Pathology for nurses

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17. renal pathology: fluids

The Cell , transport, fluid.

All cells are bounded by a plasma membrane. This membrane is selectively permeable—allowing certain things in and out while excluding others. Useful substances like oxygen and nutrients enter through the membrane, while waste products like carbon dioxide leave through it. These movements involve physical (passive) processes such as:

• Osmosis—water movement across a membrane from an area of low concentration to an area of high concentration

• Diffusion—movement of molecules from an area of high concentration to an area of low concentration

• Facilitative diffusion—movement of molecules from an area of high concentration to an area of low concentration using a carrier cell to accelerate diffusion

• Filtration—selective allowance or blockage of substances across a membrane, wherein movement is influenced by a pressure gradient The movement of substances across a membrane also includes physiologic (or active) processes such as

• Active transport—molecules moving against a concentration gradient with the assistance of energy. Sodium and potassium differ greatly from the intracellular to the extracellular environment. To maintain the concentration difference, sodium and potassium move against the concentration gradient with the help of adenosine triphosphate (ATP), an energy source produced in the mitochondria of cells. This active transport process is referred to as the sodium–potassium pump. Calcium is also moved across the cell membrane through active transport.

• Endocytosis—plasma membrane surrounds the substance being transported and takes the substances into the cell with the assistance of ATP

• Exocytosis—manufactured substances are packaged in secretory vesicles that fuse with the plasma membrane and are released outside the cell

Functionally, the membrane is active and living. Many metabolic activities take place on its surface, and it contains receptors that allow it to communicate with other cells and detect and respond to chemicals in its environment. Additionally, it serves as a conduit between the cell and the extracellular fluids in the body’s internal environment, thereby helping to maintain homeostasis. If we are to understand many aspects of physiology, it is important that we also understand the mechanism by which substances cross the cell membrane.

If cells are to survive and function normally, the fluid medium in which they live must be in equilibrium. Fluid and electrolyte balance, therefore, implies constancy, or homeostasis. This means that the amount and distribution of body fluids and electrolytes are normal and constant. For homeostasis to be maintained, the water and electrolytes that enter (input) the body must be relatively equal to the amount that leaves (output). An imbalance of osmolality, the amount of force of solute per volume of solvent (measured in miliosmoles per kilogram—mOsm/kg or mmol/ kg), of this medium can lead to serious disorders or even death. Fortunately, the body maintains homeostasis through a number of self-regulating systems, which include hormones, the nervous system, fluid–electrolyte balance, and acid–base systems.

Fluid

Water is a critical medium in the human body. The chemical reactions that fuel the body occur in the body fluids. Fluid is the major element in blood plasma that is used to transport nutrients, oxygen, and electrolytes throughout the body. Considering that the human body is composed of from 50 percent (adult females) to 60 percent (adult males) to 75 percent (infants) fluids, it is easy to understand that fluid must play an important role in maintaining life. Fluid intake should approximately equal fluid output each day to maintain an overall balance. 2 Intake of fluids and solid foods that contain water accounts for nearly 90 percent of fluid intake. Cellular metabolism, which results in the production of hydrogen and oxygen combinations (H2O), accounts for the remaining 10 percent of water in the body (see Chapter 2). Fluid intake comes from the following sources (approximate percentages):

• Fluid intake (50 percent)

• Food intake (40 percent)

• Metabolism (10 percent)

Solid foods are actually high in fluid content, for example, • Fruits and vegetables—95 percent or more fluid

Excess fluid intake can result in overload for the heart and lungs and fluid deposits in tissues and extravascular spaces. Fluid loss can occur from inadequate intake or from excessive loss from the body, most commonly from the kidneys. Fluid loss occurs from :

• Urine (58 percent)

• Stool (7.5 percent)

• Insensible loss

• Lungs (11.5 percent)

• Skin—sweat and evaporation (23 percent)

Excess loss through perspiration and respiration or through vomiting or diarrhea may severely reduce circulating volume and present a threat to tissue perfusion.

Fluid is contained in the body in several compartments separated by semipermeable membranes. The major compartments are =

• Intracellular—the area inside the cell membrane, containing 65 percent of body fluids

• Extracellular—the area in the body that is outside the cell, containing 35 percent of body fluids

• interstitial area—contains 25 percent of body fluids

• Blood plasma and lymph—represents 8 percent of body fluids

• Blood plasma is contained in the intravascular spaces

• Transcellular fluid—includes all other fluids and represents 2 percent of body fluids (e.g., eye humors, spinal fluid, synovial fluid, and peritoneal, pericardial, pleural, and other fluids in the body)

Thus, most fluid is located inside the body cells (intracellular), with the next highest amount being located in the spaces and tissues outside the blood vessels (i.e., interstitial), and the smallest amount of fluid being located outside body cells in the fluid surrounding blood cells in the blood vessels (i.e., plasma).

Intracellular fluid balance is regulated primarily through the permeability of the cell membrane. Cell membranes are selectively permeable, allowing ions and small molecules to pass through while keeping larger molecules inside, such as proteins that are synthesized inside the cell.

Some electrolyes are actively transported across the cell membrane to obtain a certain electric charge difference and a resulting reaction. Water moves across the cell membrane through the process of osmosis, flow from a lesser concentration of solutes to a greater concentration of solutes inside and outside the cell. If the extracellular (outside the cell) fluid has a high concentration of solutes, water will move from the cell out to the extracellular fluid, and conversely, if the concentration of solutes inside the cell is high, water will move into the cell.

The ability of a solution to effect the flow of intracellular fluid is called tonicity.

• Isotonic fluids have the same concentration of solutes as cells, and thus no fluid is drawn out or moves into the cell.

• Hypertonic fluids have a higher concentration of solutes (hyperosmolality) than is found inside the cells, which causes fluid to flow out of the cells and into the extracellular spaces. This causes cells to shrink.

• Hypotonic fluids have a lower concentration of solutes (hypo-osmolality) than is found inside the cells, which causes fluid to flow into cells and out of the extracellular spaces. This causes cells to swell and possibly burst.

Problems arise if insufficient water is present to maintain enough intracellular fluid for cells to function normally or if excessive water flows into a cell and causes a disruption in function and even cell rupture.

Extracellular fluid balance is maintained through closely regulated loss and retention to ensure that the total level of fluid in the body remains constant. Mechanisms are in place for regulation of water loss, such as secretion of antidiuretic hormone (ADH) to stimulation retention of water in urine, which helps to prevent excessive fluid elimination. The mechanism of thirst (also stimulated by ADH, as well as by blood pressure) is used to stimulate the ingestion of fluids and fluid-containing foods.

Fluid regulation depends on the sensing of the osmolality, or solute concentration, of the blood. As more water is retained in the body solutions, the osmolality is decreased and can result in hypo-osmolar fluid that has a lower amount of solute than water. When water is lost from the body, the osmolality of body fluids increases and can result in hyperosmolar fluid that has a higher amount of solute than water. The body responds to an increase in osmolality by stimulating the release of ADH, which causes the retention of fluid and lowers the osmolality of body fluids.

Fluid exerts a pressure on membranes (i.e., hydrostatic pressure), and that pressure serves to drive fluid and some particles out through the membrane while others are held in. Solutes dissolved in fluid exert a pressure as well (i.e., oncotic pressure) that pulls fluid toward it. Inside the blood vessels in the arterial system, fluid level is high, and the hydrostatic pressure drives fluid out into the interstitial area (along with nutrients and oxygen). In the venous system, on the other hand, the hydrostatic pressure is low and the osmotic pressure is high because solute (including red blood cells and protein molecules) is concentrated; thus fluid is drawn into the veins along with carbon dioxide and metabolic waste (Figure 1–2). The pressure of the volume and solutes in the blood vessels provides blood pressure needed to circulate blood for perfusion to the tissues. Fluid volume also plays a part in regulation of fluid levels in the body. Several mechanisms, in addition to ADH, respond to the sensation of low or high fluid volumes and osmolality. Neural mechanisms, through sensory receptors, sense low blood volume in the blood vessels and stimulate a sympathetic response resulting in constriction of the arterioles, which, in turn, result in a decrease in blood flow to

The relationship between hydrostatic pressure and osmotic pressure in the arterial and venous systems. the kidneys and decreased urine output, which retains fluid. The opposite response occurs when high blood volume is noted.

• Arteriole dilation results in increased blood flow to the kidneys.

• This results in increased urine output and fluid elimination from the body.

The renin–angiotensin–aldosterone mechanism also responds to changes in fluid volume:

• If blood volume is low, a low blood pressure results.

• Cells in the kidneys stimulate the release of renin.

• This results in the conversion of angiotensinogen to angiotensin II.

• This stimulates sodium reabsorption and results in water reabsorption.

An additional mechanism for regulating sodium reabsorption is the atrial natriuretic peptide (ANP) mechanism:

• When an increase in fluid volume is noted in the atrium of the heart, ANP is secreted.

• This decreases the absorption of sodium.

• This results in sodium and water loss through urine.

When a decrease in volume is noted in the atria, ANP secretion is inhibited.

Table 1–1 shows the relationship between fluid volume and renal perfusion.

Fluid volume regulation is necessary to maintain life. Decreased and inadequate fluid volume (i.e., hypovolemia) can result in decreased flow and perfusion to the tissues. Increased or excessive fluid volume (i.e., hypervolemia) can placed stress on the heart and cause dilutional electrolyte imbalance. It is clear that the renal system plays a vital role in fluid management. If the kidneys are not functioning fully, fluid excretion and retention will not occur appropriately in response to fluid adjustment needs.

QUIZ

1. How does intracellular fluid regulation differ from extracellular fluid regulation?

(a) Intracellular water balance is regulated through ADH secretion.

(b) Extracellular water balance is regulated through fluid volume and osmolality.

(c) Intracellular water balance is regulated through aldosterone and renin secretion.

(d) Extracellular water balance is regulated by fluid passage through cell membranes.

2. The body responds to low body fluid levels and increased osmolality with what actions?

(a) Diarrhea

(b) Diuresis

(c) Tears

(d) Thirst

3. Which mechanisms of fluid regulation respond to high fluid volume in the body?

(a) Decreased ADH secretion

(b) Increased renin–angiotensin–aldosterone

(c) Decreased water excretion

(d) Increased sodium retention

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13.Circulatory pathology and blood pressure problems

the arterial system distributes blood to all the tis- sues of the body, and lesions of the arterial system exert their effects through ischemia or impaired blood flow. There are two types of arterial disorders: diseases such as atherosclerosis, vas- culitis, and peripheral arterial diseases that obstruct blood flow, and disorders such as aneurysms that weaken the vessel wall. Cholesterol relies on lipoproteins (LDLs and HDLs) for trans- port in the blood. The LDLs, which are atherogenic, carry cholesterol to the peripheral tissues. The HDLs, which are pro- tective, remove cholesterol from the tissues and carry it back to the liver for disposal (reverse cholesterol transport). LDL re- ceptors play a major role in removing cholesterol from the blood; persons with reduced numbers of receptors are at par- ticularly high risk for development of atherosclerosis. Atherosclerosis, a leading cause of death in the United States, affects large and medium-sized arteries, such as the coronary and cerebral arteries. It has an insidious onset, and its lesions usually are far advanced before symptoms appear. Although the mechanisms of atherosclerosis are uncertain, risk factors associated with its development have been identified. These include factors such as heredity, sex, and age, which can- not be controlled; factors such as smoking, high blood pres- sure, high serum cholesterol levels, diabetes, obesity, and inflammation, which can be controlled or modified; and other contributing factors such as lack of exercise and stress. The vasculitides are a group of vascular disorders charac- terized by vasculitis or inflammation and necrosis of the blood vessels in various tissues and organs of the body. They can be caused by injury to the vessel, infectious agents, or immune processes, or they can occur secondary to other disease states such as systemic lupus erythematosus. Occlusive disorders interrupt arterial flow of blood and in- terfere with the delivery of oxygen and nutrients to the tissues. Occlusion of flow can result from a thrombus, emboli, vessel compression, vasospasm, or structural changes in the vessel. Peripheral arterial diseases affect blood vessels outside the heart and thorax. They include Raynaud’s disease or phenom- enon, caused by vessel spasm, and thromboangiitis obliterans (Buerger’s disease), characterized by an inflammatory process that involves medium-sized arteries. Aneurysms are localized areas of vessel dilation caused by weakness of the arterial wall. A berry aneurysm, most often found in the circle of Willis in the brain circulation, consists of a small, spherical vessel dilation. Fusiform and saccular aneu- rysms, most often found in the thoracic and abdominal aorta, are characterized by gradual and progressive enlargement of the aorta. They can involve part of the vessel circumference (saccular) or extend to involve the entire circumference of the vessel (fusiform). Aortic dissection is an acute, life- threatening condition. It involves hemorrhage into the vessel wall with longitudinal tearing (dissection) of the vessel wall to form a blood-filled channel. The most serious consequence of aneurysms is rupture.

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12.2 aids

AIDS is an infectious disease of the immune sys- tem caused by the HIV retrovirus that causes profound im- munosuppression. First described in June 1981, the disease is one of the leading causes of morbidity and mortality world- wide. The severity of the clinical disease and the absence of a cure or preventive vaccine have increased public awareness and concern. In the most recent years, the greatest increase in incidence of the disease has been in women and young people 15 to 24 years of age. HIV is transmitted from one person to another through sexual contact, through blood-to-blood contact, or perina- tally. Transmission occurs when the infected blood, semen, or vaginal secretions from one person are deposited onto a mucous membrane or into the bloodstream of another per- son. The primary routes of transmission are through sexual intercourse, through intravenous drug use, and from mother to infant. Blood transfusions and other blood products con- tinue to be routes of transmission in some underdeveloped countries. Occupational exposure in health care settings ac- counts for only a tiny percentage of HIV transmission. HIV in- fection is not transmitted through casual contact or by insect vectors. There is growing evidence of an association between HIV infection and other STDs. Infected individuals can trans- mit the virus to others before their own infections can be detected by antibody tests.

HIV is a retrovirus that infects the body’s CD4+ T cells and macrophages. The integration of viral RNA into the DNA of infected cells allows the virus to replicate, thereby in- fecting and eventually producing a profound loss of CD4+ cells from the peripheral blood. The course of infection occurs in three phases: an acute mononucleosis-like infection that occurs shortly after infection, a latent phase that may last years, and an overt AIDS phase that occurs when the CD4+ cell count falls to 200 cell u/L or less. The AIDS phase is marked by the onset of opportunistic infections and cancers. These opportunistic pathologies can af- fect the respiratory, gastrointestinal, nervous, and other body systems causing conditions such as pneumonia, esophagitis, diarrhea, gastroenteritis, tumors, wasting syndrome, dementia, seizures, motor deficits, and metabolic disorders.

because there is no cure for HIV, risk-free or low- risk behavior is the best protection against HIV infection. Absti- nence or long-term, mutually monogamous sexual relationships between two uninfected partners, use of condoms, avoiding drug use, and the use of sterile syringes are essential to stop- ping the spread of HIV. HIV is diagnosed using the EIA together with the Western blot assay antibody detection tests. The emotional stress, feel- ings of isolation, and sadness experienced by the person with HIV or AIDS can be overwhelming, but most persons adjust to living with HIV infection. Diagnosis and treatment of cogni- tive and affective disorders are an essential part of ongoing care for the HIV-infected person. Appropriate treatment should be made available when alcohol or other drug dependence is noted. The management of HIV/AIDS incorporates the use of HAART therapy, early recognition and treatment of oppor- tunistic infections and other clinical disorders, as well as acknowledgment and support of the psychosocial issues that are an ongoing concern for those who are infected with the virus.

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12.Immune system pathologies, Immunodeificiencys, AIDS

Immunodeficiency States=

Humoral (B-Cell) Immunodeficiency Primary Transient hypogammaglobulinemia of infancy X-linked hypogammaglobulinemia Common variable immunodeficiency Selective deficiency of IgG, IgA, IgM Secondary Increased loss of immunoglobulins (nephrotic syndrome)*

Cellular (T-Cell) Immunodeficiency Primary Congenital thymic aplasia (DiGeorge syndrome) Abnormal T-cell production (Nezelof syndrome) Secondary Malignant disease (Hodgkin’s disease and others) Transient suppression of T-cell production and function due to an acute viral infection such as measles AIDS Purine nucleoside phosphorylase or adenosine deaminase deficiency

Combined B-Cell and T-Cell Immunodeficiency Primary Severe combined immunodeficiency (autosomal or sex-linked recessive) Wiskott-Aldrich syndrome (immunodeficiency, thrombocytopenia, and eczema) Ataxia-telangiectasia Secondary Irradiation Immune suppressant and cytotoxic drugs Aging

Complement Disorders Primary Angioneurotic edema (complement 1 inactivator deficiency) Selective deficiency in a complement component Secondary Acquired disorders that involve complement utilization

Phagocytic Dysfunction Primary Chronic granulomatous disease Glucose-6-phosphate dehydrogenase deficiency Job syndrome Chédiak-Higashi syndrome CD11/CD18 deficiency Secondary Drug induced (corticosteroid and immunosuppressive therapy) Diabetes mellitus

immunodeficiency is defined as an absolute or partial loss of the normal immune response, which places a person in a state of compromise and increases the risk for de- velopment of infections or malignant complications. Immuno- deficiency states can affect one or more of the four main components of the immune response: antibody or humoral (B-cell) immunity, cellular or T-cell immunity, the complement system, and the phagocytic system. The variety of defects known to involve the immune response can be classified as primary (i.e., endogenous or inherited) or secondary (i.e., caused by exogenous factors, such as drugs or infection). The extent to which any or all of these components are compromised dic- tates the severity of the immunodeficiency.

hypersensitivity disorders are responses to en- vironmental, food, or drug antigens that would not affect most of the population. There are four basic categories of hyper- sensitivity responses: (1) type I responses, which are mediated by the IgE class immunoglobulins and include anaphylactic shock, hay fever, and bronchial asthma; (2) type II antibody- mediated reactions, which are mediated by IgG antibodies di- rected against antigens on the surface of cells such as those on the red cells of donor blood, which cause hemolytic trans- fusion reactions; (3) type III reactions, which involve IgG and IgM antibodies and result from the formation of insoluble antigen–antibody complexes that become deposited in blood vessels or in the kidney and cause localized tissue injury; and (4) type IV, t-cell–mediated responses in which sensitized T lym- phocytes promote an inflammatory response when presented with the sensitizing antigen. TH2 cells and mast cells play a pivotal role in the patho- genesis of type I reactions. Exposure to antigen stimulates the production of TH2 cells, which secrete cytokines that cause B cells to produce IgE. The antigen-specific IgE binds to mast cells and basophils, sensitizing them to the antigen. Once mast cells and basophils have become sensitized, the individual is primed to develop a type I hypersensitivity response. Type II and type III hypersensitivity responses involve TH1 cells and IgG and IgM antibodies. Latex allergy can involve a type I, IgE-mediated reaction or a type IV, cell-mediated response. The most common type of allergic reaction to latex gloves is a contact dermatitis caused by a type IV, delayed-type hypersensitivity reaction to rubber additives. The type I, IgE-mediated response to the latex pro- tein is less common but can cause far more serious anaphy- lactic reactions.

autoimmune diseases represent a disruption in self-tolerance that results in damage to body tissues by the im- mune system. Autoimmune diseases can affect almost any cell or tissue of the body. The ability of the immune system to dif- ferentiate self from nonself is called self-tolerance. Normally, self-tolerance is maintained through central and peripheral mechanisms that delete autoreactive B or T cells or otherwise suppress or inactivate immune responses that would be de- structive to host tissues. Defects in any of these mechanisms could impair self-tolerance and predispose to development of autoimmune disease. The ability of the immune system to differentiate foreign from self antigens is the responsibility of HLA encoded by MHC genes. Antigen is presented to receptors of T cells in combination with MHC molecules. Among the possible mech- anisms responsible for development of autoimmune disease are failure of T-cell–mediated immune suppression, aberra- tions in MHC–antigen–TCR interactions, molecular mimicry, and superantigens. Suggested criteria for determining that a disorder results from an autoimmune disorder are evidence of an auto- immune reaction, determination that the immunologic find- ings are not secondary to another condition, and the lack of other identifiable causes for the disorder.

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11.1 pathology of white blood cells

neutropenia, a marked reduction in the number of circulating neutrophils, is one of the major disorders of the white blood cells. It can be acquired or congenital and can re- sult from a combination of mechanisms. Severe neutropenia can occur as a complication of lymphoproliferative diseases, in which neoplastic cells crowd out neutrophil precursor cells, or of radiation therapy or treatment with cytotoxic drugs, which destroy neutrophil precursor cells. Neutropenia also may be en- countered as an idiosyncratic reaction to various drugs. Because the neutrophil is essential to the cellular stage of inflammation, severe and often life-threatening infections are common in per- sons with neutropenia. Infectious mononucleosis is a self-limited lymphoproli- ferative disorder caused by the B-lymphocytotropic EBV, a member of the herpesvirus family. The highest incidence of in- fectious mononucleosis is found in adolescents and young adults, and it is seen more frequently in the upper socio- economic classes of developed countries. The virus is usually transmitted in the saliva. The disease is characterized by fever, generalized lymphadenopathy, sore throat, and the appear- ance in the blood of atypical lymphocytes and several anti- bodies, including the well-known heterophil antibodies that are used in the diagnosis of infectious mononucleosis. Most persons with infectious mononucleosis recover without inci- dent. Treatment is largely symptomatic and supportive.

the lymphomas (Hodgkin’s disease and non- Hodgkin’s lymphoma) represent malignant neoplasms of cells native to lymphoid tissue (i.e., lymphocytes and histiocytes) that have their origin in the secondary lymphoid structures such as the lymph nodes and mucosa-associated lymphoid tissues. Hodgkin’s disease is characterized by painless and progressive enlargement of a single node or group of nodes. It is believed to originate in one area of the lymphatic system and, if un- checked, spreads throughout the lymphatic network. The non- Hodgkin’s lymphomas are a group of neoplastic disorders that originate in the lymphoid tissues, usually the lymph nodes. The non-Hodgkin’s lymphomas are multicentric in origin and spread early to various lymphoid tissues throughout the body, especially the liver, spleen, and bone marrow. The leukemias are malignant neoplasms of the hematopoi- etic stem cells that originate in the bone marrow. They are clas- sified according to cell type (i.e., lymphocytic or myelogenous) and whether the disease is acute or chronic. The lymphocytic leukemias involve immature lymphocytes and their progeni- tors that originate in the bone marrow but infiltrate the spleen, lymph nodes, CNS, and other tissues. The myelogenous leukemias involve the pluripotent myeloid stem cells in bone marrow and interfere with the maturation of all blood cells, in- cluding the granulocytes, erythrocytes, and thrombocytes. The acute leukemias (i.e., ALL, which primarily affects chil- dren, and AML, which primarily affects adults) have a sudden and stormy onset with symptoms of depressed bone marrow function (anemia, fatigue, bleeding, and infections); bone pain; and generalized lymphadenopathy, splenomegaly, and hepatomegaly. The chronic leukemias, which largely affect adults, have a more insidious onset. CLL often has the most favorable clinical course, with many persons living long enough to die of other, unrelated causes. The course of CML is slow and progressive, with transformation to a course re- sembling that of AML. Multiple myeloma is a plasma cell dyscrasia characterized by expansion of a single clone of immunoglobulin-producing plasma cells and a resultant increase in serum levels of a single monoclonal immunoglobulin or its fragments. The main sites involved in multiple myeloma are the bones and bone mar- row. In addition to the abnormal proliferation of marrow plasma cells, there is proliferation and activation of osteoclasts that leads to bone resorption and destruction and predisposes to increased risk for pathologic fractures and development of hypercalcemia. Paraproteins secreted by the plasma cells may cause a hyperviscosity of body fluids and may break down into amyloid, a proteinaceous substance deposited between cells, causing heart failure and neuropathy. Bone marrow in- volvement leads to increased risk for infection because of sup- pressed humoral and cell-mediated immunity and anemia due to impaired red cell production

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11.The Pathology of blood

hemostasis is designed to maintain the in- tegrity of the vascular compartment. The process is divided into five phases: vessel spasm, which constricts the size of the vessel and reduces blood flow; platelet adherence and for- mation of the platelet plug; formation of the fibrin clot, which cements the platelet plug together; clot retraction, which pulls the edges of the injured vessel together; and clot dissolution, which involves the action of plasmin that dissolves the clot and allows blood flow to be reestablished and tissue healing to take place. Blood coagulation requires the stepwise activa- tion of coagulation factors, carefully controlled by activators and inhibitors.

hypercoagulability causes excessive clotting and contributes to thrombus formation. It results from condi- tions that create increased platelet function or that cause ac- celerated activity of the coagulation system. Increased platelet function usually results from disorders such as atherosclerosis that damage the vessel endothelium and disturb blood flow or from conditions such as smoking that cause increased sensi- tivity of platelets to factors that promote adhesiveness and aggregation. Factors that cause accelerated activity of the co- agulation system include blood flow stasis, resulting in an accumulation of coagulation factors, and alterations in the components of the coagulation system (i.e., an increase in pro- coagulation factors or a decrease in anticoagulation factors). The antiphospholipid syndrome is another cause of venous and arterial clotting and is manifest as a primary disorder or a secondary disorder associated with systemic lupus erythe- matosus. It is associated with antiphospholipid antibodies that promote thrombosis and that can affect many organs.

bleeding disorders or impairment of blood co- agulation can result from defects in any of the factors that contribute to hemostasis: platelets, coagulation factors, or vas- cular integrity. The number of circulating platelets can be de- creased (i.e., thrombocytopenia), or platelet function can be impaired (i.e., thrombocytopathia). Impairment of blood co- agulation can result from deficiencies of one or more of the known clotting factors. Deficiencies can arise because of de- fective synthesis (i.e., liver disease or vitamin K deficiency), in- herited diseases (i.e., hemophilia A or von Willebrand disease), or increased consumption of the clotting factors (DIC). Bleed- ing may also occur from structurally weak vessels that result from impaired synthesis of vessel wall components (i.e., vita- min C deficiency, excessive cortisol levels as in Cushing’s disease, or the aging process) or from damage by genetic mechanisms (i.e., hemorrhagic telangiectasia) or the presence of microthrombi.

anemia is a condition of an abnormally low number of circulating red blood cells or hemoglobin level, or both. It is not a disease but rather a manifestation of a disease process or alteration in body function. Anemia can result from excessive blood loss, red cell destruction due to hemolysis, or deficient hemoglobin or red cell production. Blood loss anemia can be acute or chronic. With bleeding, iron and other com- ponents of the erythrocyte are lost from the body. Hemolytic anemia is characterized by the premature destruction of red cells, with retention in the body of iron and the other products of red cell destruction. Hemolytic anemia can be caused by de- fects in the red cell membrane, hemoglobinopathies (sickle cell anemia or thalassemia), or inherited enzyme defects (G6PD deficiency). Acquired forms of hemolytic anemia are caused by agents extrinsic to the red blood cell, such as drugs, bacte- rial and other toxins, antibodies, and physical trauma. Iron- deficiency anemia, which is characterized by decreased hemoglobin synthesis, can result from dietary deficiency, loss of iron through bleeding, or increased demands for red cell production. Vitamin B12 and folic acid deficiency impair red cell production by interfering with DNA synthesis. Aplastic anemia is caused by bone marrow suppression and usually results in a reduction of white blood cells and platelets as well as red blood cells. The manifestations of anemia are those associated with impaired oxygen transport; alterations in red blood cell num- ber, hemoglobin content, and cell structure; and the signs and symptoms of the underlying process causing the anemia.

 polycythemia describes a condition in which the red blood cell mass is increased. It can present as a relative, primary, or secondary disorder. Relative polycythemia results from a loss of vascular fluid and is corrected by replacing the fluid. Primary polycythemia, or polycythemia vera, is a prolif- erative disease of the bone marrow with an absolute increase in total red blood cell mass accompanied by elevated white cell and platelet counts. Secondary polycythemia results from increased erythropoietin levels caused by hypoxic conditions such as chronic heart and lung disease. Many of the manifes- tations of polycythemia are related to increased blood volume and viscosity that lead to hypertension and stagnation of blood flow.

hemoglobin concentrations at birth are high, re- flecting the in utero need for oxygen delivery; toward the end of the first postnatal week, these levels begin to decline, grad- ually falling to a minimum value at approximately 2 months of age. During the early neonatal period, there is a shift from fetal to adult hemoglobin. Many infants have physiologic jaun- dice because of hyperbilirubinemia during the first week of life, probably related to increased red cell breakdown and the in- ability of the infant’s liver to conjugate bilirubin. The term kernicterus describes elevated levels of lipid-soluble, unconju- gated bilirubin, which can be toxic to brain cells. Depending on severity, it is treated with phototherapy, exchange trans- fusions, or both. Hemolytic disease of the newborn occurs in Rh-positive infants of Rh-negative mothers who have been sensitized. It involves hemolysis of infant red cells in response to maternal Rh antibodies that have crossed the placenta. Administration of Rh immune globulin to the mother within 72 hours of delivery of an Rh-positive infant, abortion, or amniocentesis prevents sensitization.

Anemia is an increasingly common health problem in the elderly, affecting approximately 12% of persons aged 60 years and older. As with many other tissue cells, the capacity for red cell replacement decreases with aging. Although most elderly persons are able to maintain their hemoglobin and hematocrit levels within a normal range, they are unable to replace their red cells as promptly as their younger counterparts during a stress situation such as bleeding. This inability to replace red blood cells closely correlates with the increased prevalence of anemia in elderly people, which is usually the result of bleed- ing, infection, malignancy, or chronic disease.

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10.ADL PATHOLOGIES: Sleep

the ICSD classifies sleep disorders into four categories: (1) dyssomnias, which are disorders of initiating and maintaining sleep and disorders of excessive sleepiness; (2) parasomnias, which are not responsible for disturbing the sleep–wake cycle but are undesirable phenomena that occur primarily during sleep; (3) sleep disorders associated with other medical and psychiatric disorders; and (4) proposed sleep dis- orders such as pregnancy-induced sleep disruptions. The dyssomnias include circadian rhythm sleep disorders, insomnia, narcolepsy, disorders of leg movement, and sleep apnea. Sleep problems due to alterations in circadian rhythm tend to fall into three categories: non–24-hour sleep–wake syndrome (disorders of visual input and SCN function); acute shifts in the sleep–wake cycle (jet lag and shift work); and changes in sleep phase disorders (advanced and delayed sleep phase disorders). Insomnia represents a subjective problem of insufficient or nonrestorative sleep despite an adequate op- portunity to sleep. It includes transient and chronic problems in falling asleep and maintaining sleep, waking up too early, or nonrefreshing sleep. Narcolepsy is a disorder of daytime sleep attacks, cataplexy, hallucinations occurring at the onset of sleep, and sleep paralysis. Among the abnormal motor dis- orders that occur during sleep are PLMD and RLS. PLMD is characterized by episodes of repetitive movement of the large toe with flexion of the ankle, knee, and hip during sleep, usu- ally involving both legs. RLS is a neurologic disorder charac- terized by an irresistible urge to move the legs, usually owing to a “creeping,” “crawling,” or uncomfortable sensation. It usu- ally is worse during periods of inactivity and often interferes with sleep. Obstructive sleep apnea is a serious, potentially life- threatening disorder characterized by brief periods of apnea or breathing cessation during sleep, loud snoring interrupted by periods of silence, and abnormal gross motor movements. It is accompanied by complaints of persistent daytime sleepi- ness, morning headache, memory and judgment problems, irritability, difficulty concentrating, and depression. Sleep apnea also is associated with sleep-related cardiac dysrhythmias and hypertension. The parasomnias are undesirable physical phenomena that occur almost exclusively during sleep or are exaggerated by sleep. They include nightmares, sleepwalking and sleep ter- rors, teeth grinding, and bed-wetting (enuresis).

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9.ADL PATHOLOGIES: Exorcise and fatigue

fatigue is a nonspecific, self-recognized state of physical and psychological exhaustion. It results in the per- son’s not being able to perform routine activities and is not re- lieved with sleep or rest. Acute fatigue results from excessive use of the body or specific muscle groups and often is related to depletion of energy sources. Chronic fatigue often is asso- ciated with a specific disease or chronic illness and may be re- lieved when the effects of the disease are corrected. CFS is a complex illness that has physiologic and psychological mani- festations. It is characterized by debilitating fatigue. Diagnosis often is made by a process of elimination, and treatment requires a holistic approach.

during the past 75 years, the use of bed rest has undergone a complete reversal as a standard of treatment for a variety of medical conditions. Over time, research findings have described the deleterious consequences of inactivity. All body systems are affected by complications of immobility and prolonged bed rest. The responses to bed rest and immobility affect all body systems. One of the important factors is the rapidity with which the changes occur and the long time required to over- come the effects of prolonged bed rest and immobility. Ad- verse effects of prolonged immobility and bed rest include a decreased cardiac output, orthostatic intolerance, dehydration, and the potential for thrombophlebitis, pneumonia, formation of renal calculi, development of pressure ulcers, sensory deprivation, and impaired thought processes.

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8.ADL PATHOLOGIES: Nutrition

obesity is defined as excess body fat resulting from consumption of calories in excess of those expended for exercise and activities. Heredity, socioeconomic, cultural, and environmental factors, psychological influences, and activity levels have been implicated as causative factors in the development of obesity. The health risks associated with obesity include hypertension and cardiovascular disease, hyperlipidemia, insulin resistance and type 2 diabetes mellitus, menstrual irregularities and infertility, cancer of the endometrium, breast,prostate, and colon, and gallbladder disease. There are two types of obesity—upper body and lower body obesity. Upper body obesity is associated with a higher incidence of complications. The treatment of obesity focuses on nutritionally adequate weight-loss diets, behavior modification, exercise, social support, and, in situations of marked obesity, surgical methods. Obesity is the most prevalent nutritional disorder affecting the pediatric population in the United States. Undernutrition can range from a selective deficiency of a single nutrient to starvation in which there is deprivation of all ingested nutrients. Malnutrition and starvation are among the most widespread causes of morbidity and mortality in the world. The body adapts to starvation through the use of fat stores and glucose synthesis to supply the energy needs of the central nervous system. Malnutrition is common during illness, recovery from trauma, and hospitalization. The effects of malnutrition and starvation on body function are widespread. They include loss of muscle mass, impaired wound healing, impaired immunologic function, decreased appetite, loss of calcium and phosphate from bone, anovulation and amenorrhea in women, and decreased testicular function in men.

Anorexia nervosa, bulimia nervosa, and binge eating are eating disorders that result in malnutrition. In anorexia nervosa, distorted attitudes about eating lead to serious weight loss and malnutrition. Bulimia nervosa is characterized by secretive episodes or binges of eating large quantities of easily consumed, high-calorie foods, followed by compensatory behaviors such as fasting, self-induced vomiting, or abuse of laxatives or diuretics. Binge-eating disorder is characterized by eating large quantities of food but is not accompanied by purging and other inappropriate compensatory behaviours seen in persons with bulimia nervosa.

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7.ADL PATHOLOGIES: Temperature

body temperature is normally maintained within a range of 36.0°C to 37.4°C (97.0°F to 99.5°F). Most of the body’s heat is produced by metabolic processes that occur within deeper core structures (i.e., muscles and viscera) of the body.

Heat loss occurs at the body’s surface when heat from core structures is transported to the skin by the circulating blood. Heat is lost from the body through radiation, conduction, convection, and evaporation.

The thermoregulatory center in the hypothalamus functions to modify heat production and heat losses as a means of regulating body temperature.

fever and hyperthermia refer to an increase in body temperature outside the normal range. True fever is a disorder of thermoregulation in which there is an upward displacement of the set point for temperature control. In hyperthermia, the set point is unchanged, but the challenge to temperature regulation exceeds the thermoregulatory center’s ability to control body temperature.

Fever can be caused by a number of factors, including microorganisms, trauma, and drugs or chemicals, all of which incite the release of endogenous pyrogens. The reactions that occur during fever consist of four stages: a prodrome, a chill, a flush, and defervescence. A fever can follow an intermittent, remittent, sustained, or recurrent pattern. The manifestations of fever are largely related to dehydration and an increased metabolic rate. Even a low-grade fever in high-risk infants or in elderly persons can indicate serious infection.

Hyperthermia, which varies in severity based on the degree of core temperature elevation and the severity of cardiovascular and nervous system involvement, includes heat cramps, heat exhaustion, and heatstroke. Among the factors that contribute to the development of hyperthermia are prolonged muscular exertion in a hot environment, disorders that compromise heat dissipation, and hypersensitivity drug reactions.Malignant hyperthermia is an autosomal dominant disorder that can produce a severe and potentially fatal increase in body temperature. The condition commonly is triggered by general anesthetic agents and muscle relaxants used during surgery. The neuroleptic malignant syndrome is associated with neuroleptic drug therapy and is thought to result from alterations in the function of the thermoregulatory center or from uncontrolled muscle contraction.

hypothermia is a potentially life-threatening disorder in which the body’s core temperature drops below 35°C (95°F). Accidental hypothermia can develop in otherwise healthy persons in the course of accidental exposure and in elderly or disabled persons with impaired perception of or response to cold. Alcoholism, cardiovascular disease, malnutrition, and hypothyroidism contribute to the risk for hypothermia. The greatest effect of hypothermia is a decrease in the metabolic rate, leading to a decrease in carbon dioxide production and respiratory rate. The signs and symptoms of hypothermia include poor coordination, stumbling, slurred speech, irrationality, poor judgment, amnesia, hallucinations, blueness and puffiness of the skin, dilation of the pupils, decreased respiratory rate, weak and irregular pulse, stupor, and coma. The treatment of moderate and severe hypothermia includes active rewarming.

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6.ADL PATHOLOGIES: Stress

physiologic and psychological adaptation involves the ability to maintain the constancy of the internal environment (homeostasis) and behavior in the face of a wide range of changes in the internal and external environments. It involves negative feedback control systems that regulate cellular function, control life’s processes, regulate behavior, and integrate the function of the different body systems.

the stress response involves the activation of several physiologic systems (sympathetic nervous system, the HPA axis, and the immune system) that work in a coordinated fashion to protect the body against damage from the intense demands made on it. Selye called this response the general adaptation syndrome.

The activation and control of the stress response are mediated by the combined efforts of the nervous and endocrine systems. The neuroendocrine systems integrate signals received along neurosensory pathways and from circulating mediators that are carried in the bloodstream. In addition, the immune system both affects and is affected by the stress response. Adaptation is affected by a number of factors, including experience and previous learning, the rapidity with which the need to adapt occurs, genetic endowment and age, health status, nutrition, sleep–wake cycles, hardiness, and psychosocial factors.

stress in itself is neither negative nor deleterious to health. The stress response is designed to be time limited and protective, but in situations of prolonged activation of the response because of overwhelming or chronic stressors, it could be damaging to health. PTSD is an example of chronic activation of the stress response as a result of experiencing a severe trauma. In this disorder, memory of the traumatic event seems to be enhanced. Flashbacks of the event are accompanied by intense activation of the neuroendocrine system. Treatment of stress should be aimed at helping people avoid coping behaviors that can adversely affect their health and providing them with other ways to reduce stress. Non-pharmacologic methods used in the treatment of stress include relaxation techniques, guided imagery, music therapy,massage techniques, and biofeedback.

Research in stress has focused on personal reports of the stress situation and the physiologic responses to stress. A number of interview guides and written instruments are available for measuring the personal responses to acute and chronic stressors. Methods used for studying the physiologic manifestations of the stress response include electrocardiographic recording of heart rate, blood pressure measurement, electro-dermal measurement of skin resistance associated with sweating, and biochemical analyses of hormone levels.

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4. neoplasia

the term neoplasm refers to an abnormal mass of tissue in which the growth exceeds and is uncoordinated with that of the normal tissues.

Unlike normal cellular adaptive processes such as hypertrophy and hyperplasia, neoplasms do not obey the laws of normal cell growth.

They serve no useful purpose, they do not occur in response to an appropriate stimulus, and they continue to grow at the expense of the host.

[[The process of cell growth and division is called the cell cycle. It is divided into four phases: G1, the postmitotic phase, during which DNA synthesis ceases while RNA and protein synthesis and cell growth take place; S, the phase during which DNA synthesis occurs, giving rise to two separate sets of chromosomes; G2, the premitotic phase, during which RNA and protein synthesis continues; and M, the phase of cell mitosis or cell division. The G0 phase is a resting or quiescent phase in which nondividing cells reside. The entry into and the progression through the various stages of the cell cycle are controlled by cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors. Cell proliferation is the process whereby cells divide and bear offspring; it normally is regulated so that the number of cells that are actively dividing is equal to the number dying or being shed.]]

Cell differentiation is the process whereby cells are transformed into different and more specialized cell types as they proliferate. It determines the structure, function, and life span of a cell. There are three types of cells: well-differentiated cells that are no longer able to divide, progenitor or parent cells that continue to divide and bear offspring, and undifferentiated stem cells that can be recruited to become progenitor cells when the need arises. As a cell line becomes more differentiated, it becomes more highly specialized in its function and less able to divide.

Benign and malignant tumors differ in terms of cell characteristics, manner of growth, rate of growth, potential for metastasis, ability to produce generalized effects, tendency to cause tissue destruction, and capacity to cause death.

The growth of a benign tumor is restricted to the site of origin, and the tumor usually does not cause death unless it interferes with vital functions. Malignant neoplasms grow wildly and without organization, spread to distant parts of the body, and cause death unless their growth is inhibited or stopped by treatment.

There are two types of cancer: solid tumors and hematologic tumors. Solid tumors initially are confined to a specific organ or tissue, whereas hematologic cancers are disseminated from the onset. Cancer is a disorder of cell proliferation and differentiation. Cancer cells often are poorly differentiated compared with normal cells. They have abnormal karyotypes, display abnormal cell membrane antigens and characteristics, and produce abnormal biochemical products. All cancers result from non-lethal genetic changes that transform a normal cell into a cancer cell.

The spread of cancer occurs through three pathways: direct invasion and extension, seeding of cancer cells in body cavities, and metastatic spread through vascular or lymphatic pathways.

Only a proportionately small clone of cancer cells is capable of metastasis. To metastasize, a cancer cell must be able to break loose from the primary tumor, invade the surrounding extracellular matrix, gain access to a blood vessel, survive its passage in the bloodstream, emerge from the blood- stream at a favorable location, invade the surrounding tissue, and begin to grow.

The rate of growth of cancerous tissue depends on the ratio of dividing to resting cells (growth fraction) and the time it takes for the total cells in the tumor to double (doubling time). A tumor is usually undetectable until it has doubled 30 times and contains more than a billion cells.

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3. Genetics and teratogens

genetic disorders can affect a single gene mendelian inheritance) or several genes (polygenic inheritance). Single-gene disorders may be present on an autosome or on the X chromosome, and they may be expressed as a dominant or recessive trait.

In autosomal dominant disorders, a single mutant allele from an affected parent is transmitted to an offspring regardless of sex. The affected parent has a 50% chance of transmitting the disorder to each offspring.

Auto-somal recessive disorders are manifested only when both members of the gene pair are affected. Usually, both parents are unaffected but are carriers of the defective gene. Their chances of having an affected child are one in four; of having a carrier child, two in four; and of having a noncarrier un-affected child, one in four.

Sex-linked disorders, which are associated with the X chromosome, are those in which an un-affected mother carries one normal and one mutant allele on the X chromosome. She has a 50% chance of transmitting the defective gene to her sons, and her daughters have a 50% chance of being carriers of the mutant gene. Because of a normal paired gene, female heterozygotes rarely experience the effects of a defective gene.

Multifactorial inheritance disorders are caused by multiple genes and, in many cases, environmental factors.

The mitochondria contain their own DNA, which is distinct from nuclear DNA. This DNA, which is inherited maternally, is subject to mutations at a higher rate than nuclear DNA and has no repair mechanisms. Disorders of mitochondrial genes interfere with production of cellular energy, lead to the production of energy-reactive oxygen species, or disrupt the generation of signals that initiate apoptosis. The range of mitochondrial gene disorders is diverse, with neuromuscular disorders predominating.

Chromosomal disorders result from a change in chromosome number or structure. A change in chromosome number is called aneuploidy. Monosomy involves the presence of only one member of a chromosome pair; it is seen in Turner’s syndrome, in which there is monosomy of the X chromosome. Polysomy refers to the presence of more than two chromo- somes in a set. Klinefelter’s syndrome involves polysomy of the X chromosome. Trisomy 21 (i.e., Down syndrome) is the most common form of chromosome disorder.

Alterations in chromosome structure involve deletion or addition of genetic material, which may involve a translocation of genetic material from one chromosome pair to another.

a teratogenic agent is one that produces abnormalities during embryonic or fetal life. It is during the early part of pregnancy (15 to 60 days after conception) that environmental agents are most apt to produce their deleterious effects on the developing embryo.

A number of environmental agents can be damaging to the unborn child, including radiation, drugs and chemicals, and infectious agents. FAS is a risk in infants of women who regularly consume alcohol during pregnancy. Of recent concern is the use of cocaine by pregnant women. Because many drugs have the potential for causing fetal abnormalities, often at an early stage of pregnancy, it is recommended that women of childbearing age avoid unnecessary use of drugs. It also has been shown that folic acid deficiency can contribute to neural tube defects. The acronym TORCH stands for toxoplasmosis, other, rubella, cytomegalo-virus, and herpes, which are the infectious agents most frequently implicated in fetal anomalies.

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2. cellular pathology

cells adapt to changes in their environment and in their work demands by changing their size, number, and characteristics.

These adaptive changes are consistent with the needs of the cell and occur in response to an appropriate stimulus. The changes are usually reversed after the stimulus has been withdrawn.

Hypo-trophy= When confronted with a decrease in work demands or ad- verse environmental conditions, cells atrophy or reduce their  size and revert to a lower and more efficient level of functioning.

Hypertrophy results from an increase in work demands and is characterized by an increase in tissue size brought about by an increase in cell size and functional components in the cell.

hyperplasia= An increase in the number of cells in an organ or tissue that is still capable of mitotic division.

Metaplasia occurs in response to chronic irritation and represents the substitution of cells of a type that are better able to survive under circumstances in which a more fragile cell type might succumb.

Dysplasia is characterized by deranged cell growth of a specific tissue that results in cells that vary in size, shape, and appearance. It is a precursor of cancer.

Under some circumstances, cells may accumulate abnormal amounts of various substances. If the accumulation reflects a correctable systemic disorder, such as the hyperbilirubinemia that causes jaundice, the accumulation is reversible. If the disorder cannot be corrected, as often occurs in many inborn errors of metabolism, the cells become overloaded, causing cell injury and death.

Pathologic calcification involves the abnormal tissue deposition of calcium salts. Dystrophic calcification occurs in dead or dying tissue. Although the presence of dystrophic calcification may only indicate the presence of previous cell injury, it is also a frequent cause of organ dysfunction (e.g., when it affects the heart valves).

Metastatic calcification occurs in normal tissues as the result of elevated serum calcium levels. Almost any condition that increases the serum calcium level can lead to calcification in inappropriate sites such as the lung, renal tubules, and blood vessels

cell injury can be caused by a number of agents, including physical agents, chemicals, biologic agents, and nutritional factors. Among the physical agents that generate cell injury are mechanical forces that produce tissue trauma, extremes of temperature, electricity, radiation, and nutritional disorders.

Chemical agents can cause cell i1njury through several mechanisms: they can block enzymatic pathways, cause coagulation of tissues, or disrupt the osmotic or ionic balance of the cell. Biologic agents differ from other injurious agents in that they are able to replicate and continue to produce injury. Among the nutritional factors that contribute to cell injury are excesses and deficiencies of nutrients, vitamins, and minerals.

Injurious agents exert their effects largely through generation of free radicals, production of cell hypoxia, or unregulated intracellular calcium levels.

Partially reduced oxygen species called free radicals are important mediators of cell injury in many pathologic conditions. They are an important cause of cell injury in hypoxia and after exposure to radiation and certain chemical agents.

Lack of oxygen underlies the pathogenesis of cell injury in hypoxia and ischemia. Hypoxia can result from inadequate oxygen in the air, cardiorespiratory disease, anemia, or the inability of the cells to use oxygen. Increased intracellular calcium activates a number of enzymes with potentially damaging effects.

Injurious agents may produce sublethal and reversible cellular damage or may lead to irreversible cell injury and death. Cell death can involve two mechanisms: apoptosis and necrosis. Apoptosis involves controlled cell destruction and is the means by which the body removes and replaces cells that have been produced in excess, developed improperly, have genetic damage, or are worn out. Necrosis refers to cell death that is characterized by cell swelling, rupture of the cell membrane, and inflammation.

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2 lifespan pathology - TBC...

GROWTH AND DEVELOPMENT=

Prenatal Growth and Development Embryonic Development Fetal Development Birth Weight and Gestational Age Abnormal Intrauterine Growth Assessment Methods

INFANCY Growth and Development Organ Systems Common Health Problems Health Problems of the Newborn Health Problems of the Premature Infant Health Problems of the Infant

EARLY CHILDHOOD Growth and Development Common Health Problems

EARLY SCHOOL YEARS TO LATE CHILDHOOD Growth and Development Common Health Problems

ADOLESCENCE Growth and Development Common Health Problems

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1.1 modern perspectives on individual and population health

health is determined by many factors, including genetics, age and sex, and cultural and ethnic differences. The WHO defines health as a “state of complete physical, mental, and social well-being and not merely the absence of disease and infirmity.”

The ability of the body to adapt to changes that occur in both health and disease is affected by such factors as age, health status, and psychosocial resources. Adaptation is further affected by the availability and number of adaptive responses. Extreme age and disease conditions, such as when changes occur suddenly rather than gradually, also affect the capacity to adapt.

The term pathophysiology may be defined as the physiology of altered health. A disease has been defined as any deviation from or interruption of the normal structure or function of any part, organ, or system of the body that is manifested by a characteristic set of symptoms or signs and whose etiology, pathology, and prognosis may be known or unknown.

The causes of disease are known as etiologic factors. Recognized etiologic agents include biologic agents (bacteria, viruses), physical forces (trauma, burns, radiation), chemical agents (poisons, alcohol), and nutritional excesses or deficits. Pathogenesis describes how the disease process evolves. Morphology refers to the structure or form of cells or tissues; morphologic changes are changes in structure or form that are characteristic of a disease.

Disease can manifest itself through signs and symptoms. A symptom is a subjective complaint, such as pain or dizziness; a sign is an observable manifestation, such as an elevated temperature or a reddened sore throat. A syndrome is a compilation of signs and symptoms that are characteristic of a specific disease state. The clinical course of a disease describes its evolution. It can be acute (relatively severe, but self-limiting), chronic (continuous or episodic, but taking place over a long period), or subacute (not as severe as acute or as prolonged as chronic).

Within the disease spectrum, a disease can be designated pre-clinical, or not clinically evident; subclinical, not clinically apparent and not destined to become clinically apparent; or clinical, characterized by signs and symptoms.

the health of individuals is closely linked to the health of the community and to the population it encompasses. Epidemiology is the study of disease in populations. It looks for patterns such as age, race, and dietary habits of persons who are affected with a particular disorder to determine under what circumstances the particular disorder will occur. Using epidemiologic methods, researchers determine how a disease is spread, how to control it, how to prevent it, and how to eliminate it.

Epidemiologists use measures of disease frequency to predict what diseases are present in a population and as an indication of the rate at which they are increasing or decreasing. Incidence is the number of new cases arising in a population during a specified time. Prevalence is the number of people in a population who have a particular disease at a given point in time or period.

Morbidity and mortality provide epidemiologists with information about the functional effects and death-producing characteristics of a disease. Mortality or death statistics provide information about the trends in the health of a population. Morbidity describes the effects an illness has on a person’s life.It is concerned with the incidence of disease as well as its persistence and long-term consequences.

Conditions suspected of contributing to the development of a disease are called risk factors. They may be inherent to a person (high blood pressure) or external (smoking). Studies used to determine risk factors include cross-sectional studies, case-control studies, and cohort studies. Cross-sectional studies use the simultaneous collection of information necessary for classification of exposure and outcome status. Case-control studies are designed to compare subjects who are known to have the outcome of interest (cases) with those who are known not to have the outcome of interest (control). Cohort studies involve groups of persons who were born at approximately the same time or share some characteristic of interest.

The natural history of disease refers to the progression and projected outcome of a disease without medical intervention. It can be used to determine disease outcome, establish priorities for health care services, provide direction for prevention and early detection programs, and compare treatment methods and their outcomes with untreated outcomes. Prognosis is the term used to designate the probable outcome and prospect of recovery from a disease.

The three fundamental types of prevention are primary prevention, secondary prevention, and tertiary prevention. Primary prevention, such as immunizations, is directed at removing risk factors so that disease does not occur. Secondary prevention, such as a Pap smear, detects disease when it still is asymptomatic and curable with treatment. Tertiary prevention, such as β-adrenergic drugs to reduce the risk for death in persons who have had a heart attack, focuses on clinical interventions that prevent further deterioration or reduce the complications of a disease.

Evidence-based practice and evidence-based practice guidlines are mechanisms that use the current best evidence to make decisions about the health care of individuals.