NR 283 Exam 1

NR 283 Exam 1

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Chamberlain University

NR-283: Pathophysiology

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Date

Chapter 1: Introduction to Pathology

Cellular Adaptations

Cellular adaptations represent the structural and functional changes cells undergo in response to environmental stress or stimuli. These include atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia, each occurring under specific physiological or pathological conditions.

Atrophy involves a reduction in cell size and, consequently, tissue mass. This is commonly triggered by factors such as disuse, inadequate nutrition, decreased hormonal or neural input, and aging. For instance, prolonged immobilization can lead to skeletal muscle atrophy.

Hypertrophy refers to an increase in cell size that results in tissue enlargement, usually due to enhanced functional demand. A common example is myocardial hypertrophy in response to chronic hypertension.

Hyperplasia denotes an increase in the number of cells, leading to enlarged tissue mass. This process may occur physiologically (e.g., hormonal changes during pregnancy) or pathologically, as seen in endometrial hyperplasia due to hormonal imbalance.

Dysplasia is characterized by disorganized cell growth, variability in cell size and shape, enlarged nuclei, and increased mitotic activity. Chronic inflammation or infection often precedes dysplastic changes, which are commonly seen in cervical epithelial cells during cancer screening.

Metaplasia involves the substitution of one mature cell type with another that can better withstand stress. A notable example is the transformation of respiratory epithelium in smokers from ciliated columnar cells to stratified squamous cells.

Table: Cellular Adaptations and Causes

Common Causes of Cellular Injury

Cellular damage primarily arises from ischemia, which reduces oxygen supply and impairs aerobic metabolism. Additional causes include:

• Physical agents: extreme temperatures, radiation
• Mechanical stress: trauma, pressure
• Chemical agents: toxins, pollutants
• Biological factors: bacteria, viruses, parasites
• Nutritional deficiencies: protein or vitamin deficits
• Metabolic imbalances: electrolyte or fluid derangements

Infection and Inflammation

Microorganisms such as bacteria and viruses can cause direct cellular damage. Some bacteria initiate pyroptosis—a cell death pathway leading to membrane rupture and inflammation due to lysosomal enzyme release. This process exacerbates tissue injury, manifesting as redness, swelling, and pain.

Chemical Injury

Chemical agents—either endogenous like metabolic byproducts or exogenous like toxins—can impair cellular membranes and generate free radicals, leading to oxidative damage and loss of cellular integrity.

Types of Necrosis

Necrosis is irreversible cell death in living tissue. Major types include:

• Liquefactive necrosis: Enzymatic digestion results in tissue softening, common in the brain.
• Coagulative necrosis: Protein denaturation preserves cell outlines; seen in myocardial infarction.
• Fat necrosis: Enzymatic breakdown of fats, often in the breast or pancreas.
• Caseous necrosis: A combination of coagulation and liquefaction, producing a cheese-like material typical in tuberculosis.

Apoptosis

Apoptosis is a genetically regulated form of cell death essential for removing aged, damaged, or unnecessary cells. Unlike necrosis, apoptosis is non-inflammatory and results in the phagocytosis of apoptotic bodies by neighboring cells.

Table: Comparison of Cell Death Types

Chapter 2: Fluids and Electrolytes, Acids and Bases

Fluid Compartments

Body fluids are distributed across two main compartments:

• Intracellular fluid (ICF): Fluid inside cells, representing a larger proportion of total body water.
• Extracellular fluid (ECF): Found outside cells, including plasma, interstitial, cerebrospinal, and transcellular fluids.

Water Movement

Fluid exchange between plasma and interstitial space occurs across capillary membranes influenced by:

• Hydrostatic pressure: Pushes fluid out of capillaries.
• Osmotic pressure: Pulls fluid back into capillaries.

Edema

Edema results from fluid accumulation in interstitial spaces due to:

• Elevated capillary hydrostatic pressure
• Decreased plasma oncotic pressure from protein loss
• Lymphatic obstruction
• Increased capillary permeability from inflammation

Symptoms include skin pallor, swelling, and pulmonary congestion.

Sodium and Water Balance

Homeostasis is maintained through:

• ADH: Regulates water reabsorption in kidneys.
• Aldosterone: Promotes sodium and water retention.
• RAAS: Increases blood pressure and stimulates aldosterone release.

Table: Electrolyte Imbalances and Effects

Water Deficits and Excesses

• Hypovolemia: Caused by dehydration; signs include low BP and dry mucosa.
• Hypervolemia: Results from fluid overload; presents with edema and hypertension.

Acid-Base Balance

Maintained via:

• Respiratory regulation: Modulates CO2 excretion.
• Renal regulation: Balances H+ and bicarbonate.

Types of Acid-Base Imbalances

Chapter 5: Inflammation

Physiology of Inflammation

Inflammation is a protective, non-specific immune response triggered by tissue injury. Symptoms include redness, heat, swelling, pain, and functional loss.

Acute vs. Chronic Inflammation

• Acute: Rapid onset; dominated by neutrophils and plasma proteins.
• Chronic: Persistent; involves lymphocytes, macrophages, and fibrosis.

Phases of inflammation:

• Vascular phase: Vasodilation, increased permeability.
• Cellular phase: Leukocyte recruitment to injury site.

Clinical Manifestations

• Local: Redness, warmth, swelling
• Systemic: Fever, fatigue, leukocytosis

Inflammatory Mediators

• Histamine: Triggers vasodilation and capillary leakage
• Cytokines: Orchestrate immune response and cell signaling

Healing and Repair

• Regeneration: Replacement with identical cells
• Repair: Scar formation when regeneration isn’t possible

Wound Healing Stages

1. Hemostasis: Clot formation
2. Inflammation: Pathogen clearance
3. Proliferation: New tissue growth
4. Remodeling: Tissue maturation and strengthening

Complications of Healing

• Infection: Impedes repair
• Dehiscence: Wound reopening
• Hypertrophic scars: Excessive collagen formation

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.

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

NR 283 Exam 1

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