NUR2392, MDCII – Examination Blue Print – Exam 1

NUR2392, MDCII – Examination Blue Print – Exam 1 End-of-Life • Pathophysiology of Death- Death is defined as the cessation of integrated tissue and organ function, manifesting with lack of heartbeat, absence of spontaneous respirations, or irreversible brain dysfunction. S/S of Approaching death- As death nears, patients often have signs and symptoms of decline in • physical function- manifesting as weakness • increased sleep. • anorexia • changes in cardiovascular function • breathing patterns • genitourinary function. • Level of consciousness often declines to lethargy, unresponsiveness, or coma. • Cardiovascular dysfunction leads to decreases in peripheral circulation and poor tissue perfusion manifesting as cold, mottled, and cyanotic extremities. • Blood pressure decreases and often is only palpable. • The dying person’s heart rate may increase, become irregular, and gradually decrease before stopping. • Changes in breathing pattern are common, with breaths becoming very shallow and rapid. Periods of apnea and Cheyne-Stokes respirations (apnea alternating with periods of rapid breathing) are also common. Death occurs when respirations and heartbeat stop. o Management of symptoms Patient and Family Education: Preparing for Self-Management Common Physical Signs and Symptoms of Approaching Death With Recommended Comfort Measures Coolness of Extremities Circulation to the extremities is decreased; the skin may become mottled or discolored. 1. • Cover the patient with a blanket. 2. • Do not use an electric blanket, hot water bottle, or electric heating pad to warm the patient. Increased Sleeping Metabolism is decreased. 1. • Spend time sitting quietly with the patient. 2. • Do not force the patient to stay awake. 3. • Talk to the patient as you normally would, even if he or she does not respond. Fluid and Food Decrease Metabolic needs have decreased. 1. • Do not force the patient to eat or drink. 2. • Offer small sips of liquids or ice chips at frequent intervals if the patient is alert and able to swallow. 3. • Use moist swabs to keep the mouth and lips moist and comfortable. 4. • Coat the lips with lip balm. Incontinence The perineal muscles relax. 1. • Keep the perineal area clean and dry. Use disposable under pads and disposable undergarments. 2. • Offer a Foley catheter for comfort. Congestion and Gurgling The person is unable to cough up secretions effectively. 1. • Position the patient on his or her side. Use toothette to gently clean mouth of secretions. 2. • Administer medications to decrease the production of secretions. Breathing Pattern Change Slowed circulation to the brain may cause the breathing pattern to become irregular, with brief periods of no breathing or shallow breathing. 1. • Elevate the patient’s head. 2. • Position the patient on his or her side. Disorientation Decreased metabolism and slowed circulation to the brain. 1. • Identify yourself whenever you communicate with the person. 2. • Reorient the patient as needed. 3. • Speak softly, clearly, and truthfully. Restlessness Decreased metabolism and slowed circulation to the brain. 1. • Play soothing music and use aromatherapy. 2. • Do not restrain the patient. 3. • Talk quietly. 4. • Keep the room dimly lit. 5. • Keep the noise level to a minimum. 6. • Consider sedation if other methods do not work. o Postmortem Care • Provide all care with respect to communicate that the person was important and valued. • Ask the family or significant others if they wish to help wash the patient or comb his or her hair; respect and follow their cultural practices for body preparation. • If no autopsy is planned, remove or cut all tubes and lines according to agency policy. • Close the patient’s eyes unless the cultural or religious practice is for a family member or other person to close the eyes. • Insert dentures if the patient wore them. • Straighten the patient and lower the bed to a flat position. • Place a pillow under the patient’s head. • Wash the patient as needed and comb and arrange the patient’s hair unless the family desires to perform bathing and body preparation. • Place waterproof pads under the patient’s hips and around the perineum to absorb any excrement. • Clean the patient’s room or unit. • Allow the family or significant others to see the patient in private and to perform any religious or cultural customs they wish (e.g., prayer). • Assess that all who need to see the patient have done so before transferring to the funeral home or morgue. • Notify the hospital chaplain or appropriate religious leader if requested by the family or significant others. • Ensure that the nurse or physician has completed and signed the death certificate. • Prepare the patient for transfer to either a morgue or a funeral home; wrap the patient in a shroud (unless the family has a special shroud to use), and attach identification tags per agency policy. • Hospice vs Palliative Care • Impact of Pain & Pain Management Impact of Unrelieved Pain Physiologic Impact Quality-of-Life Impact • Prolongs stress response • Increases heart rate, blood pressure, and oxygen demand • Decreases GI motility • Causes immobility • Decreases immune response • Delays healing • Poorly managed acute pain increases risk for development of chronic pain • Interferes with ADLs • Causes anxiety, depression, hopelessness, fear, anger, and sleeplessness • Impairs family, work, and social relationships Financial Impact Costs Americans billions of dollars per year Increases length of hospital stay Leads to lost income and productivity ManagementofPain 1. •Useamultimodalap roachthatcombinesanalgesicswithdifferentunderlyingmechanismswiththedesired outcomeofachievingoptimalpainreliefwithlowerdosesthanwouldbeposiblewithasingleanalgesic;lower dosesresultinfewersideeffects. 2. •Considerthetypeofpainandbegintherapywiththefirst-lineanalgesicsthatarerecommendedforthatypeof pain. 3. •Donotgivemeperidinetoolderadultsbecausemosthavedecreasedrenalfunctionandareunabletoefficiently eliminateitscentralnervoussystem (CNS)-toxicmetabolitenormeperidine. 4. •Usearound-the-clock(ATC)dosingofanalgesicsforpainthatisofacontinuousnature(e.g.,persistent[chronic] osteoarthritisorcancerpain;persistent[chronic]neuropathicpain,first24to48hoursaftersurgery). 5. •Useas-needed(PRN)dosingforintermitentpainandbeforepainfulactivities,suchasbeforeambulationand physicaltherapy. 6. •Beawareofthemainsideeffectsoftheanalgesicsthatareadministeredandthatheymaybemorelikelyto ocurorbemoresevereinolderthaninyoungeradults. 7. •Startlowandgoslowwithdrugdosing;increasedosestoachieveadequateanalgesiabasedonthepatient’s responsetothepreviousdose. 8. •Teachthepatientandfamilyorothercaregiverabouthepainmanagementplan(analgesicsand nonpharmacologicstrategies)andwhentonotifytheprimaryhealthcareproviderforunrelievedpainor unmanageableorintolerabledrugsideeffects. 9. •Topromoteadherencetothepainmanagementplaninthehomeseting,sugestusingapilboxtoorganize eachday’smedicationsandkepingadiarytoidentifytimesofthedayoractivitiesthatincreasepain.Thediary canbepresentedtotheprimaryhealthcareprovider,whocanuseitomakenecesaryadjustmentsinthe treatmentplan. • Psychosocial Needs Psychosocial Integrity •Asesthepatient’semotionalsignsofimpendingdeath;ases copingabilityofthepatientandfamilyor othercaregiver. •Incorporatethepatient’spersonalculturalpracticesandspiritualbeliefsregardingdeathanddying •Beawarethatpeoplefacingdeathmayexperiencefearandanxietyaboutheirimpendingdeathandhave difficultycoping. •Providepsychosocialinterventionstosup orthepatientandfamilyduringthedyingproces. • Characteristics of cells o Benign o Benign Cells: A smaller nuclear-to-cytoplasmic ratio-similar to normal cells o Benign Cells: Specific differentiated function -contributes to the body function o Benign Cells: Tight adherence- bind closely together due to the production of fibronectin o Benign Cells: No migration- Do not invade other tissues o Benign Cells: Orderly growth- rate of growth is normal by expansion o Benign Cells: Euploidy- Normal chromosomes per cell 23 A benign tumor is normal cells growing in the wrong place at the wrong time. But they are not cancerous. Benign Cell Features o Harmless o Do not usually require intervention o Slow growing o Tight Adherence o Specific morphology o Small nuclear-to-cytoplasmic ratio o Specific differentiated functions o Tight adherence o Orderly growth o No migration o Normal chromosomes Benign cell looks similar to a healthy cell Examples of Benign cells • Skin Tag • Mole • Nasal Polyp • Uterine Fibroids • Endometriosis o Malignant o Malignant cells: Anaplasia- Loss of appearance of parent cell o Malignant cells: A larger nuclear-to-cytoplasmic ratio -Larger nucleus o Malignant Cells: Specific functions are lost- serve no purpose o Malignant Cells: Loose adherence- Loosely bound due to the lack of fibronectin production o Malignant Cells: Migration- Spread easily (metastasize) o Malignant Cells: Contact inhibition does not occur- Loss of cellular regulation o Malignant cells: Rapid or continuous cell division- loss of cellular regulation o Malignant cells: Aneuploidy- Abnormal chromosomes o Malignant tumor: Leukemias and lymphomas- Leukemias arise from organs that form blood and invade the production of the normal blood cell. Lymphomas affect the lymphocytes, which fight infections and produce enlarged lymph nodes in the armpits, chest, abdomen, and groin. o Malignant tumor: Carcinomas- Originate in the epithelial cells of the skin, lungs, liver, kidneys, stomach, breast, prostate, and thyroid and are likely to metastasize o Malignant tumor: Sarcomas- Originate in sof t tissues such as the muscles, blood vessels, bone, and connective tissues. Malignant cells - indicates cancer and can be harmful to normal body tissues and result in death Malignant cell features o Large nucleus o Migration o Doesn't stop and replicates (No contact inhibition) o Loose adherence o Rapid or continuous cell division o Loss of cellular regulation o Abnormal chromosomes ( or 23) Cancer development stages of malignancy o Initiation o Promotion o Progression o Metastasis • Initiation (Stage of malignancy)- Normal cells are damaged and irreversible • Promotion- Repeated exposureEnhances growth of malignant cells • Progression= Increase in production of malignant cells • Metastasis- Cells move from primary site to the rest of the body o Normal • Types of Cancers o Carcinoma, Sarcoma, Leukemia, Lymphoma Malignant tumor: Carcinomas Originate in the epithelial cells of the skin, lungs, liver, kidneys, stomach, breast, prostate, and thyroid and are likely to metastasize Malignant tumor: Sarcomas Originate in sof t tissues such as the muscles, blood vessels, bone, and connective tissues. Malignant tumor: Leukemias and lymphomas Leukemias arise from organs that form blood and invade the production of the normal blood cell. Lymphomas affect the lymphocytes, which fight infections and produce enlarged lymph nodes in the armpits, chest, abdomen, and groin. o Classification ▪ Grading ▪ Ploidy ▪ Staging Cancers are classified according to the type of tissue from which they arise (e.g., glandular, connective) Cancer Grading, Ploidy, and Staging Systems of grading and staging have been developed to help standardize cancer diagnosis, prognosis, and treatment. Grading of a tumor classifies cellular aspects of the cancer. Ploidy classifies the number and structure of tumor chromosomes as normal or abnormal. Staging classifies clinical aspects of the cancer. Grading is needed because some cancer cells are “more malignant” than others, varying in their aggressiveness and sensitivity to treatment. Some cancer cells barely resemble the mature tissue from which they arose (are “poorly differentiated”), are aggressive, and spread rapidly. These cells are a “high-grade” cancer. Less malignant cancer cells that are “well differentiated” and more closely resemble the tissue from which they arose are less aggressive. Grading compares the appearance and activity of the cancer cell with the normal parent tissue from which it arose. It is a means of evaluating the patient with cancer for prognosis and appropriate therapy. Grading also allows health care professionals to evaluate the results of management. Clinical groups have established specific grading systems for different types of cancer cells, but overall they resemble the standard system listed in Table 19.4. This system rates cancer cells, with the lowest rating given to those cells that closely resemble normal cells and the highest rating given to cancer cells that barely resemble normal cells. Grading systems for different cancers are presented in the clinical chapters in which care is discussed. Ploidy is the description of cancer cells by chromosome number and appearance. Normal human cells have 46 chromosomes (23 pairs), the normal diploid number (euploidy). When malignant transformation occurs, changes in the genes and chromosomes also occur. Some cancer cells gain or lose whole chromosomes and may have structural abnormalities of the remaining chromosomes, a condition called aneuploidy. The degree of aneuploidy increases with the degree of malignancy. Some chromosome changes are associated with specific cancers, and their presence is used for diagnosis and prognosis. One example is the Philadelphia chromosome abnormality often present in chronic myelogenous leukemia cells (see Chapter 37). Other gene changes in cancerous tumors alter the tumor’s susceptibility to specific treatment. Some changes form the basis of “targeted therapy” for cancer (see Chapter 20). Staging determines the exact location of the cancer and whether metastasis has occurred. Cancer stage influences selection of therapy. Staging is done by clinical staging, surgical staging, and pathologic staging. Clinical staging assesses the patient’s symptoms and evaluates tumor size and possible spread. Surgical staging assesses the tumor size, number, sites, and spread by inspection at surgery. Pathologic staging is the most definitive type, determining the tumor size, number, sites, and spread by pathologic examination of tissues obtained at surgery. • Metastasis o Stages o Common locations o Primary vs Secondary tumors The tumor, node, metastasis (TNM) system is used to describe the anatomic extent of cancers. The TNM staging systems have specific prognostic value for each solid tumor type. Table 19.5 shows a basic TNM staging system. TNM staging is not useful for leukemia or lymphomas (see Chapter 37). Additional specific staging systems include the Dukes staging system for colon and rectal cancer and the Clark levels method for staging skin cancer. FIG. 19.3 The steps of metastasis. TABLE 19.2 Common Sites of Metastasis for Different Cancer Types a Most common site of metastasis for the specific cancer. Tumor growth is assessed in terms of doubling time (the amount of time it takes for a tumor to double in size) and mitotic index (the percentage of actively dividing cells within a tumor). The smallest detectable tumor is about 1 cm in diameter and contains 1 billion cells. A tumor with a mitotic index of less than 10% is a slower-growing tumor; a tumor with an index of 85% is faster growing. Different tumor types have a wide range of growth rates. Metastasis occurs when cancer cells move from the primary location by breaking off from the original group and establishing remote colonies. These additional tumors are called metastatic tumors or secondary tumors. Even though the tumor is now in another organ, it is still a cancer from the original altered tissue. For example, when breast cancer spreads to the lung and the bone, it is still breast cancer in the lung and bone—not lung cancer and not bone cancer. Metastasis occurs through many steps, as shown in Fig. 19.3. Tumors first extend into surrounding tissues by secreting enzymes that open up areas of surrounding tissue. Pressure, created as the tumor increases in size, forces tumor cells to invade new territory. Spread to distant organs and tissues requires cancer cells to penetrate blood vessels. Bloodborne metastasis (tumor cell release into the blood) is a common cause of cancer spread. Enzymes secreted by tumor cells also make large pores in the patient’s blood vessels, allowing tumor cells to enter the blood and circulate. Because tumor cells are loosely held together, clumps of cells break off from the primary tumor into blood vessels for transport. o TNM Staging of Cancer—TNM Classification Primary Tumor (T) Tx Primary tumor cannot be assessed T0 No evidence of primary tumor Tis Carcinoma in situ T1, T2, T3, T4 Increasing size and/or local extent of the primary tumor Regional Lymph Nodes (N) Nx Regional lymph nodes cannot be assessed N0 No regional lymph node metastasis N1, N2, N3 Increasing involvement of regional lymph nodes Distant Metastasis (M) Mx Presence of distant metastasis cannot be assessed M0 No distant metastasis M1 Distant metastasis o Warning Signs (CAUTION) The Seven Warning Signs of Cancer C Changes in bowel or bladder habits A A sore that does not heal U Unusual bleeding or discharge T Thickening or lump in the breast or elsewhere I Indigestion or difficulty swallowing O Obvious change in a wart or mole N Nagging cough or hoarseness • Carcinogenesis process Carcinogenesis, Oncogenesis, and Malignant Transformation Carcinogenesis, oncogenesis, and malignant transformation are different terms for cancer development, which is the process of changing a normal cell into a cancer cell. This process occurs through loss of cellular regulation leading to the steps of initiation, promotion, progression, and metastasis. Initiation is the first step in carcinogenesis. Normal cells can become cancer cells if they lose cellular regulation by having their genes promoting cell division (proto-oncogenes) turn on excessively (are overexpressed), becoming oncogenes, and produce more cyclins. Initiation is a change in gene expression caused by anything that can damage cellular DNA, leading to loss of cellular regulation. Such changes can activate proto-oncogenes that should have only limited expression to oncogene status and can damage suppressor genes, which normally limit proto-oncogene activity. Thus initiation leads to excessive cell division through DNA damage that results in loss of cellular regulation by either loss of suppressor gene function or enhancement of proto-oncogene function. Initiation is an irreversible event that can lead to cancer development. After initiation a cell can become a cancer cell if the cellular regulation loss that occurred during initiation continues. If growth conditions are right, widespread metastatic disease can develop from just one cancer cell. Substances that change the activity of a cell’s genes so the cell becomes a cancer cell are carcinogens. Carcinogens may be chemicals, physical agents, or viruses. More than 62 agents, substances, mixtures, and exposures are known to cause cancer in humans, and about another 186 are suspected to be carcinogens. Promotion is the enhanced growth of an initiated cell by substances known as promoters. Once a normal cell has been initiated by a carcinogen and is a cancer cell, it can become a tumor if its growth is enhanced. Many normal hormones and body proteins, such as insulin and estrogen, can act as promoters and make cells divide more frequently. The time between a cell’s initiation and the development of an overt tumor is called the latency period, which can range from months to years. Exposure to promoters can shorten the latency period. Progression is the continued change of a cancer, making it more malignant over time. After cancer cells have grown to the point that a detectable tumor is formed (a 1-cm tumor has at least 1 billion cells in it), other events must occur for this tumor to become a health problem. First the tumor must develop its own blood supply. The tumor makes vascular endothelial growth factor (VEGF) that triggers nearby capillaries to grow new branches into the tumor, ensuring the tumor’s continued nourishment and growth. As tumor cells continue to divide, some of the new cells undergo genetic mutations that change features from the original, initiated cancer cell and form different groups. Some of the mutations, known as driver mutations, provide these cell groups with advantages (selection advantages) that allow them to live and divide no matter how the conditions around them change. These tumor changes may allow it to become more malignant. Over time the tumor cells have fewer and fewer normal cell features. Other mutations, known as passenger mutations, also occur but do not appear to induce significant changes, although they can be used as unique cancer identifiers and serve as specific “targets” for newer cancer therapies. For this reason, genetic testing of all cancers is recommended to allow more precise and effective treatment. The original group of cancer cells or tumor caused by carcinogenesis is called the primary tumor. It is usually identified by the tissue from which it arose (parent tissue) such as in breast cancer or lung cancer. When primary tumors are in vital organs such as the brain or lungs, they can grow and either lethally damage the vital organ or interfere with that organ’s ability to perform its vital function. At other times the primary tumor is located in soft tissue that can expand without damage as the tumor grows. One such site is the breast. The breast is not a vital organ, and even with a large tumor the primary tumor alone would not cause the patient’s death. When the tumor spreads from the original site into vital areas (metastasizes), life functions can be disrupted, and death may follow. • Management & Treatment Cancer Management Thepurposeofcancermanagementistocureorcontrolthediseasewhileminimizingthesideeffectsoftherapy.For certaincancertypessuchasacuteleukemia,failuretotreatthediseasewouldresultindeathwithinweekstomonths. Cancertreatmentcanincludesurgery,radiation,chemotherapy,immunotherapy,targetedtherapy,andhormonaltherapy. Thesetherapiesmaybeusedseparatelyorincombinationtokilcancercels.Thetypesoftherapyuseddependonthe specifictypeofcancer,whetherthecancerhasspread,and theoveralhealthand functionalstatusofthepatient. Treatmentregimens(protocols)havebeen established formosttypesofcancer.TheNationalComprehensiveCancer Network(NCCN)providesevidence-basedguidelinesandstandardizedtreatmentplansbasedonthediagnosisandstage ofcancerandmonitoringoftreatmentresponse. o Types of Surgery Surgery often plays a part in the diagnosis and/or management of cancer. Surgery is only one part of a comprehensive treatment approach for cancer therapy. Surgery is used for prophylaxis, diagnosis, cure, control, palliation, and tissue reconstruction. Prophylactic surgery removes potentially cancerous tissue as a means of preventing cancer development. It is performed when a patient has either an existing premalignant condition or a strong predisposition for development of a specific cancer. For example, removing the opposite breast in a patient who has a genetic mutation (e.g., BRCA1, BRCA2) to prevent cancer in the unaffected breast is considered prophylactic surgery. Diagnostic surgery (e.g. excisional biopsy) is the removal of all or part of a suspected lesion for examination and testing to confirm or rule out a cancer diagnosis. Cancer treatment is not initiated without tissue confirmation of a cancer diagnosis. Curative surgery removes all cancer tissue. Surgery alone can result in a cure when all visible and microscopic tumor is removed. It is most effective for small localized tumors or noninvasive skin cancers such as basal cell lesions. Debulking surgery removes part of the tumor if removal of the entire mass is not possible. It decreases the size of the tumor and the number of cancer cells, which may help alleviate symptoms, enhance the success of other types of cancer treatment, and increase survival time. Palliative surgery focuses on providing symptom relief and improving the quality of life but is not curative. Examples include removal of tumor tissue that is causing pain, obstruction, or difficulty swallowing. Reconstructive or restorative surgery increases function, enhances appearance, or both. Examples include breast reconstruction after mastectomy, bowel reconstruction, revision of scars, and cosmetic reconstruction in head and neck cancer. Side Effects of Surgical Treatment Cancer surgery often involves the loss of a body part or its function to ensure removal of all cancerous tissue. Surgery can remove all or part of the affected body part. Any organ loss reduces function. Some cancer surgeries result in scarring or disfigurement. For example, the tongue and part of the mandible or larynx may be removed in patients with head and neck cancers (see Chapter 26). Following some cancer surgeries, the removal of the affected area can cause significant changes in appearance or activity level. Patients may need supportive care and help in adapting to their new normal. o Radiation & Chemotherapy ▪ Management of risks ▪ Possible side effects • Nadir • Neutropenia • Thrombocytopenia nadir Theperiodinwhichthebonemarow sup resionisthegreatestandthepatientisathighestriskforcomplications. neutropenia Decreasednumbersofneutrophilwhitebloodcelsleadingtoimmunosup resion. thrombocytopenia Decreased numbers of platelets leading to impaired clotting and bleeding. Radiation Therapy Radiation therapy uses high-energy radiation to kill cancer cells, with the intent to cure or relieve symptoms (palliative). The goal of radiation is to kill the cancer cells while having minimal damaging effects on the surrounding normal tissue. The effects of radiation are seen only in tissues within the radiation field or path, and radiation is considered a local treatment. For example, radiation to the chest for lung cancer causes skin changes and hair loss only on the chest area that is treated. Occasionally, systemic radiation therapy uses an intravenous radioactive substance that travels throughout the body to target cancerous cells. Radiation therapy has both short- and long-term effects, depending on the area(s) radiated. For example, a short-term effect is redness or desquamation of the skin, whereas a long-term effect can be pulmonary fibrosis from radiation of the chest. When cancer cells are exposed to radiation, the cell’s DNA is damaged directly, resulting in a change in cellular regulation. These damaged cells usually can no longer reproduce or function, leading to cell death. Normal cells in the field of radiation are also affected by radiation. Careful planning of the radiation field by a radiation physicist, dosimetrist, and radiation oncologist is necessary to minimize damage to normal tissues and organs. The amount of radiation delivered to a tissue is the exposure; the amount of radiation absorbed by the tissue is the radiation dose. The dose is always less than the exposure because some energy is lost as it travels to the destination. The three factors determining the absorbed dose are the intensity of exposure, the duration of exposure, and the closeness (distance) of the radiation source to the cells. Absorbed radiation doses are described in units called grays (Gy). The total dose of radiation used depends on tumor size and location and on the sensitivity of the tumor and nearby tissues. Radiation therapy usually is given as a series of divided doses (fractionation) over a set time. This allows greater destruction of cancer cells while reducing the damage to normal tissues. The intensity of the radiation decreases with the increasing distance from the radiation source. Radiation may be used as a stand-alone treatment or may be combined with other cancer treatments. Combining treatments requires careful planning of sequencing, timing, and dose of each treatment to maximize tumor kill and limit damage to normal cells. Combining radiation with chemotherapy involves giving chemotherapy agents that radiosensitizer the tumor to enhance the radiation damage. This will result in a greater cell kill than either therapy used alone. Side effects of combined therapy can be more severe and may require more frequent interventions. Multiple factors, including total radiation dose, duration of radiation, and whether concurrent chemotherapy is prescribed, can affect skin response to radiation. Radiation to the head may result in permanent hair loss. Some systemic side effects such as altered taste, fatigue, and bone marrow suppression may also occur. Fatigue may be related to the increased energy demands needed to repair damaged cells. Radiation-induced fatigue can be debilitating and may last for months. Some degree of bone marrow suppression and reduced immunity occurs, regardless of the treatment site. The intensity of marrow suppression is related to the dose, site, and size of the area irradiated. Chemotherapy Overview Chemotherapy, the treatment of cancer with chemical agents, is used to cure and to increase survival. This killing effect on cancer cells is related to the ability of chemotherapy to damage DNA and interfere with cell division and cellular regulation. Tumors with rapid growth are often more sensitive to chemotherapy. As described in Chapter 19, cancer cells can separate from the original tumor and spread to surrounding areas and to distant sites within the body (metastasize). Treatment of patients with metastatic cancer is not considered to be of curative intent, but with newer treatment options, patients are living longer. Chemotherapy is useful in treating cancer because its effects are systemic, providing the opportunity to kill cancer cells, and it may provide protection from cells that have started to metastasize. Drugs used for chemotherapy also exert their cell-damaging (cytotoxic) effects on healthy cells. The normal cells most affected by chemotherapy are those that divide rapidly, including skin, hair, intestinal tissues, reproductive cells, and blood-forming cells. Chemotherapy Drug Categories Chemotherapy has many different categories and mechanisms of action specific to the way the drug kills the cell. Chemotherapy drugs can prevent cellular division, break DNA strands to prevent replication, impede cellular and enzyme reactions, and prevent mitosis. This prevents the cell from dividing, or limits division. See Table 20.3 for specific chemotherapy drug categories. Combination Chemotherapy Combination chemotherapy is using more than one drug for treatment of a specific cancer. Combination therapy is more effective in killing cancer cells than using just one drug because different mechanisms of action work together to affect cell division. However, the side effects and damage caused to normal tissues also increase with combination chemotherapy. Treatment Issues Drugs selected for use with a given patient are based on the sensitivity of cancer cells to the drug and the stage or extent of disease. Selected treatment protocols have been developed for many cancers through use of well-established clinical guidelines for initial treatment and relapsed disease (National Comprehensive Cancer Network [NCCN] guidelines). Dosages for most chemotherapy drugs are calculated according to the patient’s size, based on milligrams per square meter (mg/m2) of body surface area (BSA). This is a calculation of the patient’s height and weight at the time of chemotherapy administration. Dosages may change if the patient experiences significant weight loss between cycles. Side Effects of Chemotherapy Temporary and permanent damage can occur to normal tissues from chemotherapy. Chemotherapy is systemic and exerts its effects on all cells within the body. Common Terminology for Cancer Adverse Events (CTCAE) has a standardized grading scale to evaluate and document common side effects. Some problems include bladder toxicity (hemorrhagic cystitis), cardiac muscle damage, and loss of bone density. For some cancer drugs, agents that protect specific healthy cells (cytoprotectants or chemoprotectants) are given ahead of or with chemotherapy drugs to decrease the impact of these drugs on normal tissues. For example, mesna binds toxic metabolites to decrease bladder toxicity and prevent hemorrhagic cystitis from ifosfamide and high-dose cyclophosphamide use. Agents such as the anthracycline drug doxorubicin can result in cardiotoxicity, leading to heart failure and decreased ejection fraction (EF). Dexrazoxane can be prescribed to protect the heart. Loss of bone density is associated with the use of oral aromatase inhibitors for breast cancer treatment. These patients will require a vitamin D supplement or bisphosphonate therapy in an attempt to offset the known risk. Serious short-term side effects occur with cytotoxic chemotherapy. The side effects on the hematopoietic (blood- producing) system can be life threatening and are the most common reason for changing the dosage or the treatment plan. The suppressive effects on the bone marrow blood-forming cells cause anemia (decreased numbers of red blood cells and hemoglobin); reduced immunity with neutropenia (decreased numbers of neutrophil white blood cells, leading to immunosuppression); and thrombocytopenia (decreased numbers of platelets), which leads to impaired clotting and bleeding. Common distressing side effects include nausea and vomiting, alopecia (hair loss), mucositis (open sores or ulcers on mucous membranes), skin changes, anxiety, sleep disturbance, altered bowel elimination, and changes in cognitive function. The impact of side effects can create distress, which can vary from patient to patient. Cancer symptom distress is measured using the National Comprehensive Cancer Network (NCCN) Distress Thermometer. Assessing for distress is important to allow for prompt symptom management and overall improvement in quality of life. ▪ Teaching needs Patientand FamilyEducation:PreparingforSelf-M anagement Chemotherapy-InducedPeripheralNeuropathy 1.•Protectfetandotherbodyareaswheresensationisreduced;alwayswearshoeswithaprotectivesole. 2.•Besurethatshoesarewelfitingtopreventcreatingsoresorblistersfrom friction. 3.•Inspectyourfetdaily(withamiror,ifneded)foropenareasorrednes. 4.•Avoidextremesoftemperature;wearwarm clothinginthewinter,especialyoverhands,fet,andears. 5. •Testwatertemperaturewithathermometerwhenwashingdishesorbathing.Usewarm waterratherthanhotwater(les than105°For40.6°C). 6. •Usegloveswhenwashingdishesorgardening. 7. •Donoteatfodsthatareto hot;alow them tocolbeforeplacingthem inyourmouth. 8.•Eatfodsthatarehighinfiber(e.g.,fruit,whole-graincereals,vegetables). 9. •Drink2to3litersoffluid(nonalcoholic)dailyunlesyourprimaryhealthcareproviderordersafluid-restricteddiet. 10. •Getupslowlyfrom alyingorsitingposition.Ifyoufeldizzy,sitbackdownuntilthedizzines fadesbefore standing;thenstandinplaceforafew secondsbeforewalkingorusingthestairs. 11. •Topreventrip ingorfaling,lokatyourfetandtheflororgroundwhereyouarewalkingtoaseshowthe ground,flor,orstepchanges. 12. •Avoidusingarearugs,especialythosethatslideeasily. 13. •Kepflorsfre ofcluterthatcouldleadtoafal. 14. •Usehandrailswhengoingupordownsteps. ▪ Interprofessional care Interprofessional Collaborative Care Theprioritycareisuesduringchemotherapyareprotectingthepatientfrom thelife-threateningsideeffects andmanagingtheasociateddistresingsymptoms.Forsomepatientsthesymptomsaresounpleasantthat theychosetostoptreatment.Nursingeducationandinterventionarekeytosup ortingthepatientand helpingmanagesideeffects. • Oncologic Emergencies (Assessment, S/S, Interventions) o Metabolic ▪ Hypercalcemia ▪ Tumor Lysis syndrome ▪ SIADH o Hematologic ▪ Febrile Neutropenia ▪ Sepsis ▪ Disseminated intravascular coagulation o Structural ▪ Spinal Cord Compression ▪ Superior Vena Cava Syndrome Oncologic Emergencies With improvements in cancer treatments, many cancers have become chronic diseases. However, acute complications from the cancer or its treatment can occur at any time. This chapter presents select acute complications of cancer or cancer treatment, including sepsis and disseminated intravascular coagulation (DIC), syndrome of inappropriate antidiuretic hormone (ADH), spinal cord compression (SCC), hypercalcemia, superior vena cava (SVC) syndrome, and tumor lysis syndrome (TLS) as oncologic emergencies. Early diagnosis and immediate intervention for these emergency conditions are essential to avoid life- threatening situations. The role of the nurse is to implement interventions to prevent and detect these complications early for immediate treatment. Sepsis and Disseminated Intravascular Coagulation Sepsis, or septicemia, is a condition in which organisms enter the bloodstream through any site of skin breakdown and cause a severe infection. Severe sepsis can result in septic shock, a life-threatening condition. Adults with cancer who have low white blood cell (WBC) counts (neutropenia) and impaired immunity from cancer treatment are at risk for infection and sepsis. Chapter 34 describes the pathophysiology of sepsis and septic shock. Patients with neutropenia do not have enough WBCs to produce the typical signs and symptoms of infection (i.e., erythema, swelling, warmth, high fever). Often a low-grade fever (100.4°F or 38°C) is the only sign of infection. Infection and sepsis have a high mortality rate in adults with neutropenia (McCance et al., 2019). Teach patients the importance of notifying the primary health care provider at the first sign of infection or fever. Disseminated intravascular coagulation (DIC) is a problem with the blood-clotting process. DIC is triggered by many severe illnesses, including cancer. In patients with cancer DIC often is caused by sepsis from a variety of organisms (bacterial, fungal, viral, or parasitic). Extensive, abnormal clotting occurs throughout the blood vessels of patients with DIC. This widespread clotting depletes circulating clotting factors and platelets. As this happens, extensive bleeding occurs. Bleeding from many sites is the most common problem and ranges from oozing to fatal hemorrhage. Clots block blood vessels and decrease blood flow to major body organs and result in pain, ischemia, stroke like symptoms, dyspnea, tachycardia, reduced kidney function, and bowel necrosis. When sepsis is present and DIC is likely, management focuses on reducing the infection and halting the DIC process. IV antibiotic therapy is initiated. During the early phase of DIC, anticoagulants (especially heparin) are given to limit clotting and prevent the rapid consumption of circulating clotting factors. When DIC has progressed and hemorrhage is the primary problem, clotting factors are given. See Chapter 34 for a detailed discussion of DIC. Syndrome of Inappropriate Antidiuretic Hormone In healthy adults, antidiuretic hormone (ADH) is secreted by the posterior pituitary gland only when more fluid (water) is needed in the body, such as when plasma volume is decreased. Certain conditions induce ADH secretion when not needed by the body, which leads to syndrome of inappropriate antidiuretic hormone (SIADH). SIADH is a disorder of impaired water retention (McCance et al., 2019). Cancer is a common cause of SIADH, especially small cell lung cancer. SIADH also may occur with other cancers or when metastatic tumors are present in the brain. Some cancers make and secrete ADH, whereas others stimulate the posterior pituitary to secrete ADH. Drugs used for cancer treatment or supportive therapy also can cause SIADH. Older adults are at risk for SIADH due to medications (McCance et al., 2019). In SIADH, water is reabsorbed in excess by the kidneys and put into systemic circulation. The retained water dilutes blood sodium levels, causing hyponatremia. Normal range for sodium is 136 to 145 mEq/L (mmol/L) ( Pagana & Pagana, 2018). Mild symptoms include weakness, muscle cramps, loss of appetite, and fatigue. With greater fluid retention and decreased sodium levels, weight gain, nervous system changes, personality changes, confusion, and extreme muscle weakness occur. As the sodium level drops toward 110 mEq/L (mmol/L), seizures, coma, and death may follow depending on how rapidly hyponatremia occurs. SIADH is managed by treating the condition and the cause. Nursing priorities focus on patient safety, restoring normal fluid balance, and providing supportive care. Management includes fluid restriction, increased sodium intake, and drug therapy. Immediate cancer treatment with radiation or chemotherapy may cause enough tumor regression that ADH production returns to normal. See Chapter 57 for a detailed discussion of SIADH management. Spinal Cord Compression Spinal cord compression (SCC) is an oncologic emergency that requires immediate intervention to relieve pain and prevent permanent neurologic damage. Damage from SCC occurs either when a tumor directly enters the spinal cord or spinal column or when the vertebrae collapse from tumor degradation of the bone. The most frequent area for SCC is the thoracic spine. The symptoms of SCC can vary depending on the severity and location of the compression. Back pain is a common first symptom and occurs before other problems or nerve deficits. Other symptoms include weakness, loss of sensation, urinary retention, and constipation. Loss of or reduced deep tendon reflexes along with reduced pinprick and vibratory sensations are other findings that may be present at physical assessment. Neurologic problems are specific to the level of spinal compression and can lead to paralysis, which is usually permanent if the compression is not alleviated promptly. Early recognition and treatment of SCC are key to a positive outcome. Assess for back pain that worsens over time; neurologic changes; muscle weakness or a sensation of heaviness in the arms or legs; numbness or tingling in the hands or feet; inability to distinguish pinprick, touch, or hot and cold sensation; and an unsteady gait. Depending on how low the compression occurs, constipation, incontinence, and difficulty starting or stopping urination also may be present. Teach patients and families to recognize and report the symptoms of early SCC, and instruct them to seek help immediately. If SCC is suspected on the basis of clinical symptoms, treatment should begin immediately to preserve function. MRI is the preferred imaging test that can be used to confirm the diagnosis (Brigle et al., 2017). Treatment is often palliative, with high-dose corticosteroids given first as an IV bolus to reduce swelling around the spinal cord and relieve symptoms, followed by a tapered dose over time. High-dose radiation may be used to reduce the size of the tumor in the area and relieve compression. Surgery may be performed to remove the tumor and trim the bony tissue so less pressure is placed on the spinal cord or to repair the spine if the spinal column is unstable. External back or neck braces may be used to reduce the weight carried by the spinal column and to reduce pressure on the spinal cord or spinal nerves. Hypercalcemia Hypercalcemia (increased serum calcium level) occurs frequently in patients with cancer. It is a metabolic emergency and can lead to death. Multiple myeloma and metastatic cancer to the bone is a risk for hypercalcemia ( Brigle et al., 2017). Bone metastasis can stimulate bone breakdown (osteoclast activity) and bone resorption, which releases more calcium from bone and leads to hypercalcemia. In addition, systemic secretion of vitamin D analogs by the tumor can also cause elevated calcium levels in the bloodstream. Dehydration worsens hypercalcemia. Early symptoms of hypercalcemia are nonspecific. Common symptoms include fatigue, loss of appetite, nausea, vomiting, constipation, and increased urine output. Additional symptoms include skeletal pain, kidney stones, abdominal discomfort, and altered cognition that can range from lethargy to coma. More serious problems include severe muscle weakness, loss of deep tendon reflexes, paralytic ileus, dehydration, and ECG changes (Shane & Bereson, 2017). Symptom severity depends on how high the calcium level is and how quickly it increased (see Chapter 13). Cancer-induced hypercalcemia often develops slowly for many patients, which allows the body time to adapt to this electrolyte change. As a result, symptoms of hypercalcemia may not be evident until the serum calcium level is greatly elevated. For patients who have elevated serum calcium levels and symptoms of hypercalcemia, aggressive IV hydration with normal saline is prescribed. Correcting the dehydration that often accompanies hypercalcemia restores urine output. Assess the patient for volume overload and notify the primary health care provider if this occurs. Loop diuretics can promote calcium loss in urine. Thiazide diuretics are avoided because they can increase calcium reabsorption from urine. Many drugs such as bisphosphonates (which block bone resorption of calcium) and calcitonin (combined with corticosteroids) can temporarily lower serum calcium levels. Treatment of the cancer is needed for long-term control of calcium blood levels. When cancer-induced hypercalcemia is life threatening or occurs with kidney disease, dialysis can temporarily reduce serum calcium levels. FIG. 20.4 Compression of the superior vena cava by lymph nodes and tumors in superior vena cava syndrome. FIG. 20.5 Appearance of the face, neck, upper arms, and chest in a patient with superior vena cava syndrome. From Forbes, C.D., & Jackson, W.F. [2003]. Colour atlas and text of clinical medicine [3rd ed.]. London: Mosby. Superior Vena Cava Syndrome The superior vena cava (SVC) returns all blood from the head, neck, and upper extremities to the heart. Compression or obstruction by tumor growth or by clots in this vessel leads to congestion of blood returning to the body ( Fig. 20.4). This is known as SVC syndrome and can occur quickly or develop gradually over time. SVC syndrome occurs most often in patients with mediastinal tumors, or tumors near the chest wall or indwelling catheters. Compression of the SVC is painful and can be life threatening. Symptoms result from the blockage of venous return from the head, neck, and upper trunk. Early signs and symptoms include edema of the face, especially around the eyes (periorbital edema) on arising in the morning, and reports of head fullness. As the compression worsens, the patient develops engorged blood vessels and erythema of the upper body (Fig. 20.5), edema in the arms and hands, and dyspnea. The development of stridor (a high-pitched crowing sound) indicates narrowing of the pharynx or larynx and is an alarming sign of rapid progression. Symptoms are more apparent when the patient is in the supine position. Late symptoms include hemorrhage, cyanosis, mental status changes, decreased cardiac output, and hypotension. Imaging with CT or MRI is essential for diagnosis and treatment planning. Death results if compression is not relieved. SVC syndrome is often associated with late-stage disease when the tumor is widespread. SVC syndrome occasionally occurs from an indwelling vascular device as a result of a blood clot. This type of obstruction can be treated successfully with systemic anticoagulation as well as the removal of the catheter. High-dose radiation therapy to the upper chest area may be used to provide temporary relief of airway obstruction. Chemotherapy may be the only option for long-term control of the cancer causing the compression. Surgery is rarely performed for this condition. A metal stent can be placed in the vena cava in an interventional radiology department to relieve swelling. Follow-up angioplasty may keep this stent open for a longer period. Tumor Lysis Syndrome In tumor lysis syndrome (TLS) large numbers of tumor cells are destroyed rapidly. The intracellular contents and subsequent cellular by-products of damaged cancer cells are released into the bloodstream faster than the body can eliminate them (Fig. 20.6). Severe or untreated TLS can cause acute kidney injury (AKI) and death. Serum potassium levels increase, causing hyperkalemia, which can lead to cardiac dysfunction (see Chapter 13). The large amounts of cellular by-products form uric acid, causing hyperuricemia. These uric acid crystals precipitate in the kidney, blocking kidney tubules and leading to AKI. Sudden development of hyperkalemia, hyperuricemia, and hyperphosphatemia has life-threatening effects on the heart muscle, kidneys, and central nervous system. FIG. 20.6 Pathway of tumor lysis syndrome. TLS is usually seen in patients with high-grade cancers or those with bulky tumor burden, such as diffuse non-Hodgkin lymphoma. Adults receiving radiation or chemotherapy for high-grade cancers are at risk for TLS. Early symptoms of TLS stem from electrolyte imbalances and can include lethargy, nausea, vomiting, anorexia, flank pain, muscle weakness, cramps, seizures, and altered mental status. Hydration prevents and manages TLS by increasing the kidney flow rates, preventing uric acid buildup in the kidneys, and diluting the serum potassium levels. With tumors known to be very sensitive to cancer treatment, instruct patients to drink at least 3000 mL (3 L) a day leading up to and during treatment to help prevent TLS. Stress the importance of keeping fluid intake consistent throughout the 24-hour day, and help patients draw up a schedule of fluid intake. Because some patients have nausea and vomiting after chemotherapy and may not feel like drinking fluids, stress the importance of following the antiemetic regimen. Instruct patients to contact the oncologist immediately if nausea prevents adequate fluid intake so parenteral fluids can be started. If cancer treatment is expected to rapidly decrease tumor burden, prophylaxis is necessary. Monitor daily weights and serum electrolyte values. Management becomes more aggressive for patients who develop hyperkalemia or hyperuricemia. In addition to fluids, diuretics are given to increase urine flow through the kidney. These agents are used cautiously to avoid dehydration. Drugs that promote uric acid excretion, such as allopurinol, rasburicase, or febuxostat, are given. To reduce serum potassium levels for mild-to-moderate hyperkalemia, sodium polystyrene sulfonate can be given orally or as a retention enema. For more severe hyperkalemia, IV infusions containing glucose and insulin may be given. Patients who have severe hyperkalemia and hyperuricemia may need dialysis and intensive care. Survivorship As the landscape of cancer care is changing, patients are living longer with the disease. What used to be a death sentence is now being considered a chronic disease. Survivors have unique physical and psychosocial needs, including long-term effects from treatment. NCCN (2018) specifically outlines follow-up care and considerations for survivors. Routine imaging, blood work, and follow-up care with the primary health care provider are of utmost priority. Patients need to be educated on the importance of routine follow-ups and adherence to the recommended schedule. Chemotherapy can lead to cardiac and pulmonary toxicity, infertility, menopause, and peripheral neuropathy as well as an increased risk of secondary malignancies. If lymph nodes were removed during surgery, the risk of lymphedema is lifelong. Radiation can cause fibrosis and permanent skin changes in the radiation path. Nurses are uniquely positioned to provide acute cancer care and also support the patient through the survivorship journey. Fluid Distribution • Extracellular vs Intracellular Body fluid is divided into two main compartments (spaces)—the fluid outside the cells (extracellular fluid [ECF]) and the fluid inside the cells (intracellular fluid [ICF]). The ECF space is about one third (about 15 L) of the total body water • Filtration vs Diffusion vs Osmosis Filtration Actions Filtration is the movement of fluid (water) through a cell or blood vessel membrane because of hydrostatic pressure (water pressure) differences on both sides of the membrane. Hydrostatic pressure is the pressure exerted by water molecules against the surfaces (membranes or walls) of a confining space. Water molecules in a confined space constantly press outward against the membranes, creating hydrostatic pressure. This is a “water-pushing” pressure because it forces water outward from a confined space through a membrane (Fig. 13.2). The amount (volume) of water in any body fluid space determines the hydrostatic pressure of that space. Blood, which is “thicker” than water (more viscous), is confined within the blood vessels. Blood has hydrostatic pressure because of its weight and volume and also from the pressure in arteries generated by the pumping action of the heart. The hydrostatic pressures of two fluid spaces can be compared whenever a porous (permeable) membrane separates the two spaces. If the hydrostatic pressure is the same in both fluid spaces, there is no pressure difference between the two spaces, and the hydrostatic pressure is at equilibrium. If the hydrostatic pressure is not the same in both spaces, disequilibrium exists. This means that the two spaces have a graded difference (gradient) for hydrostatic pressure: one space has a higher hydrostatic pressure than the other. The human body constantly seeks equilibrium. When a gradient exists, water movement through membranes (filtration) occurs until the hydrostatic pressure is the same in both spaces (see Fig. 13.2). Water moves through the porous membrane (filters) from the space with higher hydrostatic pressure to the space with lower pressure. Filtration continues only as long as a hydrostatic pressure gradient exists. Equilibrium is reached when enough fluid leaves one space and enters the other space to make the hydrostatic pressure in both spaces equal. Then water molecules are evenly exchanged between the spaces, and neither space gains or loses water molecules. Thus the hydrostatic pressure in both spaces is the same. FIG. 13.1 Normal distribution of total body water in adults. Clinical Examples Blood pressure is an example of a hydrostatic filtering force. It moves blood from the heart to capillaries where capillary walls are thin enough for filtration to exchange water, nutrients, and waste products between the blood and the tissue spaces. The hydrostatic pressure difference between the capillary blood and the interstitial fluid (fluid in the tissue spaces between cells) determines whether water leaves the blood vessels and enters the tissue spaces. Capillary membranes are only one cell layer thick, making a thin “wall” to hold blood in the capillaries. Large spaces (pores) in the capillary membrane help water filter freely in either direction when a hydrostatic pressure gradient is present (Fig. 13.3). Thus depending on which compartment has the higher hydrostatic pressure, capillaries can allow fluid to move from the blood into the interstitial space or from the interstitial space back into the blood. Excess tissue fluid (edema) forms with changes in hydrostatic pressure differences between the blood and the interstitial fluid, such as in right-sided heart failure (McCance et al., 2019). In this condition the volume of blood in the right side of the heart increases because the right ventricle is too weak to pump blood well into lung blood vessels. As blood backs up into the venous and capillary systems, the capillary hydrostatic pressure rises until it is higher than the pressure in the interstitial space. Excess filtration from the capillaries into the interstitial tissue space then forms visible edema. of filtration. FIG. 13.3 Basic structure of a capillary. FIG. 13.2 Process FIG. 13.4 Diffusion of solute particles through a permeable membrane from an area of higher solute concentration to an area of lower solute concentration until an equilibrium is reached. Diffusion Actions Diffusion is the movement of particles (solute) across a permeable membrane from an area of higher particle concentration to an area of lower particle concentration (down a concentration difference or “gradient”). Particles in a fluid have random movement from the vibration of atoms in their nuclei. Random movement allows molecules to bump into each other in a confined fluid space. Each collision increases the speed of particle movement. The more particles (higher concentration) present in the confined fluid space, the greater the number of collisions. As a result of the collisions, particles in a solution spread out evenly through the available space. They move from an area of higher particle concentrations to an area of lower concentrations until an equal concentration (amount) is present in all areas. Spaces with many particles have more collisions and faster particle movement than spaces with fewer particles. A concentration gradient exists when two fluid spaces have different concentrations of the same type of particles. Particle collisions cause them to move down the concentration gradient. Any membrane that separates two spaces is struck repeatedly by particles. When the particle strikes a pore in the membrane that is large enough for it to pass through, diffusion occurs ( Fig. 13.4). The chance of any single particle hitting the membrane and going through a pore is much greater on the side of the membrane with a higher solute particle concentration. The speed of diffusion is related to the difference in amount of particles (concentration gradient) between the two sides of the membrane. The degree of difference is the steepness of the gradient: the larger the concentration difference between the two sides, the steeper the gradient. Diffusion is more rapid when the gradient is steeper (just as a ball rolls downhill faster when the hill is steep than when the hill is nearly flat). Particles move from the fluid space with a higher concentration of solute particles to the fluid space with a lower concentration of solute particles. Particle diffusion continues as long as a concentration gradient exists between the two sides of the membrane. When the concentration of particles is the same on both sides of the membrane, the particles are in equilibrium, and only an equal exchange of particles continues. Clinical Examples Diffusion transports most electrolytes and other particles through cell membranes. Cell membranes, unlike capillary membranes, are selective for which particles can diffuse. They permit diffusion of some particles but not others. Some particles cannot move across a cell membrane, even when a steep “downhill” gradient exists, because the membrane is impermeable (closed) to that particle type. For these particles the concentration gradient is maintained across the membrane. Impermeability and special transport systems cause differences in the amounts of specific particles from one fluid space to another. For example, usually the fluid outside the cell (the extracellular fluid [ECF]) has 10 times more sodium ions than the fluid inside the cell (the intracellular fluid [ICF]). This extreme difference is caused by cell membrane impermeability to sodium and by special “sodium pumps” that move any extra sodium present inside the cell out of the cell “uphill” against its concentration gradient and back into the ECF. For some particles diffusion cannot occur without help, even down steep concentration gradients, because of selective membrane permeability. One example is glucose. Even though the amount of glucose may be much higher in the ECF than in the ICF (creating a steep gradient for glucose), glucose cannot cross some cell membranes without the help of insulin. Insulin binds to insulin receptors on cell membranes, which then makes the membranes much more permeable to glucose. Then glucose can cross the cell membrane down its concentration gradient into the cell. Diffusion across a cell membrane that requires a membrane-altering system (e.g., insulin and its receptors) is called facilitated diffusion. This type of movement is still a form of diffusion because it does not require extra energy. Osmosis Actions Osmosis is the movement of water only through a selectively permeable (semipermeable) membrane to achieve an equilibrium of osmolarity. For osmosis to occur, a membrane must separate two fluid spaces and one space must have particles that cannot move through the membrane. (The membrane is impermeable to this particle.) A concentration gradient of this particle must also exist between the two spaces. Because the membrane is impermeable to these particles, they cannot cross the membrane to establish an equilibrium, but water molecules can. For the fluid spaces to have equal concentrations of all the particles, the water molecules move down their concentration gradient from the side with the higher concentration of water molecules (and a lower concentration of particles along with a greater hydrostatic pressure) to the side with the lower concentration of water molecules (and a higher concentration of particles along with a lower hydrostatic pressure). This movement continues until both spaces contain the same proportions of particles to water and thus have an equilibrium of osmolarity. At this point the concentrations of particles in the fluid spaces on both sides of the membrane are equal even though the total amounts of particles and volumes of water are different. The concentration equilibrium occurs by the movement of water molecules rather than the movement of solute particles. FIG. 13.5 The process of osmosis to generate a concentration equilibrium (but not a volume equilibrium) for a solute particle that cannot move through a cell membrane. Dilute fluid is less concentrated and has fewer particles and more water molecules than more concentrated fluid. Thus water moves by osmosis down its hydrostatic pressure gradient from the dilute fluid to the more concentrated fluid until a fluid concentration of solute (osmolarity) equilibrium occurs (Fig. 13.5). Particle concentration in body fluid is the major factor that determines whether and how fast osmosis and diffusion occur (McCance et al., 2019). This concentration is expressed in milliequivalents per liter (mEq/L), millimoles per liter (mmol/L), and milliosmoles per liter (mOsm/L). Osmolarity is the number of milliosmoles in a liter of solution; osmolality is the number of milliosmoles in a kilogram of solution. Because 1 L of water weighs 1 kg, in human physiology osmolarity and osmolality are considered the same, although osmolarity is the actual concentration measured most often. The normal osmolarity value for plasma and other body fluids ranges from 270 to about 300 mOsm/L. The body functions best when the osmolarity of all body fluid spaces is close to 300 mOsm/L. When all fluids have this solute (particle) concentration, the fluids are isosmotic or isotonic (also called normotonic) to each other. Fluids with osmolarities greater than 300 mOsm/L are hyperosmotic, or hypertonic, compared with isosmotic fluids. These fluids have a greater osmotic pressure than do isosmotic fluids and tend to pull water from the isosmotic fluid space into the hyperosmotic fluid space until an osmotic balance occurs. Clinical Examples If a hyperosmotic (hypertonic) IV solution (e.g., 3% or 5% saline) were infused into a patient with normal extracellular fluid (ECF) osmolarity, the infusing fluid would make the patient’s blood hyperosmotic. To balance this situation, the interstitial fluid would be pulled into the circulation in an attempt to dilute the blood osmolarity back to normal. In addition, fluid would also be drawn from the intracellular fluid (ICF) compartment. As a result, the interstitial and ICF volumes would shrink, and the plasma volume would expand. Fluids with osmolarities of less than 270 mOsm/L are hypo-osmotic, or hypotonic, compared with isosmotic fluids. Hypo-osmolar fluids have a lower osmotic pressure than isosmotic flui