NR 283 Exam 1

NR 283 Exam 1

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Chamberlain University

NR-283: Pathophysiology

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Chapter 1: Introduction to Pathology

Cellular Adaptations

Cellular adaptations refer to the changes that cells undergo in response to various stimuli or stressors. The following outlines the adaptations associated with atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia, along with their causative factors.

Atrophy is characterized by a decrease in cell size, resulting in a reduction in tissue mass. Common causes include reduced use of the tissue, insufficient nutrition, decreased neurologic or hormonal stimulation, and aging. For example, muscle atrophy may occur in individuals who are bedridden for an extended period.

Hypertrophy involves an increase in the size of individual cells, leading to an enlarged tissue mass. This change is often a response to increased workload, such as the enlargement of heart muscle cells due to hypertension.

Hyperplasia is defined as an increase in the number of cells within a tissue, resulting in tissue enlargement. This can occur as a compensatory mechanism to meet increased demands or may be pathologic, such as in cases of hormonal imbalance or precancerous conditions.

Dysplasia refers to abnormal cell growth, where cells vary in size and shape, often accompanied by large nuclei and increased mitotic activity. This condition can arise from chronic irritation or infection and is frequently a precursor to cancer. For instance, dysplasia is a key factor assessed during Pap smears for cervical cancer screening.

Metaplasia is the process in which one mature cell type is replaced by another mature cell type. This adaptation can occur in response to a deficiency, such as vitamin A, and may serve as an adaptive mechanism. An example is the replacement of ciliated columnar epithelium with stratified squamous epithelium in the respiratory tracts of smokers, enhancing tissue resilience at the expense of normal lung defenses.

Common Causes of Cellular Injury

The predominant cause of cellular injury is ischemia, defined as a decreased supply of oxygenated blood to tissues or organs due to circulatory obstruction. This condition leads to hypoxia, characterized by reduced oxygen levels in tissues and subsequent decreased cellular metabolism. Other factors contributing to cellular injury include:

• Physical agents: Excessive heat, cold, or radiation exposure
• Mechanical damage: Tissue pressure or tearing
• Chemical toxins
• Microorganisms: Bacteria, viruses, and parasites
• Accumulation of abnormal metabolites
• Nutritional deficits
• Fluid or electrolyte imbalances

Infection and Inflammation

Cellular injury from infection and inflammation occurs when microorganisms such as bacteria and viruses invade tissues. Certain microorganisms can induce pyroptosis, a form of cell death marked by cell lysis, which leads to the rupture of the plasma membrane and the release of destructive lysosomal enzymes. This process triggers inflammation, manifesting as swelling, redness, and pain, and can damage surrounding cells and impair their functions.

Chemical Injury

Chemical injuries can result from both exogenous (external) and endogenous (internal) sources, damaging cells by altering membrane permeability or producing free radicals. These free radicals cause ongoing damage to cellular components, contributing to various pathological processes.

Types of Necrosis

Necrosis refers to the process of cell death in living tissue. The major types of necrosis include:

• Liquefactive necrosis: This process involves the liquefaction of dead cells due to cell enzymes, commonly occurring in brain tissue or in certain bacterial infections that form cavities or ulcers.
• Coagulative necrosis: Occurs when cell proteins are altered or denatured while retaining some cell structure post-mortem. An example is myocardial infarction, where oxygen deprivation leads to cell death.
• Fat necrosis: Involves the breakdown of fatty tissue into fatty acids, often occurring in infections or due to certain enzymes, potentially increasing inflammation.
• Caseous necrosis: A specific form of coagulation necrosis characterized by a thick, yellowish “cheesy” substance. This is typically seen in tuberculosis infections, where a granuloma known as the Ghon complex may form. If the infection persists, it can lead to liquefactive necrosis.

Apoptosis

Apoptosis is a process of programmed cell death that is essential for maintaining cellular homeostasis. It involves the enzymatic self-digestion of cells, which then disintegrate into apoptotic bodies that are phagocytosed without triggering an inflammatory response. Apoptosis may be upregulated in cases of abnormal cell development, excessive cell numbers, or when cells are damaged or aged.

Tissue Necrosis Types

The different types of tissue necrosis include:

• Coagulative necrosis: Commonly found in cardiac and kidney tissues due to ischemia.
• Fat necrosis: Associated with pancreatic or breast tissue damage.
• Liquefactive necrosis: Typically observed in abscesses or hypoxic death, especially in brain tissue.
• Caseous necrosis: Often observed in cavitating spaces in patients with tuberculosis, affecting the lungs and kidneys.

Chapter 2: Fluids and Electrolytes, Acids and Bases

Fluid Compartments

The body is divided into two primary functional fluid compartments:

• Intracellular fluid compartment: This fluid exists within cells and constitutes a larger percentage of body weight compared to extracellular fluid.
• Extracellular fluid compartment: This compartment exists outside the cells and includes intravascular fluid (blood), interstitial fluid (intercellular fluid), cerebrospinal fluid, and transcellular fluids (found in various secretions).

Water Movement

Water moves between plasma and interstitial fluid through semipermeable capillary membranes, influenced by hydrostatic and osmotic pressure. At the arteriolar end of the capillary, higher plasma hydrostatic pressure pushes fluid into the interstitial space. Conversely, at the venous end, increased osmotic pressure draws fluid back into the capillary.

Edema

Edema refers to an accumulation of excessive fluid in the interstitial compartment, leading to tissue swelling. The causative factors include:

1. Increased capillary hydrostatic pressure, which can stem from conditions such as kidney failure or congestive heart failure.
2. Loss of plasma proteins (e.g., albumin), resulting in decreased osmotic pressure, which reduces the capillary’s ability to return fluid.
3. Obstruction of lymphatic circulation, causing localized edema.
4. Increased capillary permeability due to inflammation or infection, allowing fluid and proteins to leak into interstitial areas.

Clinical manifestations of edema can include pale or red skin, weight gain, high blood pressure, and pulmonary congestion.

Sodium and Water Balance

The balance of sodium and water is regulated by various mechanisms, including:

• Antidiuretic hormone (ADH): Released by the pituitary gland, it controls fluid retention and prevents dilute urine formation.
• Aldosterone: This hormone regulates sodium reabsorption in the kidneys and increases fluid retention during deficits.

The renin-angiotensin-aldosterone system (RAAS) plays a significant role, where renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). This leads to vasoconstriction, increased blood pressure, and stimulation of aldosterone release.

Electrolyte Imbalances

The clinical manifestations of electrolyte imbalances can be severe and vary with each condition:

• Hypernatremia arises from excessive sodium intake, rapid water loss, or diabetes insipidus, leading to symptoms such as thirst, dry mucous membranes, and agitation.
• Hyponatremia can result from excessive fluid loss, diuretic use, or increased ADH secretion, presenting with fatigue, nausea, and confusion.
• Hyperkalemia often stems from renal failure or aldosterone deficiency, leading to arrhythmias, muscle weakness, and potential cardiac arrest.
• Hypokalemia may occur due to diuretic use, excessive losses, or poor dietary intake, manifesting as cardiac arrhythmias and muscle weakness.
• Hypercalcemia can result from malignancies or hyperparathyroidism, leading to lethargy, anorexia, and kidney stones.
• Hypocalcemia may arise from hypoparathyroidism or malabsorption, presenting with muscle spasms and arrhythmias.

Water Deficits and Excesses

Hypovolemia occurs when there is a deficit of circulating blood volume, commonly due to severe diarrhea, vomiting, or injury. Clinical signs include dehydration, low blood pressure, and concentrated urine.

Hypervolemia, characterized by an excess of fluid, can arise from kidney failure or excessive fluid administration. Symptoms may include edema, weight gain, and elevated blood pressure.

Acid-Base Balance

Hydrogen ion concentration is crucial for maintaining cellular function. The lungs and kidneys regulate acid-base balance, with the lungs adjusting carbon dioxide levels and the kidneys managing bicarbonate and hydrogen ion concentrations.

Acid-Base Disturbances

Differentiating between respiratory and metabolic disturbances is essential:

• Respiratory acidosis results from impaired ventilation and leads to increased carbon dioxide levels.
• Respiratory alkalosis occurs from hyperventilation, decreasing carbon dioxide levels.
• Metabolic acidosis is due to an accumulation of acids or loss of bicarbonate.
• Metabolic alkalosis results from excessive bicarbonate or loss of acids.

Chapter 5: Inflammation

Physiology of Inflammation

Inflammation serves as a protective mechanism, localizing and removing harmful agents from the body. It is defined as the nonspecific response to tissue injury, resulting in redness, swelling, warmth, pain, and possible loss of function. Various tissue injuries can trigger inflammation, including physical damage, chemical exposure, ischemia, allergic reactions, and infections.

Acute vs. Chronic Inflammation

Acute inflammation is characterized by a rapid onset, lasting only a few days, and involves the influx of neutrophils, plasma proteins, and fluid accumulation at the site of injury. In contrast, chronic inflammation persists for weeks or months and is marked by the presence of macrophages, lymphocytes, and fibrosis.

• Acute inflammation involves the vascular and cellular phases. The vascular phase features vasodilation and increased permeability, while the cellular phase involves the recruitment of leukocytes to the injury site.

• Chronic inflammation may result from persistent irritants, autoimmune responses, or unresolved acute inflammation, leading to tissue damage and repair processes.

Clinical Manifestations of Inflammation

Signs and symptoms of inflammation can vary depending on the nature of the injury. Common manifestations include:

• Local signs: Redness, heat, swelling, pain, and loss of function.
• Systemic signs: Fever, malaise, and leukocytosis (increased white blood cell count).

Inflammatory Mediators

Various chemical mediators regulate the inflammatory process, including:

• Histamine: Released by mast cells, it causes vasodilation and increased capillary permeability.
• Cytokines: These proteins, released by various cells, coordinate inflammatory responses and recruit immune cells to the site of injury.

Healing and Repair

The healing process involves two primary phases:

• Regeneration: Replacement of damaged cells with new cells of the same type.
• Repair: Formation of scar tissue, which can occur if regeneration is not possible.

Wound Healing

Wound healing progresses through several stages:

1. Hemostasis: Immediate vasoconstriction and clot formation to stop bleeding.
2. Inflammation: Removal of debris and pathogens, characterized by increased blood flow and immune cell activity.
3. Proliferation: Formation of new tissue through cell division, angiogenesis, and collagen deposition.
4. Remodeling: Maturation of the newly formed tissue, which can take months to years, leading to improved strength and function.

Complications of Healing

Complications during the healing process can arise, including:

• Infection: Delays healing and can lead to further tissue damage.
• Dehiscence: Wound reopening due to inadequate healing or excessive tension.
• Hypertrophic scars: Excessive collagen deposition leads to raised, thick scars.

This outline provides a concise overview of the first few chapters, focusing on key concepts and clinical implications related to pathology, fluid and electrolyte balance, and inflammation.

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The Burn Wound and Its Consequences

The surface of a burn wound is often coagulated or charred, resulting in a hard and dry appearance. This damaged tissue, referred to as eschar, undergoes shrinkage, which can exert pressure on the underlying edematous tissue. When the entire circumference of a limb is affected, a surgical procedure known as escharotomy may be required. This procedure involves making incisions through the eschar to alleviate pressure and promote improved circulation in the affected area. Initially, burn wounds may be painless due to nerve destruction, but as the surrounding tissue becomes inflamed from the release of chemical mediators by the damaged cells, significant pain often develops. Full-thickness burns necessitate skin grafts for healing since there are no remaining cells to regenerate new skin. Many burn injuries present as mixed burns, containing areas of both partial and full-thickness burns.

Consequences of Severe Burn Injuries

Fluid Shifts and Cardiovascular Compromise

In burn injuries, bleeding is typically absent, as both tissue and blood become coagulated or solidified from the heat. Beneath the burn, an inflammatory response occurs, especially in cases of large burn areas. This response results in a considerable shift of water, proteins, and electrolytes into surrounding tissues, leading to fluid excess or edema. Additionally, the loss of water and protein from the bloodstream results in reduced circulating blood volume, low blood pressure, and potential hypovolemic shock. The concentration of red blood cells increases (hemoconcentration), which complicates fluid balance due to the protein shift out of capillaries and the resultant decline in blood osmotic pressure. Such fluid imbalances pose a risk of prolonged or recurrent shock, which can ultimately result in kidney failure or damage to other vital organs. For management, fluid and electrolytes, along with plasma expanders to compensate for lost proteins, are administered intravenously using protocols tailored for burn patients. Severe shock, particularly with extensive full-thickness burns, can lead to acute renal failure.

Immunologic Alterations

The risk of infection in burn injuries exacerbates tissue loss, frequently converting partial-thickness burns into full-thickness ones. Common pathogens involved in such infections include Pseudomonas aeruginosa, Staphylococcus aureus (including resistant strains), Klebsiella, and Candida. When a serious infection occurs, there is a potential for pathogens or their toxins to disseminate systemically, leading to septic shock and other severe complications. Treatment typically involves prompt excision of infected tissue, application of antimicrobial agents, and skin grafting or alternative coverings.

Types of Infectious Microorganisms

Lymph Node Treatment and Cancer Spread

Lymph nodes are typically removed or treated to eliminate any micrometastases that might be overlooked, especially in cancers that are known for early dissemination. Many types of cancer spread through the body’s natural venous and lymphatic systems, making the lungs and liver frequent secondary sites for various tumors. The term “seeding” refers to the dispersal of cancer cells via body fluids or along membranes, typically within body cavities. Tumor cells may detach and travel easily through fluid and tissue movement; they can also be dislodged during diagnostic procedures or surgery, which can exacerbate the spread of malignant cells.

The TNM Staging System

The TNM staging system is essential for classifying the extent of cancer.

Effects of Cancer and Its Treatment

Warning Signs of Cancer

Common indicators of cancer include unusual bleeding or discharge, changes in bowel or bladder habits, alterations in warts or moles, persistent sores, unexplained weight loss, anemia or low hemoglobin levels, persistent fatigue, chronic cough or hoarseness, and solid lumps in the breast or testicles.

Local Effects of Cancer

Local effects can manifest as pain, obstruction, and tissue necrosis. Pain severity varies depending on tumor type and location, often resulting from pressure on sensory nerves or stretching of visceral capsules in organs like the kidney and liver. Tumors can cause obstructions by compressing ducts or growing within passageways, while necrosis and ulceration may lead to infections surrounding the tumor.

Systemic Effects of Cancer

Systemic effects include weight loss, anemia, severe fatigue, increased infection risk, and bleeding. Additionally, paraneoplastic syndromes may occur, where tumor cells release substances that affect neurological function, blood clotting, or hormone levels.

Adverse Effects of Cancer Treatment

Cancer treatment can lead to various adverse effects, such as bone marrow depression and epithelial cell damage, which may result in inflammation, hair loss, gastrointestinal mucosal damage, and risk of secondary infections. Abdominal radiation can damage reproductive organs, leading to sterility or teratogenic risks. Patients often experience fatigue, lethargy, and specific drug-related effects in targeted areas, such as fibrosis in the lungs or damage to myocardial cells.

Environmental Hazards and Cancer Risk Factors

Smoking

Smoking significantly increases the risk of lung disease, including emphysema, bronchitis, and lung cancer, as well as bladder cancer and cardiovascular diseases. It can impair fertility and negatively affect fetal development during pregnancy, leading to complications such as stillbirth or low birth weight.

Radiation Exposure

Radiation primarily impacts cells that undergo rapid mitosis, such as those in epithelial tissues, bone marrow, and reproductive organs. Small doses may allow cells to repair damaged DNA, while larger doses can lead to mutations and cancer development due to DNA alteration and cross-linkages. Significant radiation exposure can also cause radiation sickness, damaging the bone marrow, digestive tract, and central nervous system.

Effects of Environmental Hazards

Lead Exposure

Lead can be ingested through contaminated food or water, or inhaled, and is stored in bone. Its effects include hemolytic anemia, gastrointestinal inflammation, kidney damage, and significant neurological damage, including neuritis and encephalopathy. In children, lead toxicity can lead to severe developmental issues and seizures.

Asbestos

Exposure to asbestos can cause severe inflammation and scarring, potentially leading to malignant mesothelioma, asbestosis, and pleural thickening.

Ionizing Radiation

Ionizing radiation can significantly alter cellular structures and functions, similar to the effects of lead and other environmental hazards.

Skin Structure and Functions

The skin serves as the first line of defense against microorganisms, prevents excessive fluid loss, and regulates body temperature. The primary layers of the skin include the epidermis, dermis, and hypodermis. The epidermis consists of several layers, including the stratum basale, stratum spinosum, stratum granulosum, and stratum corneum, each playing a role in skin integrity and function. The dermis contains connective tissue, sensory receptors, and blood vessels.

Pruritus and Dermatitis

Pruritus, or itching, is often linked to allergic responses, chemical irritants, or parasitic infestations. The release of histamine in hypersensitivity reactions can cause localized inflammation, potentially leading to secondary infections due to skin barrier breaches. Various forms of dermatitis include contact dermatitis, urticaria (hives), atopic dermatitis (eczema), and psoriasis, each with distinct causes, symptoms, and treatment approaches.

Skin Cancer Incidence and Types

Keratoses are benign lesions often linked to aging or skin damage. Squamous cell carcinoma (SCC) is a common skin cancer, easily detectable and treatable, characterized by painless, malignant lesions that arise primarily due to sun exposure. Malignant melanoma, arising from melanocytes, poses a higher risk for metastasis and has a more severe prognosis. Other skin cancers, such as Kaposi sarcoma, are associated with immunocompromised states, like HIV/AIDS.

References

American Association of Critical-Care Nurses. (n.d.). Clinical considerations for burn care. Retrieved from AACN website

Burke, J. F., & K. J. (2015). Burn care: Pathophysiology and management. Journal of Trauma and Acute Care Surgery, 78(2), 307-317.

NR 283 Exam 1

Davis, A. J., & H. L. (2020). Burn injury: Understanding the complications. Journal of Burn Care & Research, 41(2), 295-302.

Miller, K. C., & H. A. (2018). The immunologic response to burn injury. Clinics in Plastic Surgery, 45(1), 57-63.