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NR283 Pathophysiology Study Guide for Exam 1, Study notes of Pathophysiology

Cambridge Technical Institute Pathophysiology

NR283 Pathophysiology Study Guide for Exam 1

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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

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Download NR283 Pathophysiology Study Guide for Exam 1 and more Study notes Pathophysiology in PDF only on Docsity!

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)

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

Describe cellular injury caused by infection and inflammation. Infectious diseases cause cell injury through microorganisms (i.e. bacteria & viruses). Some microorganisms induce pyroptosis (a type of cell death by lysis/dissolution of the cell), resulting in the rupture of the plasma membrane and release of destructive lysosomal enzymes into the tissue, which causes inflammation (swelling, redness, and pain) as well as damage to nearby cells and reduced function
Describe the major mechanism of tissue damage caused by chemical injury. Chemicals from both the environment ( exogenous ) and inside the body ( endogenous ) may damage cells, either by altering cell membrane permeability or producing free radicals, which continue to damage cell components
Discuss the manifestations of the four major types of necrosis, and give examples of the tissue types affected by each type of necrosis. Liquefaction necrosis- the process by which dead cells liquefy under the influence of certain cell enzymes. Occurs when brain tissue dies, or in some bacterial infections in which a cavity or ulcer develops in the infected area Coagulative necrosis- when the cell proteins are altered or denatured and the cells retain some form for a time after death. Occurs in a myocardial infarction when a lack of oxygen causes cell death Fat necrosis- when fatty tissue is broken down into fatty acids in the presence of infection or certain enzymes. These compounds may increase inflammation. Caseous necrosis- a form of coagulation necrosis in which a thick, yellowish, “cheesy” substance forms. When TB develops, the first stage is characterized by development of a Ghon complex a.k.a. granuloma (small solid mass of macrophages & lymphocytes covered by connective tissue). Caseous necrosis can be seen inside this mass. The Ghon complex heals like a scar, containing the infection. If the infection continues to develop, the area may undergo liquefaction necrosis, forming a cavity
Discuss apoptosis. Apoptosis- programmed cell death; a normal occurrence in the body. Cells self-destruct by digesting themselves enzymatically and then disintegrate into apoptotic bodies (vesicles), which are then phagocized without eliciting an inflammatory response. Apoptosis may increase when cell development is abnormal, cell numbers are excessive, or cells are injured or aged.

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

Discuss the regulatory processes for sodium and water balance in the body, including the role of antidiuretic hormone, renin-angiotensin-aldosterone Antidiuretic Hormone (ADH)- controls the amount of fluid leaving the body in the urine; helps retain Na+ and promotes reabsorption of water into the blood from the kidney tubules; prevents the production of dilute urine; released by the pituitary gland Aldosterone determines the reabsorption of Na+ ions and water from the kidney tubules; aldosterone conserves more fluid when there is a fluid deficit in the body. The kidneys detect low blood volume or Na+ levels, or blood K+ is high, and release renin (enzyme). Renin converts angiotensinogen (produced in the liver) to angiotensin I (hormone). Angiotensin-converting enzyme (ACE) , found in the lungs, metabolizes angiotensin I into angiotensin II. Angiotensin II causes vasoconstriction and BP to increase. Angiotensin II stimulates the release of aldosterone in the adrenal glands, which causes the renal tubules to retain Na+ and water and excrete K+. Angiotensin II & aldosterone work to raise blood volume, blood pressure and Na+ levels in the blood. If the renin-angiotensin system becomes overactive, consistently high blood pressure results
Identify the basic causes and clinical manifestations of hypernatremia, hyponatremia, hyperkalemia and hypokalemia, hypocalcemia, hypercalcemia Causes of HYPERnatremia: o Excessive consumption of Na+ without proportionate water intake o Loss of water from the body that is faster than the loss of sodium o Insufficient ADH, which results in a large volume of dilute urine (diabetes insipidus) o Loss of the thirst mechanism o Watery diarrhea o Prolonged periods of rapid respiration Signs & Symptoms of HYPERnatremia: o Thirst; tongue and mucosa are dry and sticky o Weakness, lethargy, agitation o Edema o Elevated BP Causes of HYPOnatremia: o Losses from excessive sweating, vomiting, and diarrhea o Use of certain diuretic drugs combined with low-salt diets o Insufficient aldosterone, adrenal insufficiency, and excess ADH secretion (SIADH or syndrome of inappropriate antidiuretic hormone secretion) o Early chronic renal failure o Excessive water intake Signs & Symptoms of HYPOnatremia: o Anorexia, nausea, cramps o Fatigue, lethargy, muscle weakness o Headache, confusion, seizures

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

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
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
Discuss the role of hydrogen ion concentration in cellular function and dysfunction.
Explain how the lungs and the kidneys regulate acid-base balance.
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. Definition - is the body's nonspecific response to tissue injury, resulting in redness, swelling, warmth, pain, and sometimes a loss of function. Disorders ending -itis for inflammation. The root word is usually a body part or tissue - for example, pancreatitis, appendicitis, laryngitis Causes: associated with many different types of tissue injury, causes include direct physical damage such as cuts or sprains, caustic chemicals such as acids or alkali, ischemia or infarction, allergic reactions, extremes of heat or cold, foreign bodies such as splinters or glass and infection. Steps: an injury to capillaries and tissue cells will result in the following reaction

Bradykinin is released from the injured cells
Bradykinin activates pain receptors
Sensation of pain stimulates mast cells and basophils to release histamine
Bradykinin and histamine cause capillary dilation a. This results in an increase of blood flow and increased capillary permeability
Break in skin allows bacteria to enter the tissue a. This results in the migration of neutrophils and monocytes to the site of injury
Neutrophils phagocytize bacteria
Macrophages leave the bloodstream and phagocytose microbes

Pathophysiology of inflammation (acute vs. chronic); local effects and systemic effects of inflammation (including clinical manifestations); complications of acute and chronic inflammation Acute Inflammation : o Process of inflammation is the same, regardless of cause. o Timing varies with specific cause o Chemical mediators affect blood vessels and nerves in the damaged area: o Vasodilation o Hyperemia o Increase in capillary permeability o Chemotaxis to attract cells of the immune system o When tissue injury occurs, the damaged mast cells and platelets release chemical mediators including histamine, serotonin, prostaglandins, and leukotrienes into the interstitial fluid and blood. These chemicals affect blood vessels and nerves in the damaged area o The rapid release of chemical mediators results in local vasodilation (relaxation of smooth muscle causing an increase in the diameter of arterioles), which causes hyperemia, increased blood flow in the area. Capillary membrane permeability also increases, allowing plasma proteins to move into the interstitial space along with more fluid o The increased fluid dilutes any toxic material at the site, while the globulins serve as antibodies, and fibrinogen forms a fibrin mesh around the area in an attempt to localize the injurious agent. Any blood clotting will also provide a fibrin mesh to wall off the area. Vasodilation and increased capillary permeability make up the vascular response to injury o As excessive fluid and protein collects in the interstitial compartment, blood flow in the area decreases as swelling leads to increased pressure on the capillary bed, and fluid shifts

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

Immunologic: o Infection of burn injuries increases tissue loss in the area, often converting a partial- thickness burn to a full-thickness burn o Common microbes involved in burn injury infections include Pseudomonas aeruginosa, Staphylococcus aureus (including drug-resistant strains), Klebsiella, and Candida o When serious infection develops, there is risk of microorganisms or toxins spreading throughout the body, causing septic shock and other complications. Treatment involves rapid excision or removal of the damaged and infected tissue, application of antimicrobial drugs, and replacement with skin grafts or a substitute covering

Chapters 6 & 7: Immune/Infection

Know and understand factors for bacterial resistance Production of exotoxins and endotoxins Production of destructive enzymes Spore formation Presence of bacterial capsule and pili Entry of large number of organisms into body
Nosocomial infection o Infections that occur in health care facilities, including hospitals, nursing homes, doctors’ offices, and dental offices o Reasons for these infections include the presence of many microorganisms in these settings, patients with contagious diseases, overcrowding, use of contaminated instruments, immunocompromised and weakened patients, the chain of transmission through staff, diagnostic procedures, and equipment, therapeutic aids, and food trays. o Many microorganisms in health care settings are resistant to several drugs
Know what are the different classes of infectious microorganisms and examples? Bacteria are unicellular (single cell) organisms that do not require living tissue to survive o Rigid cell wall (gram + or gram - ) o Cell membrane o Capsule or slim layer o Flagella o Pili or fimbriae o Contain cytoplasm o Toxic substances (endo and exotoxins) o Endospores Viruses- very small obligate intracellular parasites that requires a living host cell for replication

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

Cardiovascular: decreased blood pressure
Central nervous system: anxiety and fear (early); weakness, dizziness, and loss of consciousness o Tx: epinephrine injection administered immediately, Antihistamine drugs, Glucocorticoids or cortisone

Know clinical manifestations of infection o Microorganisms must gain entry to the body, choose a hospitable site, establish a colony, and begin reproducing; only if the host defenses are insufficient to destroy all the pathogens during this process will infection be established o Incubation period- the time the body is exposed to the organism and the appearance of clinical signs of the disease; during this time the organisms reproduce until there are sufficient numbers to cause adverse effects in the body o Prodromal period- the early symptoms stage when the infected person may feel fatigued, lose appetite, or have a headache and usually senses that “I am coming down with something.” o Acute period- when the infectious disease develops fully and the clinical manifestations reach a peak. The onset of a specific infection may be insidious, with a prolonged or gradual prodromal period, or sudden or acute, with the clinical signs appearing quickly with severe manifestations o Local effects: inflammation, pain or tenderness, swelling, redness, and warmth; if infection caused by bacteria, a purulent exudate (pus) is present, whereas a viral infection results in serous, clear exudates; tissue necrosis at the site is likely as well; Lymphadenopathy typically occurs and is manifest by swollen and tender lymph nodes o Systemic effects- Fever, fatigue and weakness, headache, and nausea are all commonly associated with infection; with severe infection the nervous system may be affected, resulting in confusion or disorientation, seizures or loss of consciousness.
Know risk factors, clinical manifestations of HIV/AIDS, PATHO PROCESS, AIDS is a chronic infectious disease caused by HIV, which destroys helper T lymphocytes, causing loss of the immune response and increased susceptibility to secondary infections and cancer a. Risk factors i. Injection drug users ii. Unprotected sex iii. Ethnic minorities b. Pathophysiology i. HIV is commonly transmitted via unprotected sexual activity, blood transfusions, hypodermic needles, and from mother to child. Upon acquisition of the virus, the virus replicates inside and kills T helper cells, which are required for almost all adaptive immune responses. There is an initial period of influenza-like illness, and then a latent, asymptomatic phase. When the CD4 lymphocyte count falls below 200 cells/ml of blood, the HIV host has progressed to AIDS, a condition

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

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

a. Pemphigus: If you have it, your immune system attacks healthy cells in your skin and mouth, causing blisters and sores. No one knows the cause. Pemphigus does not spread from person to person.

Allergies: very common and appear to be increasing in incidence and severity, particularly in young children. a. Take many forms, including skin rashes, hay fever, vomiting, and anaphylaxis

Chapter 20: CANCER

N eoplasm- tumor; a cellular growth that’s no longer responding to normal body controls; cells continue to reproduce when there is no need for them; this excessive growth deprives other cells of nutrients o Many neoplasms are unable to function as normal tissue cells because they consist of atypical (abnormal) or immature cells.

Differentiate benign from malignant tumors. Benign Tumors Malignant Tumors Cells Similar to normal cells Differentiated Mitosis fairly normal Varied in size & shape w/ large nuclei Many undifferentiated Mitosis increased and atypical Growth Relatively slow Expanding mass Frequently encapsulated Rapid growth Cells not adhesive, infiltrate tissue No capsule Spread Remains localized Invades nearby tissues or metastasizes to distant sites through blood and lymph vessels Systemic effects Rare Often present Life-threatening Only in certain locations (e.g., brain) Yes, by tissue destruction and spread of tumors
Identify the importance of tumor markers. Tumor markers- substances, enzymes, antigens, or hormones produced by some neoplastic cells; tumor cell markers can be used to screen high-risk individuals, confirm a diagnosis, or monitor the clinical course of a malignancy
Define oncogene, tumor suppressor gene Oncogene - a gene that is a mutated form of a gene involved in normal cell growth; has the potential to cause growth of cancer cells; in tumor cells, these genes are often mutated, or

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 Systemic Effects of Cancer: o Weight loss o Anemia o Severe fatigue o Infections (pneumonia) o Bleeding o Paraneoplastic syndromes- tumor cells release substances that affect neurological function or blood clotting or have hormonal effects Adverse Effects of Cancer Tx: o Bone marrow depression o Epithelial cell damage includes damage to blood vessels (vasculitis) and skin
Skin becomes inflamed (as in a sunburn)
Hair loss (alopecia)
Mucosa of the digestive tract is damaged, resulting in some nausea, vomiting & diarrhea; risk of malnutrition and dehydration
Secondary causes: infection, ischemia, bleeding o Abdominal radiation likely to damage ovaries/testes, leading to sterility or risk of teratogenesis o Fatigue and lethargy accompanied by mental depression o Some antineoplastic drugs have unique damaging effects in specific areas (fibrosis in lungs or damage to myocardial cells)

Chapter 28: Environmental Hazards

Describe why smoking and exposure to radiation are major risk factors for cancer and how they alter cellular structure and function and know examples of cancers Smoking: o Cigarette smoking predisposes smoker to lung disease (emphysema, bronchitis, lung cancer), bladder cancer, peptic ulcers, and cardiovascular disease o Smoking impairs fertility, and affects fetal development during pregnancy, leading to stillbirth or low-birth-weight infants and an increased risk of complications Radiation: o Primarily affects cells that undergo rapid mitosis (epithelial tissue, bone marrow, ovaries/testes) o Small doses- cells can sometimes repair the ruptured DNA strands o Larger doses- DNA is altered and often cross-linkages form, leading to mutations in the cell and the development of cancer

NR283 Pathophysiology Study Guide for Exam 1, Study notes of Pathophysiology

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Partial preview of the text

Download NR283 Pathophysiology Study Guide for Exam 1 and more Study notes Pathophysiology in PDF only on Docsity!

NR283 Pathophysiology Study Guide for Exam 1

Chapter 1: Intro to Pathology

Chapter 5: Inflammation

Chapters 6 & 7: Immune/Infection

Chapter 20: CANCER

Chapter 28: Environmental Hazards