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Terms in this set (29)

Gross Level- Organ or system level
Microscopic Level- cellular level
Biopsy- excision of a small amount of living tissue
Autopsy- Examination of the body and organs after death
Diagnosis- identification of a specific disease
Etiology- causative factors in a particular disease in an individual
Predisposing factors- tendencies that promote development of a disease in an individual
Pathogenesis- development of the disease
idiopathic-unknown cause
iatrogenic- caused by treatment, error or procedure
Clinical manifestations: signs and symptoms
Acute disease- develops quickly, marked signs, short term
Chronic- Often milder, develops gradually, persists for a long time
Subclinical state- pathologic changes occur, no obvious manifestations
Latent state- no symptoms or clinical signs are evident
Prodromal period- early development of disease, signs are non-specific or absent
Syndrome- collection of signs and symptoms, often affecting more than one organ
Remissions- manifestations of disease subside or are absent
Precipitating factors- condition that might trigger an acute episode
Complications- New secondary or additional problems
Therapy- treatment measures to promote recovery or slow the progress of a disease
Sequelae- unwanted outcomes of primary condition
Convalescence- period of recovery
Prognosis- probability for recovery or for other outcomes
Rehabilitation- Maximizing function of diseased tissues
Epidemiology- Science of identifying the causative factors and tracking the pattern or occurrence of disease
Morbidity- indicates the number of people with a disease within a group
Mortality- indicates the number of deaths resulting from a particular disease w/in a group
Epidemics- occur when a higher than expected number of cases of an infectious disease occur w/in a given area
Pandemic- involve a higher number of cases in many regions of the globe
Occurrence of disease- tracked by incidence and prevalence
Incidence- number of new cases in a given population w/in a specified time period
Prevalence- # of new and old or existing cases in a specific population and w/in a specified time period
• Atrophy refers to a decrease in the size of cells, resulting in a reduced tissue mass (Fig. 1-2). Common causes include reduced use of the tissue, insufficient nutrition, decreased neurologic or hormonal stimulation, and aging. An example is the shrinkage of skeletal muscle that occurs when a limb is immobilized in a cast for several weeks.
• Hypertrophy refers to an increase in the size of individual cells, resulting in an enlarged tissue mass. This increase may be caused by additional work by the tissue, as demonstrated by an enlarged heart muscle resulting from increased demands (see Fig. 18-23). A common example of hypertrophy is the effect of consistent exercise on skeletal muscle, leading to an enlarged muscle mass. Excessive hormonal stimulation may also stimulate cell growth.
• Hyperplasia is defined as an increased number of cells resulting in an enlarged tissue mass. In some cases, hypertrophy and hyperplasia occur simultaneously, as in the uterine enlargement that occurs during pregnancy. Hyperplasia may be a compensatory mechanism to meet increased demands, or it may be pathologic when there is a hormonal imbalance. In certain instances there may be an increased risk of cancer when hyperplasia occurs.
• Metaplasia occurs when one mature cell type is replaced by a different mature cell type. This change may result from a deficit of vitamin A. Sometimes, metaplasia may be an adaptive mechanism that provides a more resistant tissue; for instance, when stratified squamous epithelium replaces ciliated columnar epithelium in the respiratory tracts of cigarette smokers. Although the new cells present a stronger barrier, they result in decreased defenses for the lungs because cilia are no longer present as a defense mechanism for the simpler squamous cells in the mucosa.
LOCAL: The cardinal signs of inflammation are redness (rubor or erythema), heat, swelling, and pain:

•Redness and warmth are caused by increased blood flow into the damaged area (Fig. 2-3).
•Swelling or edema is caused by the shift of protein and fluid into the interstitial space.
•Pain results from the increased pressure of fluid on the nerves, especially in enclosed areas, and by the local irritation of nerves by chemical mediators such as bradykinins.
•Loss of function may develop if the cells lack nutrients or swelling interferes mechanically with function, as happens in restricted joint movement.
Exudate refers to a collection of interstitial fluid formed in the inflamed area. The characteristics of the exudate vary with the cause of the trauma: • Serous or watery exudates consist primarily of fluid with small amounts of protein and white blood cells. Common examples of serous exudates occur with allergic reactions or burns.
• Fibrinous exudates are thick and sticky and have a high cell and fibrin content. This type of exudate increases the risk of scar tissue in the area.
• Purulent exudates are thick, yellow-green in color, and contain more leukocytes and cell debris as well as microorganisms. Typically, this type of exudate indicates bacterial infection, and the exudate is often referred to as "pus."
• An abscess is a localized pocket of purulent exudate or pus in a solid tissue (e.g., around a tooth or in the brain).
• A hemorrhagic exudate may be present if blood vessels have been damaged.
Mild fever (pyrexia): common if inflammation is extensive, release of pyrogens
Malaise: feeling unwell
Acetylsalicylic acid (Aspirin, ASA) has long been used as an anti-inflammatory agent, sometimes in very large doses. ASA is never recommended for children with viral infections because the combination of ASA and a viral infection is believed to contribute to the development of Reye's syndrome, a serious complication involving the brain and liver, which may be fatal.
Acetaminophen (Tylenol or Paracetamol) decreases fever and pain, but does not diminish the inflammatory response.
Nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen (Advil or Motrin), piroxicam (Feldene), or diclofenac sodium (Arthrotec) are now used extensively to treat many types of inflammatory conditions. These drugs have anti-inflammatory, analgesic, and antipyretic activities.
Glucocorticoids, sometimes referred to as corticosteroids or steroidal anti-inflammatory drugs, are synthetic chemicals that are related to the naturally occurring glucocorticoids (hydrocortisone), hormones produced by the adrenal cortex gland in the body (see Chapter 25). These drugs are extremely valuable in the short-term treatment of many disorders, but also have significant undesirable effects that may affect health care. However, with long-term use and high dosages of glucocorticoids, marked side effects occur, similar to Cushing's disease (see Chapter 25). These side effects (or adverse effects) should be considered when taking a medical history from a patient because they may complicate the care of the person.

The adverse effects of glucocorticoids include:

•Atrophy of lymphoid tissue and reduced numbers of WBCs, leading to an increased risk of infection and a decreased immune response
•Catabolic effects (increased tissue breakdown with decreased protein synthesis and tissue regeneration), including osteoporosis (bone demineralization), muscle wasting, and a tendency to thinning and breakdown of the skin and mucosa (e.g., peptic ulcer)
•Delayed healing
•Delayed growth in children
•Retention of sodium and water, often leading to high blood pressure and edema

A newer type of NSAID is celecoxib (Celebrex), which appears to be effective without unwanted effects on the stomach. This group of drugs (COX-2 inhibitors) is currently under further investigation following the withdrawal from the market of one drug in this class (rofecoxib, Vioxx). This followed reports of serious side effects such as increased incidence of heart attacks. This is an example of the necessity for long-term data collection from a large population in order to to determine all the facts about new drugs or medical procedures.
Rejection is a complex process, primarily involving a type IV cell-mediated hypersensitivity reaction (see the next section on hypersensitivity reactions), but also involving a humoral response, both of which cause inflammation and tissue necrosis. The rejection process eventually destroys the organ, so that transplanted organs often must be replaced after a few years. Survival time of a transplant is increased when the HLA match is excellent, when the donor is living (less risk of damage to donor tissue), and when immunosuppressive drugs are taken on a regular basis. Corneas and cartilage lack a blood supply, and therefore rejection is not a problem with these transplanted tissues. With improved surgical techniques and better drug therapy, transplants are now lasting a longer time and significantly prolonging the recipient's life.
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.
Immunosuppression techniques are used to reduce the immune response and prevent rejection. The common treatment involves drugs such as cyclosporine, azathioprine (Imuran), and prednisone, a glucocorticoid (see Chapter 2). The drugs must be taken on a continuous basis and the patient monitored for signs of rejection.The major concern with any immunosuppressive drug is the high risk of infection, because the normal body defenses are now limited.
CAUSES: Immunodeficiency results from a loss of function, partial or total, of one or more components of the immune system leading to increased risk of infection and cancer. Primary deficiencies involve a basic developmental failure somewhere in the system (for example, in the bone marrow's production of stem cells), the thymus, or the synthesis of antibodies. Many defects result from a genetic or congenital abnormality and are first noticed in infants and children. Secondary or acquired immunodeficiency refers to loss of the immune response resulting from specific causes and may occur at any time during the lifespan. These causes include infection, particularly viral infection, splenectomy (removal of the spleen), malnutrition or liver disease (hypoproteinemia—low serum protein level), use of immunosuppressive drugs in clients with organ transplants, and radiation and chemotherapy for cancer treatment. Immunodeficiency associated with cancer is a result of malnutrition and blood loss as well as the effects of treatment, all of which depress bone marrow production of leukocytes. Glucocorticoid drugs such as prednisone, a common long-term treatment for chronic inflammatory diseases as well as for cancer, cause decreased leukocyte production, atrophy of lymph nodes, and suppression of the immune response.

EFFECTS: Immunodeficiency states predispose patients to the development of opportunistic infections by normally harmless microorganisms. This may involve multiple organisms and be quite severe. These infections are difficult to treat successfully. They often arise from resident flora of the body; for example, fungal or candidal infection in the mouth of someone whose normal defenses are impaired. Sometimes severe, life-threatening infections result from unusual organisms that are normally not pathogenic or disease causing in healthy individuals, such as Pneumocystis carinii.
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 infection and cancer. It is characterized by a prolonged latent period followed by a period of active infection. 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. AIDS 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.
The virus is transmitted in body fluids, such as blood, semen, and vaginal secretions. Blood contains the highest concentration of virus, with semen next. HIV may be present in small numbers in other secretions, such as saliva, but transmission in such cases has not been established. There is a slight risk that blood donated by newly infected persons will not test positive for antibodies during the "window" period; therefore blood products are now tested for the virus and treated when possible. This has reduced the risk for hemophiliacs and others who must have repeated treatment with blood products. Infected organ donors can also transmit the infection. Individuals who have a history of high-risk activities such as IV drug use, unprotected sex, or untreated STDs are not accepted as organ or blood donors to reduce the possibility of transmitting the virus.
Health care workers should assume there is a risk of some infection (there is a higher risk of transmitting other infections such as hepatitis B or C) from contact with body fluids from any individual and follow universal precautions (see Chapter 4). Patients infected with HIV are not isolated or labeled because such information may not include those infected and in the "window period." All clients must be treated as though they may be infected if transmission by blood and body fluids is to be prevented.
The clinical effects of HIV infection vary among individuals, and differences are also apparent between men, women, and children. During the first phase, a few weeks after exposure, viral replication is rapid and there may be mild, generalized flulike symptoms such as low fever, fatigue, arthralgia, and sore throat. These symptoms disappear without treatment. Many persons are asymptomatic. In the prolonged second, or latent, phase, many patients demonstrate no clinical signs, whereas some have a generalized lymphadenopathy or enlarged lymph nodes. It appears that viral replication is reduced during this time.

The final acute stage, when immune deficiency is evident, is marked by numerous serious complications. The categories include general manifestations of HIV infection, gastrointestinal effects, neurologic effects, secondary infections, and malignancies. Secondary infections and cancer are caused by the immunodeficiency. Each patient may demonstrate more effects in one or two categories as well as minor changes in the other systems.

• Generalized effects include lymphadenopathy, fatigue and weakness, headache, and arthralgia. Gastrointestinal effects seem to be related primarily to opportunistic infections, including parasitic infections. The signs include chronic severe diarrhea, vomiting, and ulcers on the mucous membranes. Necrotizing periodontal disease is common, with inflammation, necrosis, and infection around the teeth in the oral cavity. Severe weight loss, malnutrition, and muscle wasting frequently develop.
• HIV encephalopathy (general brain dysfunction), sometimes called AIDS dementia, refers to the direct infection of brain cells by HIV. This is often aggravated by malignant tumors, particularly lymphomas, and by opportunistic infections such as herpesvirus, various fungi, and toxoplasmosis in the brain. Nutritional deficits, particularly of vitamins, are a contributing factor. Encephalopathy is reflected by confusion, progressive cognitive impairment, including memory loss, loss of coordination and balance, and depression. Eventually the person cannot talk or move and seizures or coma may develop.
• Secondary infections are common with AIDS and are the primary cause of death. They are frequently multiple, and more extensive and severe than usual. Drug treatment of secondary infection is often ineffective. In the lungs, Pneumocystis carinii, now considered a fungus, is a common cause of severe pneumonia (see Chapter 19) and is frequently the cause of death (Fig. 3-17A). Herpes simplex, a virus causing cold sores, is common (see Fig. 27-8), and Candida, a fungus, involves the mouth and often extends into the esophagus (see Fig. 3-17C). The incidence of tuberculosis in AIDS patients is quite high and climbing rapidly.