Patho LO Exam 1 PDF

MODULE 1 INTRODUCTION TO PATHOPHYSIOLOGY: 1. Define pathophysiology and outline the need for the practical nurse to understand pathological / processes Pathophysiology - involves the study of functional or physiologic changes in the body that result from a disease process. Pathogene...

MODULE 1 INTRODUCTION TO PATHOPHYSIOLOGY: 1. Define pathophysiology and outline the need for the practical nurse to understand pathological / processes Pathophysiology - involves the study of functional or physiologic changes in the body that result from a disease process. Pathogenesis refers to the development of the disease or the sequences of events involved in the tissue changes that are related to the specific disease process 2. Identify and define the terms used to characterize a disease Diagnosis- Identification of a basic disease - Evaluation of signs and symptoms - Laboratory test Etiology- causative factors in a particular disease - congential defects, inherited or genetic disorders, microorganisms, immunologic dysfunctions, degenerative changes, malignacy, metabolic, nutritional problems, trauma, burns, environmental factors. CAUSES OF DISEASE, TERMS: - Idiopathic- causes of disease is unknown Iatrogenic- error/treatment/procedure may cause the disease. Predisposing factors- age, gender, inherited, factors, environmental, etc. Prophylaxis- measure to preserve health; prevent spread of disease Prevention- vaccinations; dietary/lifestyle modifications; prevention of potentially harmful activities etc. CHARACTERISTIC OF DISEASE, TERMS: - Pathogenesis- development of disease Onset of disease- sudden/acute - insidious: gradual, vague, or mild signs Acute disease- short-term, develops quickly - high fever, severe pain etc. Chronic disease- develops gradually - milder symptoms, often intermitted with acute episodes Subclinical state- pathological changes, no obvious manifestations Latent state- no symptoms or clinical signs evident - - in infectious diseases: incubation period Prodromal period- early development of the disease - signs are nonspecific or absent Manifestations- clinical evidence with signs and symptoms - local: at site of the problem - systemic: general indicators of illness, i.e. fever - MORE signs- objective indicators of disease Symptoms- subjective feelings Lesions- specific local change of tissue Syndrome- collection of signs and symptoms Diagnostic test- various laboratory test - appropriate to manifestations and nedical history - CHARACTERISTICS OF DISEASE: Remissions and exacerbations - mark the course of progress of disease - remission: period which manifestations subside - exacerbation: a worsening of severity Percipitating factor - condition that triggers an acute episode Complications - new secondary or additional problems - MORE TERMS: Therapy- measures to promote recovery/slow progress Sequelae- potential unwanted outcomes Convalescence or rehabilitation- period of recovery and return to healthy state 3. Outline common predisposing risk factors for disease - diet, lack of exercise, lack of calcium, radiation exposure, asbestos, alcohol or drugs intake, smoking, stress, genetics, age, pre-existing conditions. 4. Explain the cellular adaptations most common in health disruption Cellular Adaptations: can be reversible Atrophy: decrease in the size of cells - results in reduced tissue mass Hypertrophy: increase in cell size - results in enlargement tissue mass. Hyperplasia: increased number of cells - results in enlarged tissue mass. Metaplasia: Mature cell type is replaced by a different mature cell type. Dysplasia: Cells vary in size and shape within a tissue. Anaplasia: Undifferentiated cells, with variable nuclear and cell structures Neoplasia: “New growth”―commonly called tumor 5. Explain the causes of cell injury Apoptosis- normal programmed cell death. For example, after 120 days a red blood cell (erythrocyte) dies Ischemia- deficit of oxygen in the cells. For example, myocardial ischemia affecting the heart, can cause angina (chest pain) Hypoxia- reduced oxygen in tissues leading to nutritional deficits (this can lead to cyanosis) Ischemia is insufficient blood flow to provide adequate oxygenation. This, in turn, leads to tissue hypoxia (reduced oxygen) or anoxia (absence of oxygen) Pyroptosis- Results in lysis causing nearby inflammation CELL INJURY - Physical damage Microorganisms - Excessive heat or cold - Bacteria and viruses, for example - Radiation exposure Abnormal metabolites Mechanical damage - Genetic disorders - Pressure or tearing of tissue - inborn errors of metabolism Chemical toxins - Altered metabolism - Exogenous: from environment Imbalances of fluids or electrolytes - Endogenous: from inside the body Nutritional deficits 6. Describe the process of cell damage and necrosis Necrosis: - When cell damage becomes irreversible, necrosis occurs, leading to cell death and further tissue damage due to the disintegration of the cell. Types of Necrosis: - Liquefaction Necrosis: Cells are destroyed and liquefied by enzymes, often occurring in brain tissue or bacterial infections. - Coagulative Necrosis: Cell proteins denature, typically seen in myocardial infarction (heart attack). - Fat Necrosis: Fatty tissue is broken down into fatty acids, which may increase inflammation. - Caseous Necrosis: A type of coagulation necrosis with a thick, yellowish “cheesy” substance, often seen in tuberculosis. - Gangrene: Necrotic tissue invaded by bacteria, commonly in areas with compromised blood supply, leading to wet or dry gangrene. *In conclusion, necrosis is a process that not only affects the individual cell but can lead to widespread inflammation and further damage to surrounding tissues due to the release of cellular components. 7. Identify the difference between acute and chronic illnesses Acute disease (gastroenteritis, flu, food poisoning) - Short-term, develops quickly - High fever, severe pain etc. Chronic disease (arthritis, diabetes, etc.) - Develops gradually - Milder symptoms, often intermitted with acute episodes 8. Analyze the impact stress has on health ↑ blood pressure and ↑ heart rate Bronchodilation and ↑ ventilation ↑ blood glucose levels Arousal of the central nervous system ↓ inflammatory and immune responses …. Potential Effects of prolonged stress: Renal failure Stress ulcers Infection Slowed healing Following trauma or surgery Increased secretion of glucocorticoid—reduction in protein synthesis and tissue regeneration Increased catecholamine levels— vasoconstriction, reduced nutrients and oxygen to the tissue Posttraumatic stress disorder Serious consequence of major disaster or personal threat Usually occurs within 3 months of event May cause symptoms years later High risk of developing dependence on drugs and/or alcohol MODULE 2 INFLAMMATION AND HEALING 1. Describe the body defenses for the prevention of disease First line of defense: mechanical barriers, nonspecific, unbroken skin and mucous membrane, - secretion such as tears and gastric juices Second line of defense: other nonspecific mechanisms, phagocytes, inflammation - Third line of defense: specific mechanisms, production of specific antibodies or cell-mediated immunity > First line of defense: skin, saliva, tears, mucous lining of nose, throat, etc., stomach acid, normal flora > Second line of defense: (innate immunity) – > Phagocytosis (macrophages and neutrophils engulf and destroy bacteria and other foreign debris) & inflammation - final stage of the acute inflammatory process > Third line of defense: (adaptive immunity) – Response to specific pathogens using specialized cells such as B and T cells Production of specific antibodies, or cell-mediated immunity 2. Describe the physiology of inflammation A protective mechanism and important basic concept in pathophysiology Disorders are named using the ending –it is. Inflammation is a normal non-specific defense mechanism in response to tissue injury Intended to localize and remove the injurious agent Signs and symptoms of inflammation serve as warning for a problem: > Problem may be hidden within the body. It is not the same as infection. > Infection, however, is one cause of inflammation. 3. Differentiate between local and systemic effects of inflammation - LOCAL EFFECTS Redness and heat > Caused by increased blood flow to damaged area by vasodilation Swelling (edema) > Increased capillary permeability, causing shift of protein and fluid into the interstitial space Pain > Increased pressure of fluid on nerves; release of chemical mediators (e.g., bradykinins) Loss of function > May develop if cells lack nutrients; edema may interfere with movement. LOCAL EFFECTS; EXUDATE i n te re Exudate is the collection of interstitial fluid formed in the inflamed area. > Serous - Watery, consists primarily of fluid, some proteins, and white blood cells > Fibrinous- *increases risk for scar tissue - Thick, sticky, high cell and fibrin content > Purulent *pus, typically indicates infection - Thick, yellow-green, contains more leukocytes, cell debris, and microorganisms > Abcess - Localized pocket of purulent exudate or pus in a solid tissue - SYSTEMIC EFFECTS Mild fever > Common if inflammation is extensive > Results from the release of pyrogens (released from WBCs or macrophages -> once in blood -> stimulate the hypothalamus to increase body temp) > One gets cold, shivers (↑ cell metabolism) and looks pale from cutaneous vasoconstriction = body trying to reduce heat loss Malaise > feeling unwell Fatigue Headache Anorexia 4. Compare and contrast te effects of chronic and acute inflammation - CHRONIC Inflammation Follows the acute episode of inflammation Less swelling and less exudate Presence of MORE lymphocytes, macrophages and fibroblasts Leads to continued tissue destruction More fibrous scar tissue due to increased collagen in the area Granuloma may develop around the foreign object > Small mass of cells with a necrotic center, covered with connective tissue  … ACUTE INFLAMMATION: ~ CHRONIC INFLAMMATION: > Allergic reaction > Cardiovascular Disease > Chemical Irritants > Neurological Disease > Infection > Autoimmune Disease > Trauma Injury > Rheumatoid Arthritis > Burns > Cancer > Laceration, Cuts, Wounds > Lupus > Fibromyalgia 5. Describe the purposes and procedures of the common diagnostic tests for inflammation 1. Leukocytosis: Purpose: Measures an increase in white blood cell (WBC) count, particularly neutrophils, which is indicative of an inflammatory response. Procedure: A blood test is conducted to count WBCs. An elevated count, especially of neutrophils, signals active inflammation or infection. 2. Differential WBC Count: Purpose: Helps determine the specific type of WBC that is elevated, offering clues about the underlying cause of inflammation. Procedure: Blood analysis is performed to assess the proportions of different types of WBCs (neutrophils, lymphocytes, eosinophils, etc.). 3. Plasma Proteins (Fibrinogen and Prothrombin): Purpose: Increased levels of fibrinogen and prothrombin indicate inflammation and are involved in blood clotting and tissue repair. Procedure: Blood tests measure the concentration of these proteins to assess the extent of inflammation. 4. C-Reactive Protein (CRP): Purpose: CRP is not normally present in the blood, but it appears during acute inflammation and tissue necrosis. Procedure: A CRP blood test detects its presence and concentration to monitor inflammation levels. 5. Erythrocyte Sedimentation Rate (ESR): Purpose: Elevated plasma proteins increase the rate at which red blood cells settle in a blood sample, indicating inflammation. Procedure: A blood sample is taken, and the time it takes for red blood cells to settle is measured. A faster rate indicates inflammation. 6. Cell Enzymes: Purpose: Enzymes released from necrotic cells enter the blood and can indicate the site of tissue damage and inflammation. Procedure: Blood tests measure the levels of specific enzymes such as Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST), and others associated with liver, heart, and muscle damage. These diagnostic tests are used to identify the presence, severity, and cause of inflammation, guiding treatment decisions and monitoring the progress of the inflammatory response. 6. Outline common medical treatments for inflammation z Acetylsalicylic acid (ASA) **Adults only** RICE: - Aspirin Rest Acetaminophen Ice - Tylenol Compression Nonsteroidal anti-inflammatory drugs (NSAIDs) Elevation - Ibuprofen Glucocorticoids - Corticosteroids 7. Describe the types of healing Resolution > Minimal tissue damage > Cell recover and everything goes back to normal Regeneration > Damaged tissue replaced with cells that are functional through mitosis > If complex tissue is altered, may not contribute functionally Replacement > Functional tissue replaced by scar tissue (connective tissue, fibrous tissue) cells are incapable of mitosis (brain or heart) > Loss of function First intention > Wound is clean and free of debris/necrotic tissue > Edges are held close together (well approximated) > Seen in surgical incisions Second intention > Large break in tissue, more inflammation > Longer healing, more scar tissue > Seen with compound factures, other large wounds with missing tissue 8. Discuss the classifications and effects of burns Superficial (first-degree) > 1st degree- red and painful and heal readily. Sunburn, burns scalding - Involve epidermis and part of > 2nd degree- red, edematous, blistered, hypersensitive and dermis painful. Can appear waxy with a reddened margin. Dead - Little, if any, blister formation skin sloughs off. Grafts may be necessary in large areas. Partial-thickness (second- Can easily become infected. degree) burns > 3rd destruction of all skin layers and underlying tissues. - Epidermis and part of dermis Burn area is often coagulated or charred and is hard and - Blister formation dry on the surface. Damaged tissue (eschar) shrinks and Full-thickness (third-degree) causes pressure on the edematous tissue under it. burns Escharotomy (cutting through this crust) might be - Destruction of all skin layers necessary to relieve pressure. May be painless because of and destruction of the nerves but becomes very painful due to often underlying tissues massive inflammatory response. Require skin grafts because there are no cells available 9. Outline treatments for patients with burns 1. Immediate Covering: Cover the wound immediately to prevent infection. 2. Non-stick Dressings: Use non-stick dressings to cover the wound and protect it from infection and damage. 3. Scar Tissue Management: Scar tissue develops even with skin grafting. Physiotherapy and occupational therapy may be required to maintain movement and function. 4. Skin Grafting: Grafting skin is a common procedure, but temporary solutions like pig skin or cadaver skin are often rejected over time. Biosynthetic or synthetic skin substitutes are used, though there is no ideal solution for scar-free healing yet. 5. Nutritional Support: Increased protein and carbohydrate intake is necessary due to hypermetabolism during the healing period. 6. Infection Prevention: Prevent infection through proper wound care and management, as infections are common due to the compromised skin barrier. 7. Long-term Care: Surgery may be needed to release restrictive scar tissue, particularly in severe cases. These are the key treatments mentioned in the presentation for managing burn injuries. 10. Identify the complications that can occur with burns 1. Dehydration and Edema: The inflammatory response from burns leads to a massive shift of water, proteins, and electrolytes into the tissues, causing fluid imbalance and edema. 2. Shock: Burn injuries can result in hypovolemic shock due to the loss of fluids and electrolytes, which lowers blood volume and blood pressure. Prolonged or recurrent shock can lead to kidney failure or damage to other organs. 3. Respiratory Problems: Inhalation of toxic or irritating fumes, such as carbon dioxide, can cause respiratory complications, as CO2 binds to hemoglobin, reducing the body’s oxygen supply. 4. Infection: Due to the compromised skin barrier and the presence of microbes in deep glands and follicles, burns are highly susceptible to bacterial and fungal infections. 5. Increased Metabolic Needs: The healing process from burns leads to increased metabolic demands for nutrients, especially protein and carbohydrates, as well as heat loss until the skin is restored. 6. Anemia: Anemia can develop as a complication due to the destruction of erythrocytes (red blood cells) and the suppression of bone marrow function from the injury. 11. Discuss the implications of the inflammatory process to the Spheres of Caring Conceptual Framework The Bow Valley College Practical Nurse curriculum is built around four key concepts: health, the person or patient, the environment, and nursing. These concepts form the foundation of the program’s Conceptual Framework – The Spheres of Caring. This framework visually represents the values and beliefs central to practical nursing. To understand this framework, it’s important to start with three main ideas: 1. The individual (or patient). 2. The health care environment. 3. The role of the professional nurse. At the center of the framework is the individual and their family. These are seen as interconnected with their community and society. The framework emphasizes that practical nursing is an interactive process. The arrows in the diagram highlight the dynamic and active nature of how practical nurses engage with patients, families, and their surroundings. The Determinants of Health describe factors that affect a person’s environment, such as socioeconomic status, education, and living conditions. Practical nurses work within this environment to help influence a person’s health outcomes. Their relationship with individuals and families is complex, involving caring, responding to needs, and adapting to changes in the patient’s health. As students progress through the program, they develop the skills to provide person-centered care, focusing on compassion, responsiveness, and flexibility in addressing patient needs. Additionally, as part of the college’s commitment to the Truth and Reconciliation Commission of Canada’s Call to Action #24, the Medicine Wheel is incorporated into the curriculum. This is an ancient healing tool used by Plains First Nations people, representing the interconnectedness of mental, spiritual, emotional, and physical health. It guides students to approach their nursing practice holistically, promoting peace, healing, and enlightenment on their professional journey. MODULE 3 NEOPLASMS AND PAIN 1. Discuss the causes and types of pain The causes of pain, as discussed in the presentation, include several underlying factors: 1. Inflammation – Pain caused by inflammatory responses in the body. 2. Infection – Such as stomach pain due to infection. 3. Ischemia – Pain caused by reduced blood supply, such as in myocardial infarction. 4. Stretching of tissues – Pain resulting from the stretching of tissues, tendons, ligaments, or joints, as seen in a sprained ankle. 5. Muscle spasms – Occurring in conditions like multiple sclerosis or due to dehydration and diabetes. 6. Chemical triggers – Pain can also be triggered by chemical irritants. 7. Burns – Pain from thermal injury. 8. Tissue necrosis – Pain due to tissue death. … The types of pain described are: Somatic Pain: Originating from skin, bone, or muscle, and typically well-localized and described as throbbing or aching. Visceral Pain: Originating from internal organs and often poorly localized. It may be associated with autonomic symptoms like nausea or increased heart rate and blood pressure. Neuropathic Pain: This results from nervous system dysfunction, manifesting as burning, tingling, or numbness. It can be either peripheral or central in origin. Ischemic Pain: Caused by a sudden loss of blood flow, leading to symptoms like burning or aching. Cancer-Related Pain: Associated with disease progression, treatment, or coexisting conditions. These causes and types of pain highlight the diversity of pain experiences, ranging from localized somatic pain to widespread, poorly localized visceral or neuropathic pain. 2. Describe the physiology of pain pathways 1. Nociceptors (pain receptors): Pain is detected by nociceptors, which are free sensory nerve endings. These can be stimulated by various factors: Temperature: Extremes in temperature can activate nociceptors. Chemicals: Substances like acids, bradykinin, histamine, and prostaglandins. Physical stimuli: For example, pressure can also activate nociceptors. 2. Afferent fibers: These are sensory neurons that transmit pain signals from the body to the central nervous system (CNS). There are two main types: Myelinated A-delta fibers: These fibers conduct impulses very rapidly and are responsible for transmitting acute pain, which is sharp and localized. Unmyelinated C fibers: These fibers transmit impulses more slowly and are associated with chronic pain, which is dull, diffuse, and often described as aching or burning. 3. Dermatome: Each spinal nerve innervates a specific area of the skin, called a dermatome. This mapping helps localize pain based on the nerve affected. For example, sciatica, a condition where pain radiates down the leg, follows the dermatome of the sciatic nerve. 4. Spinothalamic Tract: Pain signals travel up the spinal cord through the spinothalamic tracts. These include: Neospinothalamic tract: Responsible for transmitting fast impulses related to acute pain. Paleospinothalamic tract: Responsible for transmitting slower impulses related to chronic, dull pain. … 5. Brain Involvement: Once the pain signal reaches the spinal cord, it is relayed to the brain through the following pathway: 1. Spinal decussation (cross-over): The pain signal crosses over to the opposite side of the spinal cord. 2. Lateral spinothalamic tract: The signal travels up to the brain. 3. Reticular formation: Located in the brainstem, this area is involved in pain awareness. 4. Thalamus: Acts as a relay station for sensory information, including pain. 5. Somatic sensory area (parietal lobe): The pain is perceived and localized here. 6. Hypothalamus: Triggers the stress response, involving the sympathetic nervous system (SNS). 7. Limbic system: This region is responsible for the emotional response to pain. 6. Reflex response: A reflex response to pain is also initiated when a pain signal reaches the spinal cord. This results in an involuntary motor response, such as pulling away from a painful stimulus, which is carried out by efferent fibers. This pathway outlines how pain is sensed, transmitted, and processed from the site of injury to its perception in the brain 3. Outline the gate control theory of pain ~ Gate control theory: Control systems, “gates” built into normal pain pathways Can modify pain stimuli Gates open allowing pain impulse to be conduction and transmission in carried along the normal pain pathway the spinal cord and brain Gates open When closed there is a reduction of > Pain stimulates transmitted from pain impulses- reduces or modifies the periphery to brain passage of the pain response Gates closed > reduces or modifies the passage of pain impulses 4. Identify factors that influence the pain experience Emotional State Fatigue Stress/Anxiety/Fear Hunger Age Culture Prior experiences Personality/Temperament 5. Identify the purpose of analgesics in the management of pain Remove cause of pain as soon as possible Use of analgesic medications > Orally > Parenterally (injection) > Transdermal patch > Classified by ability to relieve 1. Mild pain 2. Moderate pain 3. Severe pain 6. Describe the role of anesthesia in the control of pain Local anesthesia Injected or applied to skin or mucous membranes Spinal or regional anesthesia Blocks pain from legs or abdomen General anesthesia Causes loss of consciousness (gas or injection) Neuroleptanesthesia (Conscious/Procedural Sedation) 7. Outline the pathological processes contributing to the development of cancer 1. Carcinogenesis: This is the process through which normal cells become cancerous. It happens in several stages: Initiation: An irreversible change occurs in the DNA of a cell. This could be due to exposure to carcinogens like radiation, chemicals, or viruses. The change in DNA does not create an active tumor at this stage, but it sets the stage for further mutations. Promotion: Additional changes in the cell’s DNA lead to increased cell division (mitosis) and decreased differentiation (the ability of cells to specialize). Promoters, such as certain hormones or chemicals, encourage these changes, which may result in the development of a tumor. Progression: As changes in the DNA continue, the tumor becomes malignant. The cells are less differentiated, meaning they look and act less like normal cells, and the tumor grows more aggressively. Dysplasia (abnormal development of cells) and anaplasia (loss of cell differentiation) may occur. Metastasis: In the final stage, cancer cells gain the ability to spread from their original location to other parts of the body. They break away from the primary tumor, travel through the bloodstream or lymphatic system, and form secondary tumors in other tissues. 2. Tumor Characteristics: Growth and Structure: Tumors form as abnormal (dysplastic) cells grow and divide uncontrollably. They lack normal cell organization and structure. Invasion: Cancer cells do not adhere well to each other, which allows them to invade nearby tissues and organs. Necrosis and Inflammation: As tumors grow, they can compress nearby blood vessels, leading to reduced blood flow, tissue death (necrosis), and inflammation. Secretion of Enzymes: Some cancer cells release enzymes, such as collagenase, which break down surrounding tissues and help the tumor spread further.  … 3. Angiogenesis: Tumor cells can secrete growth factors that stimulate the formation of new blood vessels (angiogenesis). This helps supply the tumor with the nutrients and oxygen it needs to continue growing. 4. Invasion and Metastasis: Local Invasion: Tumor cells spread into surrounding tissues near the original tumor. Metastasis: Cancer cells break off from the primary tumor, enter the bloodstream or lymphatic system, and travel to distant parts of the body, where they form new tumors. Seeding: In some cases, cancer cells spread along membranes or within body fluids, especially in body cavities like the abdomen. 8. Compare and contrast the characteristics of benign and malignant tumors Benign Tumors: - Cell differentiation: Cells are usually well-differentiated, meaning they resemble normal cells and perform normal functions. Growth rate: Benign tumors grow at a slower rate compared to malignant tumors. Encapsulation: They are typically encapsulated, which limits their growth and prevents them from invading surrounding tissues. Spread: Benign tumors do not spread (metastasize) to other parts of the body. Tissue damage: Although they do not invade other tissues, they can cause damage by compressing nearby structures, especially if located in a confined space like the brain, which can make them life-threatening. Outcome: They are generally considered less harmful than malignant tumors, though they can still pose risks depending on their location. Malignant Tumors: Mumm Cell differentiation: Malignant tumors consist of undifferentiated, non-functional cells. These cells often lose the characteristics of the tissue from which they originated. Growth rate: They grow rapidly, often exhibiting abnormal mitotic figures. Encapsulation: Malignant tumors lack a capsule, allowing them to invade surrounding tissues. Spread: They have the ability to metastasize, meaning they can spread to distant sites in the body via the bloodstream or lymphatic system. Tissue damage: Malignant tumors invade nearby tissues, causing significant destruction. They can compress blood vessels, leading to tissue necrosis and inflammation. Outcome: These tumors are considered harmful and are often life-threatening, particularly because of their invasive and metastatic nature. Key Differences: ~ Benign tumors are encapsulated, slow-growing, and do not spread, while malignant tumors are invasive, fast-growing, and can spread (metastasize) to other parts of the body. Benign tumors consist of well-differentiated cells, whereas malignant tumors contain undifferentiated, non-functional cells.  9. Describe the systemic and localized effects of cancer on the body Localized Effects of Cancer: - 1. Pain: May not occur until the cancer is well advanced. The severity of pain depends on the type of tumor and its location. 2. Obstruction: Cancer can compress ducts or passageways, restricting blood supply or lymphatic flow. This can also block the digestive tract or airflow in the bronchi. 3. Tissue Necrosis and Ulceration: As tumors grow, they can lead to the death of nearby tissues (necrosis). This can cause ulceration, potentially leading to bleeding or infection around the tumor. Systemic Effects of Cancer: - 1. Weight Loss and Cachexia: Cancer often leads to significant weight loss and a wasting syndrome known as cachexia. This is caused by anorexia, fatigue, pain, stress, and increased demands on the body from the tumor cells. 2. Anemia: Anemia can develop due to blood loss at the tumor site or because nutritional deficits reduce hemoglobin synthesis. 3. Severe Fatigue: Fatigue is common and may be caused by inflammatory changes, anemia, and the stress of the cancer treatment schedule. 4. Infections: Infections occur frequently as the body’s resistance declines, making it more vulnerable to opportunistic infections. 5. Bleeding: Tumor cells can erode blood vessels, leading to bleeding, which may be a common complication of advanced cancer. 6. Effusions: Inflammation caused by the cancer may lead to fluid buildup in body cavities (effusions), such as pleural or peritoneal effusions. 7. Paraneoplastic Syndromes: Certain tumors release substances that affect neurological function, blood clotting, or have hormonal effects, leading to additional problems. For example, some bronchogenic carcinoma tumors may produce adrenocorticotropic hormone (ACTH), leading to symptoms of Cushing syndrome.  10. List common signs of cancer 1. Unusual bleeding or discharge anywhere in the body. 2. Change in bowel or bladder habits (e.g., prolonged diarrhea or discomfort). 3. A change in a wart or mole (i.e., color, size, or shape). 4. A sore that does not heal (on the skin or in the mouth, anywhere). 5. Unexpected weight loss. 6. Anemia or low hemoglobin and persistent fatigue. 7. Persistent cough or hoarness without reason. 8. A solid lump, often painless, in the breast or testes or anywhere onn the body. 11. Describe common screening methods for early detection of cancer Breast Cancer Prostate > Self-exams - Digital rectal exam > Mammograms - PSA > Ultrasound Cervical > MRI > PAP test Colorectal > Vaccination > FOB > CA-125 > GI Endoscopy Testicular > CEA > Self-exams 12. Describe the purposes and procedures of the common diagnostic tests for cancer detection Laboratory Tests: Medical imaging: - Cytology - X-ray, mammogram, & ultrasound > FNA, surgery, fluid sample - MRI, CT scan, & PET scan - Blood Tests Procedures: > Baselines - Bone Marrow Bx, Lumbar Puncture, > Tumor markers bronchoscopy, GI scopes 13. Outline common treatment for cancer Radiation Chemotherapy Stem cell Transplants Immunotherapy Complementary and Alternative (CAM) therapies 14. Discuss the implications of the cancer process as it relates to the Spheres of Caring Conceptual Framework Determinants of Health: Cancer impacts key factors like socio-economic status, access to care, and environmental factors, all of which affect health outcomes. Society: Cancer treatment requires resources and societal support. Nurses advocate for equitable healthcare and policies. Caring: Nurses provide emotional and physical support, addressing holistic needs like pain management and patient dignity. Responding: Nurses and healthcare systems must respond promptly with appropriate cancer treatments and adjustments based on disease progression. Adapting: Patients and families need to adjust to the physical and emotional changes cancer brings, with nurses guiding the adaptation process. Community: The support from community networks, including healthcare teams and social services, is essential for managing cancer care. Individual/Family: Cancer affects both the patient and their family, requiring personalized care and emotional support from the nursing team. This framework emphasizes holistic, patient-centered cancer care across all spheres. MODULE 4 FLUID AND ELECTROCYTE DISORDER 1. Review the anatomy and physiology of fluid and electrocytes within the body water carries nutrients into cells and removes wastes, transports enzymes in digestive secretions, and moves blood cells around the body > Water is found within and outside the cells in the human body > Cells cannot function without water What is intracellular fluid? > Fluid inside cells What is extracellular fluid? Prefixes: > Fluid outside cells inter- = between What is interstitial fluid? intra- = within > Extracellular fluid between cells inside tissue extra- = outside of Besides interstitial fluid, what else does iso- = the same extracellular fluid include? hyper- = high, higher - Intravascular (plasma, lymph) - Transcellular (synovial joints) 2. Describe the diagnostic tests used to evaluate fluid and electrolyte imbalances 1. Renal Panel Includes electrolytes such as creatinine (normal range: 50-100 µmol/L) and BUN (3.6-7.1 mmol/L). Increased BUN indicates dehydration or kidney disease. 2. Serum Osmolarity Measures water and electrolyte balance. Increases with dehydration, decreases with fluid overload. 3. Urinalysis Tests for glucose, electrolytes, pH, protein, and osmolarity in urine. 4. Urine Osmolarity Assesses the concentration of urine, providing more information on renal function when combined with serum osmolarity. 5. Urine Specific Gravity (SG) Indicates the kidneys’ ability to concentrate urine. Higher values suggest more concentrated urine, while lower values suggest more diluted urine. 6. Liver Panel Measures blood levels of total protein, albumin, bilirubin, and liver enzymes. Serum Albumin: Albumin is the most abundant protein in the blood and is essential for wound healing and maintaining blood cells. 7. Serum Electrolytes Measures key electrolytes like sodium, potassium, calcium, and others to detect imbalances. 8. Skin Turgor Assesses the elasticity of the skin, typically used in cases of severe dehydration to evaluate fluid status. 3. Compare and contrast the causes, signs and symptoms, treatment, and usual course of: a. edema and dehydration b. electrolyte imbalances of: i. sodium ii. potassium iii. calcium iv. magnesium c. acid-base imbalances (See next page for the answer) … A. Edema vs. Dehydration CAUSES: Edema: Increased capillary hydrostatic pressure, loss of plasma proteins, obstruction of lymphatic circulation, increased capillary permeability. Dehydration: Inadequate intake or excessive loss (vomiting, diarrhea, sweating). Signs and Symptoms: Edema: Swelling, pitting, pale or red skin, increased body weight. Dehydration: Dry mucous membranes, decreased skin turgor, low blood pressure, decreased urine output. TREATMENT: Edema: Treat the underlying cause, reduce salt intake. Dehydration: Fluid replacement (oral or IV). OUTCOME: Edema: Can impair circulation, leading to ischemia and tissue breakdown. Dehydration: If severe, can lead to hypovolemic shock or organ failure. B. Electrolyte Imbalances i. Sodium (Hyponatremia & Hypernatremia) remem ~ Normal Range: 135-145 mEq/L. CAUSES: Hyponatremia: Diuretics, diarrhea, dehydration. Hypernatremia: Excessive sodium intake, insufficient water intake, excessive water loss. SIGNS & SYMPTOMS: Hyponatremia: Fatigue, muscle weakness, headache, seizures. Hypernatremia: Thirst, restlessness, edema. TREATMENT: Hyponatremia: Sodium replacement, fluid restriction. Hypernatremia: Fluid replacement, restrict sodium intake. OUTCOME: Hyponatremia: Can lead to neurological issues, seizures. Hypernatremia: Can cause fluid shifts leading to cell dehydration. … ii. Potassium (Hypokalemia & Hyperkalemia) ~ Normal Range: 3.5-5 mEq/L. CAUSES: Hypokalemia: Diuretics, diarrhea, Cushing’s syndrome. Hyperkalemia: Renal failure, excessive potassium intake. SIGNS & SYMPTOMS: Hypokalemia: Muscle cramps, cardiac dysrhythmias, weakness. Hyperkalemia: Muscle weakness, cardiac arrest. TREATMENT: Hypokalemia: Potassium supplements. Hyperkalemia: Dialysis, potassium-lowering drugs. OUTCOME: Hypokalemia: Can lead to muscle dysfunction and cardiac issues. Hyperkalemia: Can result in life-threatening cardiac arrhythmias. iii. Calcium (Hypocalcemia & Hypercalcemia) ~ Normal Range: 8.5-10.5 mEq/L. CAUSES: Hypocalcemia: Hypoparathyroidism, vitamin D deficiency. Hypercalcemia: Hyperparathyroidism, bone cancer. SIGNS & SYMPTOMS: Hypocalcemia: Muscle spasms, tingling, Chvostek and Trousseau signs. Hypercalcemia: Bone pain, kidney stones, muscle weakness. TREATMENT: Hypocalcemia: Calcium supplements. Hypercalcemia: Hydration, diuretics. OUTCOME: Hypocalcemia: Can result in neuromuscular irritability, spasms. Hypercalcemia: Can cause kidney stones, and if severe, cardiac issues. iv. Magnesium (Hypomagnesemia & Hypermagnesemia) re m e m ~ Normal Range: 1.3-2.1 mEq/L. CAUSES: Hypomagnesemia: Malnutrition, diuretics, alcoholism. Hypermagnesemia: Renal failure. SIGNS & SYMPTOMS: Hypomagnesemia: Tremors, personality changes, arrhythmias. Hypermagnesemia: Lethargy, depressed neuromuscular function. TREATMENT: Hypomagnesemia: Magnesium replacement. Hypermagnesemia: Diuresis, dialysis, calcium gluconate. OUTCOME: Hypomagnesemia: Can result in neuromuscular irritability, cardiac issues. Hypermagnesemia: Can cause respiratory and cardiac arrest. … C. Acid-Base Imbalances TYPES: Respiratory Acidosis: Results from an increase in carbon dioxide levels (CO2 retention) due to conditions like respiratory depression, COPD, or airway obstruction. Respiratory Alkalosis: Caused by hyperventilation, leading to a loss of carbon dioxide, often due to anxiety, pain, or high altitudes. Metabolic Acidosis: Occurs when bicarbonate levels decrease due to conditions like diarrhea, renal failure, or diabetic ketoacidosis. Metabolic Alkalosis: Results from excessive loss of hydrogen ions (e.g., vomiting, use of diuretics), or excessive bicarbonate intake. SIGNS & SYMPTOMS: Respiratory Acidosis: Confusion, lethargy, headache, and eventually, coma. Respiratory Alkalosis: Dizziness, tingling, muscle spasms, and possible seizures. Metabolic Acidosis: Rapid, deep breathing (Kussmaul respirations), weakness, fatigue, confusion. Metabolic Alkalosis: Restlessness, muscle twitching, tetany, seizures. TREATMENT: Respiratory Acidosis: Improve ventilation, treat underlying respiratory issues. Respiratory Alkalosis: Slow breathing or treat the underlying cause (e.g., anxiety). Metabolic Acidosis: Administer bicarbonate, correct underlying causes like ketoacidosis or renal failure. Metabolic Alkalosis: Administer fluids with chloride or treat underlying issues like vomiting. OUTCOME: Acidosis: Can result in coma or death if not corrected. Alkalosis: Severe cases may cause tetany or seizures, and if untreated, coma. 4. Discuss the implications of fluid and electrolyte imbalances as they relate to the Spheres of Caring Conceptual Framework Fluid and electrolyte imbalances, when viewed through the Spheres of Caring Conceptual Framework, highlight the importance of holistic care. These imbalances affect the physical sphere by disrupting normal body function, which can impact the emotional sphere due to discomfort or distress. In the relational sphere, the nurse’s ability to build trust and communicate effectively is essential to supporting the individual through these challenges. Overall, addressing fluid and electrolyte imbalances requires comprehensive care that integrates physical needs with emotional and relational support.  MODULE 5 INFECTION AND IMMUNITY 1. Explain the relationship between microorganisms and infectious diseases The relationship between microorganisms and infectious diseases, as outlined in the slides, is that pathogens—disease-causing microbes—such as bacteria, viruses, fungi, and protozoa invade the body and multiply. This invasion leads to damage in body tissues, resulting in infectious diseases. Microbes require specific conditions to thrive, such as particular temperatures, pH levels, or living hosts. Pathogenic microorganisms cause infection by reproducing within the host and disrupting normal bodily functions. 2. Describe the characteristics of microorganisms (bacteria, virus, fungi, protozoa) most commonly associated with infectious diseases in humans 1. Bacteria: Unicellular organisms with a cell wall. Do not require living tissue to survive. Reproduce by binary fission (simple division). Some bacteria secrete toxins (exotoxins and endotoxins). Can form endospores to survive extreme conditions. 2. Viruses: Not considered living organisms; they require a host to replicate. Obligate intracellular parasites that take over a host cell’s functions to reproduce. Contain either DNA or RNA and mutate frequently. 3. Fungi: Eukaryotic organisms (contain a nucleus). Can be single-celled (yeasts) or multicellular (molds). Fungal infections often affect immunocompromised individuals. Reproduce by budding, hyphae extension, or spores, which can easily spread and resist environmental changes. 4. Protozoa: Complex eukaryotic organisms, lacking a cell wall. Some live independently, while others are obligate parasites. Protozoan pathogens cause diseases such as malaria, amebic dysentery, and trichomoniasis. 3. Differentiate between infectious and non-infectious microorganisms Infectious disease Non-infectious diseases 1. Caused due to attack of 1. Caused by factors other than pathogens pathogens 2. Caused due to intrinsic factors 2. Caused due to extrinsic factors 3. Do not get transmitted from one person 3. Transmitted from one person to to another another 4. Transmission in case of hereditary 4. Transmission of diseases occurs diseases is from parent to offspring through direct contact or some 5. Community hygiene is ineffective in medium (air, water, vectors) reducing the occurrence of these diseases 5. Community hygiene can reduce E.g. Diabetes, Goitre the occurence of these diseases E.g. Cholera, Malaria 4. Identify the location of resident flora on body sites Normal flora, otherwise called commensal bacteria, is important to our immune system for a variety of reasons. It supports the mucosal immune system (innate immunity) by improving its function to defend against foreign pathogens. > Skin > Nose, pharynx > Mouth > Colon, Rectum > Vagina > Distal urethra/ Perineum 5. Explain the term nosocomial infection Nosocomial infections are infections that occur in health care facilities, including hospitals, nursing homes, doctors' offices, and dental offices. > 10-15% of patients acquire an infection in the hospital Why? > Presence of many microorganisms, contagious diseases, over crowding, contaminated instruments, immunocompromised patients, chain transmissions, diagnostic tests… C. Diff, causing severe diarrhea, normal flora disrupted by antibiotics Methicillin-resistant Staphylococcus aureus (MRSA) 6. Compare and contrast the local and systemic signs of infection LOCAL SIGNS: ~ SYSTEMIC SIGNS: e Swelling Fever Erythema (redness) Leukocytosis Pain and tenderness Elevated erythrocyte sedimentation rate Lymphadenopathy Fatigue, weakness, anorexia Exudate, purulent Headache, arthralgia 7. Recognize sepsis as life-threatening organ dysfunction caused by a dysregulated immune response Sepsis is recognized as a life-threatening organ dysfunction caused by a dysregulated immune response to infection. It results from the multiplication of pathogenic organisms in the blood, leading to septicemia. Sepsis can cause a toxic inflammatory condition as large amounts of inflammatory mediators are released into systemic circulation, leading to fever, hypotension, tachycardia, and tachypnea. If not treated promptly, sepsis can lead to septic shock, organ failure, and ultimately death. 8. Outline the diagnostic tests and common medical treatments for infection Diagnostic Tests: 1. Culture and Staining Techniques: Specific clinical specimens are used to grow and identify bacteria. 2. Drug Sensitivity Tests: Determine the most effective antibiotics. 3. Blood Tests: Variations in the number of leukocytes: Leukocytosis: Increase in WBCs (bacterial infection). Leukopenia: Decrease in WBCs (viral infection). Differential counts, C-reactive protein (CRP), and Erythrocyte Sedimentation Rate (ESR) indicate inflammation. 4. Immunological Testing: Antigen identification and antibody titers. 5. Radiologic Examinations: Help identify the site of infection. Common Medical Treatments: 1. Antimicrobial Drugs: Antibiotics: Used to treat bacterial infections. Antiviral Drugs: Block viral entry, gene expression, or assembly. Antifungal Drugs: Interfere with fungal mitosis and increase membrane permeability. Antiprotozoal Drugs: Similar to antifungals but vary based on the life cycle of the protozoa. 2. Supportive Treatments: May include fluid replacement, medications to reduce fever or inflammation, and pain relief. 9. Review the anatomy and physiology of the bone marrow, the lymphatic system, and the immune response Bone Marrow: - The bone marrow is the source of stem cells, which develop into various blood cells, including leukocytes (white blood cells). It is also where B lymphocytes mature. Lymphatic System: - The lymphatic system consists of lymph nodes, lymphoid structures, and lymphatic vessels. It filters body fluids, removes foreign material, and activates the immune system when necessary. It helps return excess fluid and proteins from tissues back to the bloodstream. Immune Response: - The immune response is the body’s defense against foreign substances. It involves recognizing self from non-self antigens and producing specific antibodies or activating immune cells to destroy the invaders. - The major components include immune cells (such as B and T lymphocytes) and chemical mediators (like histamines and interleukins). 10. Compare and contrast the causes, signs and symptoms, treatment, and usual course of: a. multiple myeloma b. acute and chronic leukemias c. aplastic anemia a. Multiple Myeloma: Causes: Neoplastic disease involving increased production of plasma cells (mature B lymphocytes) in the bone marrow. Signs and Symptoms: Frequent infections, bone pain, anemia, and kidney failure. Treatment: Chemotherapy to encourage remission; analgesics for bone pain; treatment for kidney impairment. Usual Course: Poor prognosis with a median survival of 3 years. Patients often experience bone destruction, hypercalcemia, and pathologic fractures. b. Acute and Chronic Leukemias: Acute Leukemia: Causes: Uncontrolled proliferation of immature, nonfunctional white blood cells in the bone marrow. Signs and Symptoms: Abrupt onset, frequent infections, anemia, bone pain, and severe hemorrhage. Treatment: Chemotherapy, blood transfusions, and sometimes bone marrow transplants. Usual Course: Rapid progression and fatal without treatment. Chronic Leukemia: Causes: Gradual increase in mature but dysfunctional white blood cells. Signs and Symptoms: Slow onset, fatigue, weakness, and frequent infections. Treatment: Chemotherapy and other supportive care. Usual Course: Slower progression with a longer course compared to acute leukemia. c. Aplastic Anemia: Causes: Failure of bone marrow leading to loss of stem cells and pancytopenia (reduced production of all blood cells). Signs and Symptoms: Fatigue, pallor, frequent infections, and bleeding tendencies. Treatment: Bone marrow transplant, blood transfusions, and removal of any causative agents. Usual Course: Can be life-threatening without treatment, requiring long-term care for symptom management.  11. Describe and compare the diagnostic tests to evaluate hypersensitivity reactions and immune system disorders Diagnostic Tests to Evaluate Hypersensitivity Reactions and Immune System Disorders: 1. Skin Tests: Used to identify specific allergens in Type I hypersensitivity reactions (e.g., allergies). A small amount of purified antigen is applied to the skin, and a positive reaction is indicated by redness or swelling at the site. 2. Serum Antibody Testing: Detects the presence of specific antibodies in the blood to assess immune response and diagnose immune system disorders. This is useful for conditions like autoimmune diseases. 3. Blood Tests: Look for variations in white blood cell (WBC) count. Increased WBCs may indicate an immune response or infection. Specific tests like measuring C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) can indicate inflammation. 4. Antigen Identification: Involves testing body fluids to detect specific antigens that trigger immune responses, helping to identify immune system disorders. 5. Antibody Titer: Measures the concentration of specific antibodies in the blood, indicating the strength of an immune response or prior exposure to antigens. 12. Examine the etiology and effects of immunodeficiency Etiology of Immunodeficiency: Primary Immunodeficiency: Caused by basic developmental failures in the immune system, such as defects in bone marrow production or the thymus. Secondary (Acquired) Immunodeficiency: Results from external factors such as infections (e.g., HIV/AIDS), malnutrition, immunosuppressive drugs, chemotherapy, or diseases affecting the bone marrow. Effects of Immunodeficiency: Increased risk of opportunistic infections by normally harmless microorganisms. Higher susceptibility to infections, which can be more severe and frequent. Treatment often involves replacement therapy, such as administering gamma globulin to boost antibodies.  13. Compare and contrast the causes, signs and symptoms, treatment, and usual course of: a. Types I, II, III, and IV hypersensitivity reactions b. systemic lupus erythematosus c. the immunodeficiency disorder HIV-AIDS d. lymphomas (Hodgkin and non-Hodgkin) e. lymphedema a. Types I, II, III, and IV Hypersensitivity Reactions: Type I (Allergic Reactions): Causes: Exposure to allergens, leading to IgE binding to mast cells and histamine release. Signs and Symptoms: Immediate inflammation, pruritus, and can include anaphylaxis. Treatment: Antihistamines, corticosteroids, epinephrine for anaphylaxis. Usual Course: Symptoms occur immediately after exposure. Type II (Cytotoxic Hypersensitivity): Causes: IgG or IgM reacts with antigens on cells (e.g., blood transfusion reactions). Signs and Symptoms: Cell lysis and phagocytosis. Treatment: Discontinue exposure to the antigen (e.g., stop transfusion). Usual Course: Can result in rapid destruction of targeted cells. Type III (Immune Complex Hypersensitivity): Causes: Antigen-antibody complexes deposit in tissues (e.g., autoimmune disorders like systemic lupus erythematosus). Signs and Symptoms: Inflammation, vasculitis, tissue destruction. Treatment: Anti-inflammatory drugs. Usual Course: Chronic or progressive damage over time. Type IV (Cell-Mediated or Delayed Hypersensitivity): Causes: Sensitized T lymphocytes respond to an antigen (e.g., contact dermatitis, tuberculosis test). Signs and Symptoms: Delayed inflammation, typically appearing 48-96 hours after exposure. Treatment: Anti-inflammatory medications. Usual Course: Delayed reaction to antigens. b. Systemic Lupus Erythematosus (SLE): Causes: Autoimmune disorder where the body forms antibodies against its own tissues. Signs and Symptoms: Butterfly rash, polyarthritis, kidney inflammation, pleurisy, photosensitivity, anemia. Treatment: Glucocorticoids, NSAIDs, immunosuppressive drugs. Usual Course: Chronic disease with periods of remission and exacerbation. c. HIV-AIDS (Immunodeficiency Disorder): Causes: Infection by the HIV virus, which destroys CD4 helper T cells, weakening the immune response. Signs and Symptoms: Generalized lymphadenopathy, fatigue, secondary infections (e.g., pneumonia, oral candidiasis), Kaposi sarcoma. Treatment: Antiretroviral drugs, no cure but can manage the disease. Usual Course: Prolonged latent phase, followed by active AIDS with multiple complications and increased susceptibility to infections and cancers. … d. Lymphomas (Hodgkin and Non-Hodgkin): Hodgkin Lymphoma: Causes: Malignancy initially involving a single lymph node. Signs and Symptoms: Painless enlarged lymph nodes, splenomegaly, recurrent infections, Reed-Sternberg cells present. Treatment: Radiation, chemotherapy. Usual Course: Localized spread from node to node, more treatable. Non-Hodgkin Lymphoma: Causes: Malignant B lymphocytes, no Reed-Sternberg cells. Signs and Symptoms: Painless enlarged lymph nodes, systemic spread. Treatment: Chemotherapy, radiation. Usual Course: More widespread and less predictable than Hodgkin’s, making it harder to treat. e. Lymphedema: Causes: Blockage of lymphatic vessels, often due to surgery, radiation, or parasitic infection. Signs and Symptoms: Swelling, initially soft but can become firm, frequent infections. Treatment: Diuretics, bed rest, massage, elevation of the affected area. Usual Course: Chronic condition with risk of frequent infections. 14. Discuss the implications of infection and immunity disorders as they relate to the Spheres of Caring Conceptual Framework Caring: When individuals suffer from infections or immune disorders, holistic care becomes crucial. Nurses must provide physical care while also addressing emotional, social, and psychological impacts on the person and family. Responding: The healthcare system must respond swiftly to control infections and manage immune disorders to prevent further complications. This involves timely interventions and patient education. Adapting: Individuals with immune disorders often need to adapt to chronic conditions, including changes to lifestyle and managing long-term treatments. This affects their overall well-being. Community: Community support plays a role in preventing the spread of infection (e.g., vaccination campaigns) and in offering resources for those managing chronic immune disorders. Society: Public health policies and societal attitudes impact how infection control and immune disorder management are approached, influencing care standards and accessibility.