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NR 283 Patho Exam 1 Study guide
CHAPTER 1
Pathophysiology the study of functional or physiologic changes in the body that result from disease processes. Characteristics of disease- review all
- Pathogenesis refers to the development of the disease or the sequence of events involved in the tissue changes related to the specific disease process.
- The onset of a disease may be sudden and obvious or acute; for example, gastroenteritis with vomiting, cramps, and diarrhea; or the onset may be insidious, best described as a gradual progression with only vague or very mild signs. Hepatitis may manifest quietly in this way. There may be several stages in the development of a single disease.
- An acute disease indicates a short-term illness that develops very quickly with marked signs such as high fever or severe pain; for example, acute appendicitis.
- A chronic disease is often a milder condition developing gradually, such as rheumatoid arthritis, but it persists for a long time and usually causes more permanent tissue damage. Often a chronic disease is marked by intermittent acute episodes.
- A subclinical state exists in some conditions in which pathologic changes occur, but no obvious manifestations are exhibited by the patient, perhaps because of the great reserve capacity of some organs. For example, kidney damage may progress to an advanced stage of renal failure before symptoms are manifested. •An initial latent or “silent” stage, in which no clinical signs are evident, characterizes some diseases. In infectious diseases this stage may be referred to as the incubation period, which is the time between exposure to the microorganism and the onset of signs or symptoms; it may last for a day or so or may be prolonged, perhaps for days or weeks. Often the disease agent may be communicable during this incubation period. •The prodromal period comprises the time in the early development of a disease when one is aware of a change in the body, but the signs are nonspecific; for example, fatigue, loss of appetite, or headache. A sense of feeling threatened often develops in the early stage of infections. Laboratory tests are negative during the prodromal period; thus it is difficult to confirm a diagnosis. •The manifestations of a disease are the clinical evidence or effects, the signs and symptoms, of disease. These manifestations, such as redness and swelling, may be local, or found at the site of the problem. Or signs and symptoms may be systemic, meaning they are general indicators of illness, such as fever.
- Signs are objective indicators of disease that are obvious to someone other than the affected individual. Examples of a sign are a fever or a skin rash.
- Symptoms are subjective feelings, such as pain or nausea. Both signs and symptoms are significant in diagnosing a particular problem.
- Lesion is the term used to describe a specific local change in the tissue. Such a change may be microscopic, as when liver cells are examined for pathologic change, or highly visible, such as a blister or pimple observed on the skin. •A syndrome is a collection of signs and symptoms, often affecting more than one organ, that usually occur together in response to a certain condition.
- Diagnostic tests are laboratory tests that assist in the diagnosis of a specific disease. The appropriate tests are ordered on the basis of the patient's manifestations and medical history, the clinical examination, and the patient's answers to specific questions. These tests may also be used for monitoring the response to treatment or the progress of the disease. Such tests may involve chemical analysis of body fluids such as blood, examination of tissues and cells from specimens (e.g., biopsies or body secretions), identification of microorganisms in body fluids or tissue specimens, or radiologic examination of the body. It is important that medical laboratories have a Quality Assurance (QA) program in place to ensure accurate test results. Also, it is often helpful for a patient to have any future or repeated tests done by the same laboratory to provide a more accurate comparison of results.
- Remissions and exacerbations may mark the course or progress of a disease. During a remission, the manifestations of the disease subside, whereas during an exacerbation the signs increase. Rheumatoid arthritis typically has periods of remission when pain and swelling are minimal, alternating with acute periods when swelling and pain are severe. •A precipitating factor is a condition that triggers an acute episode, such as a seizure in an individual with a seizure disorder. Note that a precipitating factor differs from a predisposing factor. For example, a patient may be predisposed to coronary artery disease and angina because of a high-cholesterol diet. An angina attack can be precipitated by shoveling snow on a very cold day.
- Complications are new secondary or additional problems that arise after the original disease begins. For example, following a heart attack, a person may develop congestive heart failure, a complication.
- Therapy or therapeutic interventions are treatment measures used to promote recovery or slow the progress of a disease. These measures may include surgery, drugs, physiotherapy, alternative therapies or behavior modification (see Chapter 3).
- Sequelae describe the potential unwanted outcomes of the primary condition, such as paralysis following recovery from a stroke.
- Convalescence or rehabilitation is the period of recovery and return to the normal healthy state; it may last for several days or months. Systemic signs of disease
Atrophy degeneration and wasting of tissue, organs, or muscle due to decrease in cell size. Dysplasia disorganized cells that vary in size and shape with large nuclei. Apoptosis normal programmed cell death in tissues.
CHAPTER 2
Insensible fluid loss Fluid is lost in the urine and feces as well as through insensible (unapparent) losses through the skin (perspiration) and exhaled air. Causes of edema 1.The first cause is increased capillary hydrostatic pressure (equivalent to higher BP or blood pressure), which prevents return of fluid from the interstitial compartment to the venous end of the capillary, or forces excessive amounts of fluid out of the capillaries into the tissues. The latter is a cause of pulmonary edema, in which excessive pressure, often due to increased blood volume, can force fluid into the alveoli, interfering with respiratory function.Specific causes of edema related to increased hydrostatic pressure include increased blood volume (hypervolemia) associated with kidney failure, pregnancy, congestive heart failure, or administration of excessive fluids. In pregnancy, the enlarged uterus compresses the pelvic veins in the seated position and when a pregnant woman must stand still for long periods of time, the pressure in the leg veins can become quite elevated, causing edema in the feet and legs. In some people with congestive heart failure, the blood cannot return easily through the veins to the heart, raising the hydrostatic pressure in the legs and abdominal organs and causing ascites, or fluid in the abdominal cavity. 2.Second, edema may be related to the loss of plasma proteins, particularly albumin, which results in a decrease in plasma osmotic pressure. Plasma proteins usually remain inside the capillary and seldom move through the semipermeable capillary membrane. The presence of fewer plasma proteins in the capillary allows more fluid to leave the capillary and less fluid to return to the venous end of the capillary.Protein may be lost in the urine through kidney disease, or synthesis of protein may be impaired in patients with malnutrition and malabsorption diseases or with liver disease. Protein levels may drop acutely in burn patients who have large areas of burned skin; the subsequent inflammation and loss of the skin barrier allow protein to easily leak out of the body.Frequently excessive sodium levels in the extracellular fluid accompany the two causes just mentioned. When sodium ions are retained, they promote accumulation of fluid in the interstitial compartment by increasing the ISF osmotic pressure and decreasing the return of fluid to the blood. Blood volume and blood pressure are usually elevated as well. High sodium levels are common in patients with heart failure, high blood pressure, kidney disease, and increased aldosterone secretion.
3.Edema may result from obstruction of the lymphatic circulation. Such an obstruction usually causes a localized edema because excessive fluid and protein are not returned to the general circulation. This situation may develop if a tumor or infection damages a lymph node or if lymph nodes are removed, as they may be in cancer surgery. 4.The fourth cause of edema is increased capillary permeability. This usually causes localized edema and may result from an inflammatory response or infection (see Chapter 5). In this case, histamine and other chemical mediators released from cells following tissue injury cause increased capillary permeability and increased fluid movement into the interstitial area. Protein also leaks into the interstitial compartment, increasing the osmotic pressure in ISF and thus holding more fluid in the interstitial area. A general increase in capillary permeability can result from some bacterial toxins or large burn wounds, leading to both hypovolemia and shock. Third spacing Third-spacing refers to a situation in which fluid shifts out of the blood into a body cavity or tissue where it is no longer available as circulating fluid. Examples include peritonitis, the inflammation and infection of the peritoneal membranes, and burns. Fluid deficit- Dehydration Dehydration refers to insufficient body fluid resulting from inadequate intake or excessive loss of fluids or a combination of the two. Losses are more common and affect the extracellular compartment first. Signs of dehydration The signs of dehydration include thirst, dry oral mucous membrane and decreased skin turgor, fatigue, decreased urine output, and low blood pressure with rapid, weak pulse. Electrolyte imbalances Electrolyte disorders result in an imbalance of minerals in the body. ... Electrolytes refer to minerals that include calcium, chloride, magnesium, phosphate, potassium, and sodium. They are present in your blood, body fluids, and urine. They are ingested with food, drink, and medicines and supplements. Water loss is often accompanied by a loss of electrolytes and sometimes of proteins, depending on the specific cause of the loss. For example, sweating results in a loss of water and sodium chloride. Electrolyte losses can influence water balance significantly because electrolyte changes lead to osmotic pressure change between compartments. To restore balance, electrolytes as well as fluid must be replaced. Isotonic dehydration refers to a proportionate loss of fluid and electrolytes, hypotonic dehydration to a loss of more electrolytes than water, and hypertonic dehydration to a loss of more fluid than electrolytes. The latter two types of dehydration cause signs of electrolyte imbalance and influence the movement of water between the intracellular and extracellular compartments. Intracellular and extracellular cations
•Weakness, agitation •Firm subcutaneous tissues •Increased thirst, with dry, rough mucous membranes •Decreased urine output because ADH is secreted Note that the manifestations can change depending on the cause of the problem: If the cause of hypernatremia is fluid loss caused by lack of ADH, urine output is high. Acid base (AB) Imbalance Acid-base balance is essential to homeostasis because cell enzymes can function only within a very narrow pH range. The normal serum pH range is 7.35 to 7.45. Death usually results if serum pH is below 6.8 or above 7.8 (Fig. 2-10). For example, a pH of less than 7.35 depresses central nervous system function and decreases all cell enzyme activity. Briefly review concepts and processes of AB imbalance There are four basic types of acid-base imbalance (Table 2-8). An increase in hydrogen ions or a decrease in serum pH results in acidosis, which can result either from an increase in carbon dioxide levels (acid) due to respiratory problems or from a decrease in bicarbonate ions (base) because of metabolic or renal problems. The first category is termed respiratory acidosis (increased carbon dioxide), and the second is called metabolic acidosis (decreased bicarbonate ions). Alkalosis refers to an increase in serum pH or decreased hydrogen ions. It may be respiratory alkalosis if increased respirations cause a decrease in carbon dioxide (less acid), or metabolic alkalosis if serum bicarbonate increases. Imbalances may be acute or chronic. In some situations, combinations of imbalances may occur; for example, metabolic acidosis and respiratory alkalosis can occur simultaneously. Normal serum PH range The normal serum pH range is 7.35 to 7.45. Death usually results if serum pH is below 6.8 or above 7.8 (Fig. 2-10). For example, a pH of less than 7.35 depresses central nervous system function and decreases all cell enzyme activity. Basic review of the following (in italics) and the impact on PCO2. Respiratory acidosis and examples Respiratory acidosis, in which there is an increase in carbon dioxide levels, may occur under several conditions: •Acute problems such as pneumonia, airway obstruction (aspiration or asthma), or chest injuries, and in those taking drugs such as opiates, which depress the respiratory control center •Chronic respiratory acidosis, common in people with chronic obstructive pulmonary diseases (COPD) such as emphysema
•Decompensated respiratory acidosis, which may develop if the impairment becomes severe or if, for example, a patient with a chronic problem develops an additional infection Respiratory alkalosis and examples Alkalosis does not occur as frequently as acidosis. Respiratory alkalosis results from hyperventilation, usually caused by anxiety, high fever, or an overdose of aspirin (ASA). Head injuries or brainstem tumors may lead to hyperventilation. Stress-related alkalosis may develop rapidly. If the individual cannot quickly be calmed enough to hold his or her breath repeatedly, then it is best treated by rebreathing exhaled air containing excreted carbon dioxide from a paper bag placed over the face. Even if renal compensation is not impaired it is slow to take place. There will be no questions on compensation and decompensation
CHAPTER 21
Diagnostic tools- Karyotype Is a visual demonstration of the pairs of cell chromosomes arranged in order of size. Down syndrome Down syndrome, or trisomy 21, is a common chromosomal disorder, resulting in numerous defects in physical and mental development. Formerly called Down's syndrome or mongolism, it is now identified as Down syndrome in North America. The risk of bearing a child with Down syndrome increases with maternal age. For example, a woman at age 30 has a risk of approximately 1 in 1000 of bearing a child with Down syndrome, whereas at age 35 the risk increases to approximately 1 in 500 and at age 40 to 1 in 100. Whether this risk is caused by damage to the oocytes resulting from degeneration with aging or environmental agents or other factors is unknown. Recently it has been suggested that some cases may be of paternal origin. A positive triple screen test on maternal blood followed by amniocentesis can detect the disorder. Characteristics of individuals with Down syndrome include the following •The head is small and has a flat facial profile. •The eyes are slanted, and the irises contain Brushfield spots. •The mouth tends to hang open, revealing a large, protruding tongue and a high-arched palate. •The hands are small and have a single palmar (simian) crease. •The muscles tend to be hypotonic, the joints are loose, cervical abnormalities and instability are often evident, and stature is short. •Developmental stages are delayed. •All children are cognitively impaired, but the severity of impairment varies with the individual, and early stimulation programs are helpful. •Sexual development is often delayed or incomplete. •Many children have an assortment of other problems, including visual problems (cataracts, strabismus), hearing problems, obstructions in the digestive tract, celiac disease, congenital heart defects, decreased resistance to infection (immune deficit), and a high risk of developing leukemia. As the life of these children has been extended as a result of improved medical care, a
are forming (Fig. 21-9). Changes in the basic cells at this time have far-reaching effects. The effects of exposure depend on the stage of development at the precise time of the exposure. In addition to an anomaly, or a developmental abnormality, exposure to damaging substances such as cocaine may cause premature birth, a high risk of further illness in the infant (low birthweight or increased respiratory problems), and increased risk of sudden infant death syndrome. Cerebral palsy is an example of the kind of brain damage that can occur before, during, or immediately after birth (see Chapter 14). The cause may be insufficient oxygen, the toxic effects of excessive bilirubin in the blood (jaundice), or trauma. The effects may be localized or may involve several areas of the brain. Impact of exposure to harmful/damaging substances In addition to an anomaly, or a developmental abnormality, exposure to damaging substances such as cocaine may cause premature birth, a high risk of further illness in the infant (low birth weight or increased respiratory problems), and increased risk of sudden infant death syndrome. Mutation a change in the genetic makeup (DNA) of a cell, which will be inherited. Meiosis is a type of cell division that reduces the number of chromosomes in the parent cell by half and produces four gamete cells. This process is required to produce egg and sperm cells for sexual reproduction. Mitosis a process of cell reproduction resulting in two daughter cells with the same DNA as the parent cell.
CHAPTER 5
Inflammatory response pathophysiology and manifestations The inflammatory response is a protective mechanism and an important basic concept in pathophysiology. Inflammation is a normal defense mechanism in the body and is intended to localize and remove an injurious agent, whatever it may be. You have probably observed the inflammatory process resulting from a cut, an allergic reaction, an insect bite, an infection, or a small burn on your body. The general signs and symptoms of inflammation serve as a warning of a problem, which may be hidden within the body. Inflammation is not the same as infection, although infection is one cause of inflammation. With infection, microorganisms such as a bacteria, viruses, or
fungi are always present at the site, causing the inflammation. This microbe can be identified and appropriate treatment instituted to reduce the infection, and the inflammation will subside. When inflammation is caused by an allergy or a burn, no microbes are present. Inflammation is the body's nonspecific response to tissue injury, resulting in redness, swelling, warmth, and pain, and perhaps loss of function. Disorders are named using the ending -itis for inflammation. The root word is usually a body part or tissue; for example, pancreatitis, appendicitis, laryngitis, or ileitis. Causes Inflammation is associated with many different types of tissue injury. Causes include direct physical damage such as cuts or sprains, caustic chemicals such as acids or drain cleaners, ischemia or infarction, allergic reactions, extremes of heat or cold, foreign bodies such as splinters or glass, and infection. Steps of Inflammation An injury to capillaries and tissue cells will result in the following reactions: •Bradykinin is released from the insured cells. •Bradykinin activates pain receptors. •Sensation of pain stimulates mast cells and basophils to release histamine. •Bradykinin and histamine cause capillary dilation. •This results in an increase of blood flow and increased capillary permeability. •Break in skin allows bacteria to enter the tissue. •This results in the migration of neutrophils and monocytes to the site of injury. •Neutrophils phagocytize bacteria. •Macrophages leave the bloodstream and phagocytose microbes. Acute Inflammation Pathophysiology and General Characteristics The inflammatory process is basically the same regardless of the cause. The timing varies with the specific cause. Inflammation may develop immediately and last only a short time; it may have a delayed onset (e.g., a sunburn), or it may be more severe and prolonged. The severity of the inflammation varies with the specific cause and duration of exposure. When tissue injury occurs, the damaged mast cells and platelets release chemical mediators including histamine, serotonin, prostaglandins, and leukotrienes into the interstitial fluid and blood (Table 5-1). These chemicals affect blood vessels and nerves in the damaged area. Cytokines serve as communicators in the tissue fluids, sending messages to lymphocytes and macrophages, the immune system, or the hypothalamus to induce fever. Chemical mediators such as histamine are released immediately from granules in mast cells and exert their effects at once. Other chemical mediators such as leukotrienes and prostaglandins must be synthesized from arachidonic acid in mast cells before release and, therefore, are responsible for the later effects, prolonging the inflammation. Many of these chemicals also intensify the effects of other chemicals in the response. Note that many anti-inflammatory drugs and antihistamines reduce the effects of some of these chemical mediators.
reduces heat loss from the body. Voluntary actions such as curling up or covering the body conserve heat. These mechanisms continue until the body temperature reaches the new, higher setting. Following removal of the cause, body temperature returns to normal by reversing the mechanisms. Chemical mediators and examples Burns and classification of burns A burn is a thermal (heat) or nonthermal (electrical or chemical) injury to the body, causing acute inflammation and tissue destruction. Burns may be mild or cover only a small area of the body, or they may be severe and life threatening, as when an extensive area is involved. Burns may be caused by direct contact with a heat source such as flames or hot water (a scald), by chemicals, radiation, electricity, light, or friction. Most burns occur in the home. Any burn injury causes an acute inflammatory response and release of chemical mediators, resulting in a major fluid shift, edema, and decreased blood volume. Major burns constitute a medical emergency requiring specialized care as quickly as possible. The severity of the burn depends on the cause of the burn, and the temperature, duration of the contact, as well as the extent of the burn surface and the site of the injury. Young children with their thin skin frequently receive severe burns from immersion in excessively hot water in a bathtub. The elderly also have thinner skin; therefore they can suffer much deeper burn injuries than younger adults. Skin thickness varies over the body, with facial skin being much thinner than the skin on the palms and soles. Thus, facial burns are more often more damaging than burns to the soles of the feet. Classifications of Burns Burns are classified by the depth of skin damage and the percentage of body surface area involved. Partial-thickness burns involve the epidermis and part of the dermis (Fig. 5-10). Superficial partial-thickness burns (formerly known as first-degree burns) damage the epidermis and may involve the upper dermis. They usually appear red and painful but heal readily without scar tissue. Examples include sunburn or a mild scald. Deep partial-thickness burns (formerly second-degree burns) involve the destruction of the epidermis and part of the dermis (Fig. 5-11). The area is red, edematous, blistered, and often hypersensitive and painful during the inflammatory stage. In severe cases, the skin appears waxy with a reddened margin. The dead skin gradually sloughs off, and healing occurs by regeneration from the edges of the blistered areas and from epithelium lining the hair follicles and glands. If the area is extensive, healing may be difficult, and complications occur. Grafts may be necessary to cover larger areas. These burns easily become infected, causing additional tissue destruction and scar tissue formation.
Full-thickness burns (formerly third- and fourth-degree burns) result in destruction of all skin layers and often underlying tissues as well (see Fig. 5-11C). The burn wound area is coagulated or charred and therefore is hard and dry on the surface. This damaged tissue (eschar) shrinks, causing pressure on the edematous tissue beneath it. If the entire circumference of a limb is involved, treatment (escharotomy—surgical cuts through this crust) may be necessary to release the pressure and allow better circulation to the area. This procedure may also be required when a large area of the chest is covered by eschar, impairing lung expansion. Initially the burn area may be painless because of destruction of the nerves, but it becomes very painful as adjacent tissue becomes inflamed due to chemical mediators released by the damaged tissues. Full-thickness burns require skin grafts for healing because there are no cells available for the production of new skin. Many burn injuries are mixed burns, consisting of areas of partial burns mixed with full-thickness burns. First aid measures First aid directives for injury-related inflammation frequently recommend the RICE approach: Rest, Ice, Compression, and Elevation. Cold applications are useful in the early stage of acute inflammation. Application of cold causes local vasoconstriction, thereby decreasing edema and pain. The use of hot or cold applications during long-term therapy and recovery periods depends on the particular situation. In some instances, for example, acute rheumatoid arthritis, heat, and moderate activity may improve the circulation in the affected area, thereby removing excess fluid, pain-causing chemical mediators, and waste metabolites, as well as promoting healing. Factors affecting healing- also see box 5- A small gap in the tissue results in complete healing within a short period of time and with minimal scar tissue formation. A large or deep area of tissue damage requires a prolonged healing time and results in a large scar. Factors Promoting Healing
- Youth
- Good nutrition: protein, vitamins A and C
- Adequate hemoglobin
- Effective circulation
- Clean, undisturbed wound
- No infection or further trauma to the site Leukocytosis an above-normal number of leukocytes (WBCs) in the blood.
CHAPTER 6
Anti-viral agents- Mode of action
•Vector-borne, when an insect or animal serves as an intermediary host in a disease such as malaria. Local and systemic signs of infection The local signs of infection are usually those of inflammation: pain or tenderness, swelling, redness, and warmth (Fig. 6-14). If the infection is caused by bacteria, a purulent exudate, or pus, is usually present, whereas a viral infection results in serous, clear exudates. The color and other characteristics of the exudates and tissue may help to identify the microorganism. Figure 5- 13 illustrates infection of a burn wound by two different microorganisms. Tissue necrosis at the site is likely as well. Lymphadenopathy occurs and is manifest by swollen and tender lymph nodes (Table 6-4). Other local signs depend on the site of infection. For instance, in the respiratory tract, local signs probably include coughing or sneezing and difficulty in breathing. In the digestive tract, local signs might include vomiting or diarrhea. Systemic Signs Systemic signs include signs and symptoms common to significant infections in any area of the body. Fever, fatigue and weakness, headache, and nausea are all commonly associated with infection. The characteristics of fever (pyrexia) may vary with the causative organism. The body temperature may be very high or spiking and Nosocomial infection Nosocomial infections are infections that occur in health care facilities, including hospitals, nursing homes, doctors' offices, and dental offices. The CDC estimates that 10% to 15% of patients acquire an infection in the hospital. Reasons for these infections include the presence of many microorganisms in these settings, patients with contagious diseases, overcrowding, use of contaminated instruments, immunocompromised and weakened patients, the chain of transmission through staff, diagnostic procedures, and equipment, therapeutic aids, and food trays. Also, many microbes in health Bacteremia Presence of bacteria in the blood
CHAPTER 7
Humoral immunity and mediation The immune response is a specific defense mechanism in the body. When a foreign antigen enters the body, specific matching antibodies (humoral immunity) or sensitized T-lymphocytes (cell-mediated immunity) form, which then can destroy the matching foreign antigen. Specialized memory cells ensure immediate recognition and destruction of that antigen during future exposures. The B lymphocytes or B cells are responsible for humoral immunity through the production of antibodies or immunoglobulins. B cells are thought to mature in the bone
marrow and then proceed to the spleen and lymphoid tissue. After exposure to antigens, and with the assistance of T lymphocytes, they become antibody-producing plasma cells (see Fig. 7-2). B lymphocytes act primarily against bacteria and viruses that are outside body cells. B-memory cells that provide for repeated production of antibodies also form in humoral immune responses. Passive and active immunity and examples Passive immunity occurs when antibodies are transferred from one person to another. These are effective immediately, but offer only temporary protection because memory has not been established in the recipient, and the antibodies are gradually removed from the circulation. There are also two forms of passive immunity: •Passive natural immunity occurs when IgG is transferred from mother to fetus across the placenta. Breast milk also supplies maternal antibodies. These antibodies protect the infant for the first few months of life. •Passive artificial immunity results from the injection of antibodies from a person or animal into a second person. An example is the administration of rabies antiserum or snake antivenom. Sometimes immunoglobulins are administered to an individual who has been exposed to an organism but has not been immunized to reduce the effects of the infection (for example, hepatitis B). Active immunity develops when the person's own body develops antibodies or T cells in response to a specific antigen introduced into the body. This process takes a few weeks, but the result usually lasts for years because memory B and T cells are retained in the body. •Active natural immunity may be acquired by direct exposure to an antigen, for example, when a person has an infection and then develops antibodies. •Active artificial immunity develops when a specific antigen is purposefully introduced into the body, stimulating the production of antibodies. For example, a vaccine is a solution containing dead or weakened (attenuated) organisms that stimulate the immune system to produce antibodies but does not result in the disease itself. Work continues on the development of vaccines using antigenic fragments of microbes or genetically altered forms. A long list of vaccines is available, including those for protection against polio, diphtheria, measles, and chickenpox. Infants begin a regular schedule of immunizations/vaccines shortly after birth to reduce the risk of serious infections and in hopes of eradicating some infectious diseases. Immunization recommendations for all age groups are published by the CDC. A toxoid is an altered or weakened bacterial toxin that acts as an antigen in a similar manner. A booster is an additional immunization given perhaps 5 or 10 years after initial immunization that “reminds” the immune system of the antigen and promotes a more rapid and effective secondary response. Booster immunizations are currently used for tetanus. Type 1 hypersensitivity reactions and pathophysiology
Self-antigens are usually tolerated by the immune system, and there is no reaction to one's own antigens. When self-tolerance is lost, the immune system is unable to differentiate self from foreign material. The autoantibodies then trigger an immune reaction leading to inflammation and necrosis of tissue. Some individuals may lose their immune tolerance following tissue destruction and subsequent formation of antibodies to the damaged cell components. Aging may lead to loss of tolerance to self-antigens. There also appears to be a genetic factor involved in autoimmune diseases, as evidenced by increased familial incidence. Example: Systemic Lupus Erythematosus Systemic lupus erythematosus pathophysiology and causes Systemic lupus erythematosus (SLE) is a chronic inflammatory disease that affects a number of systems; therefore it can be difficult to diagnose and treat. The name of this systemic disorder is derived from the characteristic facial rash, which is erythematous and occurs across the nose and cheeks, resembling the markings of a wolf (lupus) (Fig. 7-10). The rash is now often referred to as a “butterfly rash,” reflecting its distribution. The condition is becoming better known and more cases are identified in the early stages, improving the prognosis. Certain drugs may cause a lupus-like syndrome, which usually disappears when the drug is discontinued. Discoid lupus erythematosus is a less serious version of the disease affecting only the skin. Occurrence is uncertain because many cases are probably not diagnosed in the early stages. Systemic lupus erythematosus affects primarily women and becomes manifest between the ages of 20 and 40 years. The incidence is higher in African Americans, Asians, Hispanics, and Native Americans. The specific cause has not been established, but it appears to be multifactorial and includes genetic, hormonal (estrogen levels), and environmental (ultraviolet light exposure) factors. A single lupus gene has not been identified, but genes increasing susceptibility to autoimmune disorders have been identified. A number of research projects are in process, including studies of the complement system and immune systems in affected individuals and their families. Another focus concerns identification of a possible genetic defect interfering with normal apoptosis and removal of damaged cells, leaving cell contents such as nucleic acids in the tissues. Pathophysiology Systemic lupus erythematosus is characterized by the presence of large numbers of circulating autoantibodies against DNA, platelets, erythrocytes, various nucleic acids, and other nuclear materials (antinuclear antibodies [ANAs]). Immune complexes, especially those with anti-DNA antibody, are deposited in connective tissues anywhere in the body, activating complement and causing inflammation and necrosis. Vasculitis, or inflammation of the blood vessels, develops in many organs, impairing blood supply to the tissue. The resulting ischemia (inadequate oxygen for the cells) leads to further inflammation and destruction of the tissue. This process usually takes place in several organs or tissues. Common sites include the kidneys, lungs, heart, brain, skin, joints, and digestive tract. Diagnosis is based on the presence of multiple system involvement (a minimum of four areas) and laboratory data showing the presence of autoantibodies. HIV pathophysiology and transmission
Acquired immunodeficiency syndrome (AIDS) is a chronic infectious disease caused by HIV, which destroys helper T-lymphocytes, causing loss of the immune response and increased susceptibility to secondary infections and cancer. It is characterized by a prolonged latent period followed by a period of active infection (Fig. 7-12). An individual is considered HIV- positive when the virus is known to be present in the body, but few if any clinical signs have developed. Acquired immunodeficiency syndrome is the stage of active infection, with marked clinical manifestations and multiple complications. An individual may be HIV positive for many years before he or she develops AIDS. Current therapy has extended the time before development of symptomatic AIDS; however, eventually the active stage develops. The infection may not be diagnosed in the early stages because of this latent asymptomatic period; this contributes to greater spread of the disease. If a patient presents with an unusual infection such as Pneumocystis carinii pneumonia or a cancer such as Kaposi's sarcoma (termed an AIDS indicator disease) and no other pathology, this often marks the presence of active HIV infection and signals the need for HIV testing. Host-versus-graft disease pathophysiology One type of rejection occurs when the host, or recipient's, immune system rejects the graft (host- versus-graft disease [HVGD]), a possibility with kidney transplants. The other type of rejection that occurs is when the graft tissue contains T cells that attack the host cells (graft-versus-host disease [GVHD]), as may occur in bone marrow transplants. Rejection may occur at any time: •Hyperacute rejection occurs immediately after transplantation as circulation to the site is re- established. This is a greater risk in patients who have pre-existing antibodies, perhaps from prior blood transfusions. The blood vessels are affected, resulting in lack of blood flow to the transplanted tissue. •Acute rejection develops after several weeks when unmatched antigens cause a reaction. •Chronic or late rejection occurs after months or years, with gradual degeneration of the blood vessels. Tolerance Self-antigens are usually tolerated by the immune system, and there is no reaction to one's own antigens. When self-tolerance is lost, the immune system is unable to differentiate self from foreign material. The autoantibodies then trigger an immune reaction leading to inflammation and necrosis of tissue. Some individuals may lose their immune tolerance following tissue destruction and subsequent formation of antibodies to the damaged cell components. Aging may lead to loss of tolerance to self-antigens. There also appears to be a genetic factor involved in autoimmune diseases, as evidenced by increased familial incidence.
CHAPTER 20
