Pathophysiology textbook, Summaries of Pathophysiology

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J. Rogers,

Pathophysiology

NR283 Pathophysiology Study Guide for Exam 1

Chapter 1: Intro to Pathology

1 & 2. Describe the cellular adaptations made in each of the following processes and their causative factors: atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia Atrophy - a decrease in the size of cells, resulting in a reduced tissue mass. Common causes include reduced use of the tissue, insufficient nutrition, decreased neurologic or hormonal stimulation, and aging Hypertrophy - 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 Hyperplasia - an increased number of cells resulting in an enlarged tissue mass. Hyperplasia may be a compensatory mechanism to meet increased demands, or pathologic when there is a hormonal imbalance, or it may mean there is an increased risk of cancer Dysplasia - tissue in which the cells vary in size and shape, large nuclei are frequently present, and the rate of mitosis is increased. May result from chronic irritation infection, or may be a precancerous change. Detection of dysplasia is the basis of routine screening tests for atypical cells such as the Pap smear Metaplasia - when one mature cell type is replaced by a different mature cell type. May result from a deficit of vitamin A. Metaplasia is sometimes an adaptive mechanism that provides a more resistant tissue (i.e. when stratified squamous epithelium replaces ciliated columnar epithelium in the respiratory tracts of cigarette smokers. The new cells make a stronger barrier but they decrease defenses for the lungs because they lack cilia)

3. Identify the most common cause of cellular injury. The most common cause of cellular injury is ischemia (decreased supply of oxygenated blood to a tissue or organ, due to circulatory obstruction), which results in hypoxia (reduced oxygen in tissue) and reduced cellular metabolism Other causes of cell injury: ● Physical agents - excessive health or cold or radiation exposure ● Mechanical damage such as pressure or tearing of tissue ● Chemical toxins ● Microorganisms such as bacteria, viruses, and parasites ● Abnormal metabolites accumulation in cells ● Nutritional deficits ● Imbalance of fluids or electrolytes

8. Discuss the types of tissue necrosis.
   • Coagulative o Cardiac o Kidney caused by ischemia
   • Fat o Pancreas o Breast tissue
   • Liquefactive o Abscess and hypoxic death o Commonly found in the brain
   • Caseous o Spaces of cavitation (cystic spaces) o Found in TB patients and the bronchi o Lungs, kidney

Chapter 02: Fluids and Electrolytes, Acids and Bases

1. Discuss the two functional fluid compartments of the body. o Intracellular fluid compartment - fluid inside cells; makes up greater % of body weight than ECF o Extracellular fluid compartment - fluid outside the cells ▪ Includes: - Intravascular fluid (blood/fluid in blood) - Interstitial fluid (intercellular fluid) - Cerebrospinal fluid - Transcelluar fluids (present in various secretions like pericardial (heart) cavity or synovial cavities)
2. Discuss the ways water moves between plasma and interstitial fluid. Water moves between the plasma (vascular component/blood vessels) and the interstitial compartment through a semipermeable capillary membranes based on hydrostatic pressure and osmotic pressure. At the arteriolar end of the capillary, the plasma hydrostatic pressure (blood pressure) is greater than the interstitial hydrostatic pressure and the plasma osmotic pressure of the blood so fluid moves/pushes out from the capillary into the interstitial compartment. At the venous end of the capillary, the plasma hydrostatic pressure is decreased and the osmotic pressure is increased (because of the greater concentration of plasma proteins and other solutes) so fluid is pulled back into the capillary from the interstitial compartment

3. Describe the causation, pathophysiologic process, and clinical manifestations of edema. Edema- an excessive amount of fluid in the interstitial compartment, which causes a swelling or enlargement of the tissues. Causes of Edema : 1. Increased capillary hydrostatic pressure (higher BP)- 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 (pulmonary edema). Specific causes of edema related to increased hydrostatic pressure include increased blood volume (hypervolemia) associated with kidney failure, pregnancy, CHF, or administration of excessive fluids. 2. Loss of plasma proteins (albumin)- results in decreased plasma osmotic pressure because there are less proteins/solutes in the plasma. 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. Proteins are lost in urine through kidney disease; protein synthesis is impaired in patients with malnutrition/malabsorption diseases or with liver disease. Protein levels drop acutely in burn patients with large burn areas because the subsequent inflammation and loss of skin barrier allows proteins to easily leak out of the body Excessive Na+ levels in the ECF accompany the two causes just mentioned. When Na+ 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 BP are usually elevated. High Na+ levels are common in patients with heart failure, high BP, kidney disease, and increased aldosterone secretion. 3. Obstruction of the lymphatic circulation- causes localized edema because excessive fluid & protein are not returned to the general circulation. May occur if a tumor or infection damages lymph nodes or if lymph nodes are removed (cancer surgery) 4. Increased capillary permeability- causes localized edema; results from an inflammatory response or infection. 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. Increase in capillary permeability can result from some bacterial toxins or large burn wounds, leading to both hypovolemic and shock Signs & Symptoms of Edema: o Pale, gray, or red skin color o Weight gain o Slow, bounding pulse, high BP o Lethargy, possible seizures o Pulmonary congestion, cough, rales o Laboratory values: Decreased HCT, decreased serum Na+ o Urine: low specific gravity, high volume
4. Discuss the regulatory processes for sodium and water balance in the body, including the role of antidiuretic hormone, renin-angiotensin-aldosterone

Causes of HYPERkalemia: o Renal failure o Aldosterone deficit o “K+ sparing” diuretic drugs o Leakage of intracellular K+ into ECF in pts with extensive tissue damage/traumatic injuries o Displacement of K+ from cells by prolonged acidosis Signs & Symptoms of HYPERnatremia: o Arrhythmias, cardiac arrest o Nausea, diarrhea o Muscle weakness, paralysis beginning in leg o Paresthesias (fingers, toes, face, tongue) o Oliguria o pH < 7.35 (acidosis) Causes of HYPOkalemia: o Excessive losses from the body due to diarrhea o Diuresis associated with certain diuretic drugs o Excessive aldosterone or glucocorticoids in the body o Decreased dietary intake, which may occur with alcoholism, eating disorders, or starvation o Treatment of diabetic ketoacidosis with insulin Signs & Symptoms of HYPOkalemia: o Cardiac arrhythmias, cardiac arrest o Anorexia, nausea, constipation o Fatigue, muscle twitch, weakness, leg cramps o Shallow respirations, paresthesias o Postural hypotension, polyuria, and nocturia o pH > 7.45 (alkalosis) Causes of HYPERcalcemia: o Uncontrolled release of Ca2+^ ions from the bones due to neoplasms; malignant bone tumors destroying bone, or tumors secreting PTH in excess of body needs o Hyperparathyroidism o Immobility, which may decrease stress on the bone, leading to demineralization o Increased intake of Ca2+^ due to excess vitamin D or excess dietary Ca2+ o Milk-alkali syndrome associated w/ increased milk & antacid intake Signs & Symptoms of HYPERcalcemia: o Apathy, lethargy o Anorexia, nausea, constipation o Polyuria, thirst o Kidney stones o Arrhythmias, prolonged strong cardiac contractions, increased BP

Causes of HYPOcalcemia: o Hypoparathyroidism- decreased parathyroid hormone causes decreased intestinal Ca2+ absorption o Malabsorption syndrome- decreased intestinal absorption of vitamin D or Ca2+ o Deficient serum albumin o pH > 7.45 (alkalosis) Signs & Symptoms of HYPOcalcemia: o Tetany- involuntary skeletal muscle spasm, carpopedal spasm, laryngospasm o Tingling fingers o Mental confusion, irritability o Arrhythmias, weak heart contractions

6. Discuss the causes, clinical manifestations, complications of water deficit (hypovolemia). Hyponatremia results in decreased osmotic pressure in the extracellular compartment which may cause a fluid shift into cells, resulting in hypovolemia and decreased blood pressure Decreased volume of circulating blood in the body. Can be caused by severe diarrhea and vomiting, injury from deep cut or hard impact, illnesses like damage in organ like spleen, liver, kidneys, tear in heart or a large blood vessel. Problems with digestive track such as ulcers. S/S are dehydration, sunken, soft eyes, dry mucous membrane, concentrated urine, thirst, weight loss, fatigue, weakness, dizziness, possible stupor, increased body temperature, low blood pressure, thread pulse
7. Discuss the causes, clinical manifestations, complications, of water excess (hypervolemia). Increased hydrostatic pressure includes increased blood volume. It is associated with kidney `failure, pregnancy, congestive heart failure, or administration of excessive fluids. S/S are edema, weight gain, slow, bounding pulse, high blood pressure, lethargy, possible seizures, pulmonary congestion
8. Discuss the role of hydrogen ion concentration in cellular function and dysfunction.
9. Explain how the lungs and the kidneys regulate acid-base balance.
10. Differentiate between respiratory acidosis, respiratory alkalosis, metabolic alkalosis, and metabolic acidosis by causes and mechanisms of compensation.

Chapter 5: Inflammation

• Physiology of inflammation; definition of inflammation; causes; and steps of inflammation Physiology - protective mechanism. Normal defense mechanism in the body and is intended to localize and remove an injurious agent.

o Complications: ▪ local complications depend on the site of inflammation (ex: inflammation in the lungs may impair he expansion of the lungs, decreasing the diffusion of oxygen) ▪ Infection - may develop in an inflamed tissue because microorganisms can more easily penetrate when the skin or mucosa is damaged and the blood supply is impaired. ▪ Skeletal muscle spasms - strong muscle contractions may be initiated by inflammation. o Local effects - redness (rubor or erythema), heat, swelling, and pain o Systemic effects - mild fever, malaise (feeling unwell), fatigue, headache, and anorexia (loss of appetite) Chronic Inflammation: o May develop after acute episode of inflammation when the cause is not eradicated o Pathophysiology - swelling and exudate but the presence of more lymphocytes, macrophages, and fibroblasts (connective tissue cells) than in acute inflammation o Complications

• disorders such as rheumatoid arthritis are characterized by chronic inflammation with periodic exacerbations of acute inflammation
• Deep ulcers may result from severe or prolonged inflammation because cell necrosis and lack of cell regeneration cause erosion of tissue
• This in turn can lead to complications such as perforation (erosion through the wall) of viscera or the development of extensive scar tissue

• Types of healing o Resolution is the process that occurs when there is minimal tissue damage. The damaged cells recover, and the tissue returns to normal within a short period of time—for example, after a mild sunburn. o Regeneration is the healing process that occurs in damaged tissue in which the cells are capable of mitosis. Some types of cells (eg, epithelial cells) are constantly replicating, whereas other cells such as hepatocytes in the liver are able to undergo mitosis when necessary. The damaged tissue is thus replaced by identical tissue from the proliferation of nearby cells. This type of healing may be limited if the organization of a complex tissue is altered. For instance, sometimes fibrous tissue develops in the liver, distorting the orderly arrangement of cells, ducts, and blood vessels. Although nodules of new cells form, they do not contribute to the overall function of the liver. o Replacement by connective tissue (scar or fibrous tissue formation) takes place when there is extensive tissue damage or the cells are incapable of mitosis—for example, the brain or myocardium. The wound area must be filled in and covered by some form of tissue. Chronic inflammation or complications such as infection result in more fibrous material

• Know classifications of burns and signs and symptoms o First-degree burns (also known as superficial 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. o Second-degree burns (also known as partial-thickness 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. o Third-degree burns (also known as full-thickness burns) result in destruction of all skin layers and in cases of fourth-degree burns, often underlying tissues as well. The burn wound area is coagulated or charred so it’s 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. Burn area may be painless initially because of destruction of 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
• Discuss the consequences of body fluid shifts, cardiovascular compromise, and immunologic alterations related to severe burn injuries. Fluid Shifts: o No bleeding occurs with a burn injury (tissue and blood are coagulated or solidified by the heat). Under the burn surface, an inflammatory response occurs o Where the burn area is large, the inflammatory response results in a massive shift of water, protein, and electrolytes into the tissues, causing fluid excess or edema o Loss of water and protein from the blood leads to decreased circulating blood volume, low blood pressure, and hypovolemic shock, as well as an increased HCT due to hemoconcentration o The fluid imbalance is aggravated by the protein shift out of the capillaries and the resulting lower osmotic pressure in the blood, making it difficult to maintain blood volume until the inflammation subsides o Prolonged or recurrent shock may cause kidney failure or damage to other organs o Fluid and electrolytes as well as plasma expanders (a substitute for lost protein) are replaced intravenously using formulas designed to treat burn patients o Severe shock, particularly with extensive full-thickness burns, may lead to acute renal failure

Ex: Influenza A, B, and C, mumps, measles, rubella virus (German measles), hepatitis C virus, herpes simplex, infectious mononucleosis, varicella (chickenpox), West Nile virus, encephalitis, Poliovirus, hepatitis A virus, Hepatitis B virus, HPV, HIV Chlamydiae, Rickettsiae, and Mycoplasmas o Chlamydiae- Elementary body (EB) is infectious, possessing a cell wall and the ability to bind to epithelial cells. Reticulate body (RB) is noninfectious but uses the host cell to make adenosine triphosphate (ATP) and reproduce as an obligate intracellular organism; Chlamydial infection is a common sexually transmitted disease that causes pelvic inflammatory disease and sterility in women. Infants born to infected mothers may develop eye infections or pneumonia o Rickettsiae are tiny gram-negative bacteria that live inside a host cell (obligate intracellular parasites); transmitted by insect vectors, such as lice or ticks, and cause diseases such as typhus fever and Rocky Mountain spotted fever; attack blood vessel walls, causing a typical rash and small hemorrhages o Mycoplasma infection is a common cause of pneumonia; lack cell walls (not affected by many antimicrobial drugs) and they can appear in many shapes. They are the smallest cellular microbes Fungi- eukaryotic and consist of single cells or chains of cells o The long filaments or strands of a fungus are hyphae, which intertwine to form a mass called the mycelium, the visible mass o Fungi reproduce by budding, extension of the hyphae, or producing various types of spores. Spores can spread easily through the air and are resistant to temperature change and chemicals. Inhaled spores can stimulate an allergic reaction in humans o Ex: tinea pedis (athlete's foot), Candida, Histoplasma Protozoa- complex eukaryotic organisms. They are unicellular, usually motile, and lack a cell wall o Ex: Trichomonas vaginalis, Plasmodium species, Giardia, Entamoeba histolytica Helminths- worms Prions- protein-like agents that are transmitted by consumption of contaminated tissues such as muscle or the use of donor tissues contaminated with the protein o Induces proteins within the brain to undergo abnormal folding and change of shape, rendering the protein molecule nonfunctional and causes degenerative disease of the nervous system o Ex: Creutzfeldt-Jakob disease

• Understand the 4 types of hypersensitivity, know pathological process, and examples Type Example Mechanism Effects Hypersensitivity I: Allergic Reactions Hay fever, anaphylaxis IgE bound to mast cells; release of histamine and chemical mediators Immediate inflammation and pruritus Hypersensitivity II: Cytotoxic hypersensitivity ABO blood incompatibility IgG or IgM reacts with antigen on cell- complement activated Cell lysis and phagocytosis Hypersensitivity III: Immune complex hypersensitivity Autoimmune disorders: SLE, glomerulonephritis Antigen-antibody complex deposits in tissue-complement activated Inflammation, vasculitis Hypersensitivity IV: Cell-mediated or delayed hypersensitivity Contact dermatitis: transplant rejection Antigen binds to T- lymphocyte; sensitized lymphocyte releases lymphokines Delayed inflammation
• Anaphylactic shock: risk factors, clinical manifestations, pathological process, complications Anaphylaxis is a severe, life-threatening, systemic hypersensitivity reaction resulting in decreased blood pressure, airway obstruction, and severe hypoxia o Large amounts of chemical mediators are released from mast cells into the general circulation quickly o General or systemic vasodilation occurs with a sudden, severe decrease in blood pressure o In the lungs, edema of the mucosa and constriction of the bronchi and bronchioles occur, obstructing airflow o Lack of oxygen that results from both respiratory and circulatory impairment causes loss of consciousness o Signs & Symptoms:

• Skin: pruritus, tingling, warmth, hives
• Respiration: difficulty in breathing, cough, wheezing, tight feeling

characterized by deficiency in cell-mediated immunity and the resulting increased susceptibility to opportunistic infections and certain forms of cancer c. Clinical manifestations i. Vary among individuals, and differences are also apparent among men, women, and children ii. First phase: (few weeks after exposure) viral replication is rapid and may be mild, flu-like symptoms such as low fever, fatigue, arthralgia and sore throat

1. Disappear without treatment; some are asymptomatic iii. Second (latent) phase: demonstrate no clinical signs; some have lymphadenopathy or enlarged lymph nodes iv. Final acute phase: serious complications
2. Generalized effects: lymphadenopathy, fatigue and weakness, headache, arthralgia
3. HIV encephalopathy, AIDS dementia: direct infection of brain cells by HIV
4. Secondary infections are common with AIDS and are the primary cause of death a. Drug treatment inefficient b. Extensive and severe c. Pneumocystis carinii: common cause of pneumonia d. Herpes simplex e. Candida f. TB
5. Increased incidence of all cancers, unusual cancers are a markers for AIDS a. Kaposi’s sarcoma : affects the skin, mucous membranes, and internal organs; Skin lesions appear purple or brown, nonpruritic, painless and eventually become nodular b. Non-Hodgkin's lymphoma is also frequent

• Know pathological process and clinical manifestations of Systemic Lupus Erythematosus Systemic lupus erythematosus (SLE) is a chronic inflammatory disease o “butterfly rash” o affects primarily women and becomes manifest between the ages of 10 and 50 years o characterized by the presence of large numbers of circulating autoantibodies against DNA, platelets, erythrocytes, various nucleic acids, and other nuclear materials (antinuclear antibodies [ANA]) o Immune complexes, especially those with anti-DNA antibody, are deposited in connective tissues anywhere in the body, activating complement and causing inflammation and necrosis o Vasculitis, or inflammation of the blood vessels, develops in many organs, impairing blood supply to the tissue, resulting in ischemia (inadequate oxygen for the cells) which leads to further inflammation and destruction of the tissue (kidneys, lungs, heart, brain, skin, joints, and digestive tract)

o Presence of numerous ANAs, especially anti-DNA, as well as other antibodies in the serum is indicative of SLE o Signs & Symptoms:

• Joints- Polyarthritis, with swollen, painful joints, without damage; arthralgia
• Skin- Butterfly rash w/ erythema on cheeks & over nose or rash on body; photosensitivity (exacerbation with sun exposure); ulcerations in oral mucosa; hair loss
• Kidneys- Glomerulonephritis with antigen–antibody deposit in glomerulus, causing inflammation with marked proteinuria and progressive renal damage
• Lungs- Pleurisy (inflammation of the pleural membranes) causing chest pain
• Heart- Carditis (inflammation of any layer of the heart, commonly pericarditis)
• Blood vessels- Raynaud phenomenon (periodic vasospasm in fingers and toes, accompanied by pain)
• Central nervous system- Psychoses, depression, mood changes, seizures
• Bone marrow- Anemia, leukopenia, thrombocytopenia o Tx: rheumatologist; specific treatment often depends on the severity and symptoms of the disease; prednisone (glucocorticoid) used to reduce the immune response and subsequent inflammation

• Active vs. Passive immunity (types?) Type Mechanism Memory Example Natural active Pathogens enter body and cause illness; antibodies form in the host Yes Person has chickenpox once Artificial active Vaccine (live or attenuated organisms) is injected into person. No illness results, but antibodies form Yes Person has measles vaccine and gains immunity Natural passive Antibodies passed directly from mother to child to provide temporary protection No Placental passage during pregnancy or ingestion of breast milk Artificial passive Antibodies injected into person (antiserum) to provide temporary protection or minimize severity of injection No Gammaglobulin if recent exposure to microbe
• Allergy, Autoimmune

1. Autoimmune disorders : occur when the immune system cannot distinguish between self and non-self-antigens; the exact causes are unknown

Tumor Suppressor Gene - antioncogene; a gene that regulates a cell from advancing to cancer; makes a protein called a tumor suppressor protein that helps control cell growth; mutations in tumor suppressor genes may lead to cancer

• Describe risk factors of cancer and know examples (TABLE 20 - 3) Risk Factors (Carcinogens) Example Genetic Factors: oncogenes that regulate all growth Breast cancer: high family incidence; retinoblastoma: inherited Leukemia: chromosomal abnormalities Viruses: Oncogenic viruses alter host cell DNA Hepatic cancer: hepatitis virus Cervical cancer: papillomavirus (HPV) or herpes simplex II; Kaposi sarcoma: HIV Radiation: Ultraviolet rays (sun), x-rays, gamma rays, and radioactive chemicals cause cumulative chromosomal damage in cells Skin cancer: sun exposure Leukemia: radiation exposure Chemicals: Exposure to both natural and synthetic products in excess may be hazardous; the effects of carcinogenic agents depend on the amount and duration of exposure Lung cancer: asbestos, nickel Leukemia: solvents (e.g., benzene) Bladder cancer: aniline dyes and rubber Biologic Factors: Chronic irritation and inflammation with increased mitosis Colon cancer: ulcerative colitis; oral cancer: leukoplakia Age: Increasing Many cancers are more common in older persons Diet: natural substances, additives, processing methods Colon cancer: high-fat diet; gastric cancer: smoked foods Hormones Endometrial cancer: estrogen
• Know and understand metastasis and how cancer is spread Metastasis- spread to distant sites by blood or lymphatic channels Usually first metastasis appears in the regional lymph nodes, which localize the tumor cells for a time. These lymph nodes are checked at the time of surgery & several are often removed. Usually the lymph nodes are removed or treated to eradicate any micrometastases that may be missed, particularly in cancers that are known to spread at an early stage Many cancers spread by normal venous and lymphatic flow, and therefore the lungs and liver are common secondary sites for many tumors Seeding- the spread of cancer cells in body fluids or along membranes, usually in body cavities; the tumor cells break away and travel easily with the movement of fluid and tissue; malignant cells

may also be dislodged from the tumor if excessive handling occurs during diagnostic procedures or surgery, leading to further spread

• Describe staging system TNM T- size of the primary tumor TX: Main tumor cannot be measured. T0: Main tumor cannot be found. T1, T2, T3, T4: Refers to the size and/or extent of the main tumor. The higher the number after the T, the larger the tumor or the more it has grown into nearby tissues. T's may be further divided to provide more detail, such as T3a and T3b N- extent of involvement of regional lymph nodes NX: Cancer in nearby lymph nodes cannot be measured. N0: There is no cancer in nearby lymph nodes. N1, N2, N3: Refers to the number and location of lymph nodes that contain cancer. The higher the number after the N, the more lymph nodes that contain cancer. M- spread (invasion or metastasis) of the tumor MX: Metastasis cannot be measured. M0: Cancer has not spread to other parts of the body. M1: Cancer has spread to other parts of the body
• Describe the effects associated with cancer AND cancer treatment. Warning Signs of Cancer: o Unusual bleeding or discharge anywhere in the body. o Change in bowel or bladder habits (e.g., prolonged diarrhea or discomfort). o A change in a wart or mole (i.e., color, size, or shape). o A sore that does not heal (on the skin or in the mouth, anywhere). o Unexplained weight loss. o Anemia or low hemoglobin and persistent fatigue o Persistent cough or hoarseness without reason o A solid lump, often painless, in the breast or testes or anywhere on the body Local Effects of Cancer: o Pain

• Severity of pain depends on type of tumor & location; may be caused by direct pressure of the mass on sensory nerves
• Dull aching results from the stretching of visceral capsule (occurs in kidney or liver)
• Inflammation contributes to pain
• Secondary causes: infection, ischemia, bleeding o Obstruction
• Results from when a tumor compresses a duct or passageway from an external position or grows inside a passageway or around a structure o Tissue necrosis and ulceration- leads to infection around the tumor