) ~ Fragile skin that may have red streaks as well as increased hair growth (hirsutism) ~ Catabolic effects such as osteoporosis and decreased protein synthesis, which will delay healing ~ Metabolic changes include increased gluconeogenesis and insulin resistance, which may lead to glucose intolerance; this may result in diabetes mellitus or exacerbate an existing diabetic state ~ Retention of sodium and water (mineralocorticoid effect), leading to hypertension, edema, and possible hyperkalemia ~ Suppression of the immune response and the inflammatory response with atrophy of the lymphoid tissue, predisposing the client to infection ~ Stimulation of erythrocyte production ~ Emotional lability and euphoria Health care professionals will have two concerns: 1. The risk of infection in the patient with Cushing syndrome and the need for precautions; infection may be local or systemic (eg, tuberculosis) 2. A decreased stress response in a patient with iatrogenic Cushing syndrome because of the atrophy of the adrenal cortex; therefore the doses of medication may have to be increased before and during a stressful event; similarly dosage must be gradually reduced over a period of time to permit resumption of normal secretory function by the gland Treatment depends on the underlying cause.

Diabetic Nephrosclerosis

Diabetic nephropathy, or vascular degeneration in the kidney glomeruli, eventually leads to chronic renal failure (Fig. 16.6). It is responsible for 40% of patients in end-stage renal failure

Action of Insulin

High blood glucose level, triggers beta cells of the pancreas to make and secrete insulin. INsullin binds to its receptor, the cell membrane is more open to glucose and glucose enters the cell. final result is a normal blood glucose level

Hypothyroidism

Mild hypothyroidism is common and is easily treated by replacement doses of thyroid hormone. Severe hypothyroidism occurs in several forms: ~ Hashimoto thyroiditis is a destructive autoimmune disorder ~ Myxedema, severe hypothyroidism in adults (myxedema refers to the nonpitting edema manifested as facial puffiness and a thick tongue); myxedema coma refers to acute hypothyroidism resulting in hypotension, hypoglycemia, hypothermia, and loss of consciousness, a life-threatening complication occurring in undiagnosed or untreated elderly patients. ~ Cretinism, untreated congenital hypothyroidism, may be related to iodine deficiency during pregnancy or may be a developmental defect. The thyroid gland may be nonfunctional or absent. Neonatal screening is standard in many areas of the country; it leads to early treatment and prevents the mental retardation that accompanies early hypothyroidism. Lack of treatment results in severe impairment of all aspects of growth and development because thyroid hormone affects the metabolism of all cells. For example, the child may have difficulty feeding, delayed tooth eruption, malocclusion, and a large protruding tongue, demonstrating stunted skeletal growth and extreme lethargy

Patient/Family Teaching

Nature of disease Importance of glucose control Treatment components: SBGM, diet exercise, A1C test, medications, foot Care: Insulin storing, adminstration, injection, site rotation, S&S hypo and Hyperglycemia

Diabetes Mellitus

caused by a relative deficit of insulin secretion from the beta cells in the islets of Langerhans or by the lack of response by cells to insulin (insulin resistance). TYPE 1 AND TYPE 2: Type 1, formerly insulin dependent diabetes mellitus, type I, or juvenile diabetes, is the more severe form. It occurs more frequently in children and adolescents but can develop at any age. Although there is a genetic factor in the development of the disease, the insulin deficit results from destruction of the pancreatic beta cells in an autoimmune reaction, resulting in an absolute deficit of insulin in the body and therefore requiring replacement therapy. The amount of insulin required is equivalent to the metabolic needs of the body based on dietary intake and metabolic activity. Acute complications such as hypoglycemia or ketoacidosis are more likely to occur in this group. About 1 in every 400 to 500 children has type 1 diabetes; type 1 diabetes occurs in approximately 10% of all individuals diagnosed with diabetes. It is a major factor predisposing to strokes (cerebrovascular accident), heart attacks (myocardial infarction), peripheral vascular disease and amputation, kidney failure, and blindness. Type 2 diabetes, formerly referred to as non-insulin dependent diabetes mellitus, type II, or mature-onset diabetes, is based on decreased effectiveness of insulin or a relative deficit of insulin. This abnormality may involve decreased pancreatic beta cell production of insulin, increased resistance by body cells to insulin, increased production of glucose by the liver, or a combination of these factors. Type 2 is a milder form of diabetes, often developing gradually in older adults, the majority of whom are overweight. However, there has been an increased incidence in adolescents and younger adults who are identified with metabolic syndrome, a complex of several pathophysiologic conditions marked by obesity, cardiovascular changes, and significant insulin resistance due to increased adipose tissue. Individuals with metabolic syndrome often have developed vascular or other chronic complications before diagnosis. A major concern at this time is the rapid climb in incidence of type 2 diabetes, with prevalence now estimated at about 9% (18 million) of the population younger than 20 years of age. With increasing obesity in the population, it is anticipated that future incidence will increase significantly. Also, it is thought that there may be one undiagnosed case for every two to three diagnosed cases. The prevalence of type 2 diabetes increases with age, with approximately half the cases found in persons older than 55 years of age. There is a higher prevalence among African Americans, Hispanic Americans, and Native Americans, some Asian Americans, some native Hawaiians, Pacific Islanders. SIGNS AND SYMPTOMS: ~ Hunger and fatigue ~ Thirst ~ Polyuria, indicated by urinary frequency, which is often noticed by the patient at night (nocturia) with the excretion of large volumes of urine ~ Dry mouth ~ Itchy skin ~ Blurred vision As type 2 diabetes develops, weight gain or increased abdominal girth is common, whereas in type 1 weight loss is common. As blood glucose rises in the early stage, fluid loss Is significant, and appetite increases. Typically, the three Bs —polyuria, polydipsia, and polyphagia—herald the onset of diabetes. If the insulin deficit continues, the patient progresses to the stage of diabetic ketoacidosis. DIAGNOSTIC TEST: Hemoglobin A1C 6.5% or higher Fasting blood glucose level 126 mg/dl or higher Casual blood glucose 200mg/dl or higher Glucose tolerence test Glycosylated hemoglobin test: Clinical and subclinical diabetes, Monitor glucose levels over several months Diabetes Treatment Goal Maintain Glycemic Control Avoid long-term complications, including death Complications: Hypertension, heart disease, stroke, blindness, renal failure neuropathy, lower limb amputations, ED, gastroparesis Treatment: Glucose level in normal range Diet and exercise- exercise blood glucose level as skeletal muscle uses glucose Oral medication: increase insulin secretion, reduce blood glucose levels Insulin

Hyperthroidism, Graves disease

caused by an adenoma, hyperplasia, or secondary to renal failure. It causes hypercalcemia, or high serum calcium levels. Hypercalcemia leads to forceful cardiac contractions (see Table 2.7 for signs of calcium imbalance). The most serious effects of hyperparathyroidism occur in the bone tissue. Increased parathyroid hormone (PTH) causes calcium to leave the bone, leading to osteoporosis, weakening the bone so that it fractures easily (see Chapter 9). Hypercalcemia also increases one's predisposition to kidney stones PATHO: Graves disease occurs more frequently in women older than 30 years of age and is related to an autoimmune factor. It is manifested by the signs of hypermetabolism, toxic goiter, and exophthalmos (Table 16.5). Increased stimulation of the sympathetic nervous system magnifies the metabolic effects. SIGNS: Exophthalmos is evident by the presence of protruding, staring eyes and decreased blink and eye movements (Fig. 16.15). It results from increased tissue mass in the orbit pushing the eyeball forward and from increased sympathetic stimulation affecting the eyelids. If untreated, visual impairment may result from optic nerve damage or corneal ulceration. Thyrotoxic crisis, or thyroid storm, is an acute situation in a patient with uncontrolled hyperthyroidism, usually precipitated by infection or surgery. It is life threatening because of the resulting hyperthermia, tachycardia, and heart failure and delirium.

Hyperglycemic Hyperosmolar Nonketotic Syndrome (HHNS)

coma develops more frequently in patients with type 2 diabetes. Often the patient is elderly with an infection or one who has overindulged in carbohydrates, thereby using more insulin than anticipated. In these cases, hyperglycemia and dehydration develop because of the relative insulin deficit, but sufficient insulin is available to prevent ketoacidosis. Therefore the condition may be difficult to diagnose initially. Severe cellular dehydration results in neurologic deficits, muscle weakness, difficulties with speech, and abnormal reflexes.

Hypoglycemia symptoms

hunger, fatigue, weakness, sweating, headache, dizziness, low bp, cold or clammy skin, fast heartbeat, irritable, sweating, anxious

Periodontal disease

inflammation and degeneration of gums, teeth, and surrounding bone

Nursing consideration for Insulin

o Monitor for hypoglycemia o Hypoglycemia: Administer PO juice, sugar, glucose tablets if pt alert and able to swallow o If patient unable to swallow, use IV glucose (D50) or subcutaneous or intramuscular glucagon o Teach patients to rotate injection sites and allow 1 inch between sites to avoid lipohypertrophy o Other medications may have additive hypoglycemic effects (sulfonylureas, beta blockers, alcohol) or may counteract insulin (thiazide diuretics) o Beta blockers may mask SNS response to hypoglycemia

Complications

related to duration and extent of abnormal blood glucose levels Many factors lead to fluctuations in serum glucose levels Hypoglycemia (insulin shock) more common with insulin replacement treatment Diabetic ketoacidosis occurs in insulin dependent clients, mostly type 1

Neuropathic Ulcer

secondary complication usually associated with a combination of ischemia and neuropathy. most often associated with diabetes. frequently found on plantar surface of foot, often beneath the metatarsal heads. wound has good granulation tissue and little or no drainage. often do not report pain due to altered sensation

Adrenal Glands

•Adrenal medulla •Pheochromocytoma •Benign tumor of the adrenal medulla—secretes epinephrine, norepinephrine, and possibly other substances •Occasionally, multiple tumors •Headache, heart palpations, sweating, intermittent or constant anxiety