NURS-340: Pathophysiology 1 (Exam 1)

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Last updated 12:17 AM on 2/10/26
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218 Terms

1
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How is health defined according to the World Health Organization (WHO)?

A state of complete physical, mental, and social well-being, not merely the absence of disease or infirmity

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What factors influence health status?

Age, genetics, gender, environment, and social factors

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How is disease defined?

A condition in which the body no longer functions normally and varies in severity and duration

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What is the difference between acute and chronic diseases?

Acute diseases occur and resolve quickly; chronic diseases last longer and may never fully resolve but can be managed

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What is homeostasis?

The body’s ability to maintain a stable internal environment despite external changes

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What are the two main mechanisms of cellular adaptation?

Proliferation (cell division) and differentiation (cells specializing in structure and function)

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When is cellular adaptation considered abnormal?

When it persists after the stimulus is removed or contributes to disease

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What is atrophy?

Decrease in cell size

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What is hypertrophy?

Increase in cell size

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What is hyperplasia?

Increase in the number of cells

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What is metaplasia?

Replacement of one mature cell type with another

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What is dysplasia?

Abnormal cell growth that is often precancerous

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What causes cellular injury?

Physical, chemical, biologic agents, nutritional deficiencies, and free radicals

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What is hypoxia?

Insufficient oxygen in the blood to sustain cellular function

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What is ischemia?

Decreased blood supply to an organ

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What is apoptosis?

Normal, programmed cell death

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What is necrosis?

Premature, abnormal cell death due to injury that triggers inflammation

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What is the difference between genetics and genomics?

Genetics studies individual genes; genomics studies the entire genome and gene-environment interactions

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What are genes?

Segments of DNA on chromosomes that code for protein production and inherited traits

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What is the difference between genotype and phenotype?

Genotype is genetic makeup; phenotype is observable traits

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What is penetrance?

The percentage of individuals with a gene mutation who express the associated phenotype

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What is expressivity?

The degree to which a gene is expressed in an individual

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What is the difference between generic and brand names?

Generic names are official, lowercase, and standardized; brand names are capitalized and manufacturer-specific

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Are generic and brand drugs interchangeable?

Yes, if FDA approved as bioequivalent

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What is onset of action?

The time it takes for a drug to begin producing an effect

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What is peak of action?

The time when the drug reaches its highest concentration and strongest effect

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What is duration of action?

The length of time the drug maintains a therapeutic effect

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What is a therapeutic effect?

The intended, desired effect of a medication

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What is an adverse effect?

An unintended, potentially harmful effect of a medication

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What is pharmacokinetics?

How the body processes a drug through absorption, distribution, metabolism, and elimination

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What is absorption?

Movement of a drug from the administration site into the bloodstream

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What is distribution?

Transport of the drug throughout the body via the bloodstream

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What is metabolism?

Chemical alteration of a drug, primarily by the liver

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What is elimination?

Removal of the drug from the body via kidneys, bile, lungs, skin, or feces

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What is a peak level?

The highest concentration of a drug in the bloodstream after administration

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What is a trough level?

The lowest concentration of a drug in the bloodstream, measured just before the next dose

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What is pharmacodynamics?

The biochemical and physiological effects of drugs on the body

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What is an agonist?

A drug that enhances or activates cellular activity

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What is an antagonist?

A drug that blocks or reduces cellular activity

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What is tolerance?

A decreased response to a drug over time, requiring higher doses

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What is dependence?

Physical or psychological reliance on a drug

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What is addiction?

Compulsive drug use despite harmful consequences

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What is drug toxicity?

Drug accumulation in the body to harmful or life-threatening levels

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What is a cumulative effect?

Drug buildup due to impaired metabolism or elimination

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Why are drug-food interactions important?

Certain foods (e.g., grapefruit juice, calcium-rich foods) can alter absorption or metabolism and increase toxicity

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Why do pharmacokinetics differ across the lifespan?

Differences in liver function, kidney function, body composition, and metabolism in infants, children, and older adults

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What is the immune response?

The collective, coordinated response of immune cells and molecules that protect the body from foreign invaders

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What are the body’s three lines of defense?

  1. Physical and chemical barriers

  2. Innate immune response

  3. Adaptive immune response

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What structures make up the first line of defense?

Skin, mucous membranes, mucus, cilia, tears, saliva, and stomach acid

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What is innate (nonspecific) immunity?

A rapid, immediate defense that responds the same way to all pathogens and has no memory

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What is adaptive (specific) immunity?

A slower but more precise immune response that targets specific antigens and has memory

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What are key characteristics of innate immunity?

Immediate response, no memory, and limited specificity

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What are key characteristics of adaptive immunity?

Specificity, diversity, memory, and stronger response on re-exposure

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Which WBCs develop into macrophages?

Monocytes

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Which WBCs are the first responders to infection?

Neutrophils

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Which cells ingest bacteria and release enzymes?

Phagocytes (macrophages, neutrophils)

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Which cells release histamine in allergic reactions?

Basophils and mast cells

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Which cells recognize and destroy abnormal cells and release cytokines?

Natural killer (NK) cells

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What is the role of B cells?

Produce antibodies

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What is the role of cytotoxic (CD8+) T cells?

Directly destroy infected or abnormal cells

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What do helper T cells do?

Coordinate and activate other immune cells

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What is the function of antigen-presenting cells (APCs)?

Present antigens to T cells to initiate adaptive immunity

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What is the complement system?

A cascade of plasma proteins that enhance inflammation and destroy pathogens

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What are cytokines?

Immune signaling molecules that stimulate, inhibit, or regulate immune responses

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What is inflammation?

An innate, automatic response to injury or infection that neutralizes harmful agents, removes damaged tissue, and promotes healing

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What are the two stages of acute inflammation?

Vascular stage and cellular stage

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What occurs during the vascular stage of inflammation?

Vasodilation and increased capillary permeability

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Which mediators cause vasodilation?

Histamine and nitric oxide

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What occurs during the cellular stage of inflammation?

WBCs migrate to tissue, destroy pathogens, remove debris, and release mediators

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What are the five cardinal signs of inflammation?

Redness (rubor), swelling (tumor), heat (calor), pain (dolor), and loss of function (functio laesa)

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What is histamine’s primary role in inflammation?

Increases vascular permeability

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What do prostaglandins and leukotrienes do?

Potentiate inflammation; prostaglandins increase platelet aggregation, leukotrienes prolong permeability

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What is the role of cytokines like TNF-α and IL-1?

Produce fever, hypotension, tachycardia, anorexia, and neutrophil release

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What does bradykinin cause?

Pain, vasodilation, and increased permeability

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What is hypersensitivity?

An exaggerated immune response that damages healthy tissue

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What is Type I hypersensitivity?

IgE-mediated; causes allergies and anaphylaxis

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What is Type II hypersensitivity?

Tissue-specific antibody reaction causing cell lysis (e.g., transfusion reactions)

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What is Type III hypersensitivity?

Immune complex deposition causing inflammation (e.g., autoimmune disorders)

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What is Type IV hypersensitivity?

Delayed, T-cell mediated response (e.g., TB skin test, transplant rejection)

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What defines an infectious disease?

Microbial invasion that causes pathologic damage to the host

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What is the difference between colonization and infection?

Colonization is presence without disease; infection involves tissue damage and symptoms

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What are opportunistic infections?

Infections caused by normal flora or low-virulence organisms in immunocompromised hosts

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What are the six links in the chain of infection?

Agent → Reservoir → Portal of exit → Mode of transmission → Portal of entry → Susceptible host

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What is virulence?

A pathogen’s ability to cause disease

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What are exotoxins?

Proteins secreted by bacteria that damage host cells

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What are endotoxins?

Lipids from gram-negative bacterial cell walls causing fever, hypotension, and inflammation

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What is the stress response?

A coordinated physiologic response designed to restore homeostasis during threats

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Which systems regulate the stress response?

Nervous, endocrine, and immune systems

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What is the HPA axis?

Hypothalamic-pituitary-adrenal axis regulating cortisol release

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What is cortisol’s role in stress?

It increases blood glucose, suppresses immune function, and conserves energy

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How does chronic stress affect immunity?

Prolonged cortisol suppresses immune responses and increases infection risk

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What factors influence stress response effectiveness?

Age, health, nutrition, sleep, genetics, psychosocial factors, and duration of stress

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How do vaccines work?

They introduce antigens that stimulate antibody production and immune memory

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What is active immunity?

Immunity developed after infection or vaccination; memory present

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What is passive immunity?

Temporary immunity from transferred antibodies; no memory

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What is the purpose of booster vaccines?

To reinforce immune memory as immunity wanes over time

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How do opioids relieve pain?

By binding to opioid receptors in the CNS to alter pain perception

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How do NSAIDs reduce inflammation?

By inhibiting prostaglandin synthesis

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How does acetaminophen differ from NSAIDs?

It provides analgesia and antipyresis but minimal anti-inflammatory effect

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What is aspirin’s unique effect among NSAIDs?

Irreversible platelet inhibition