Chapter 2 pt 1

Normal cells maintain a narrow range of structural and functional constraints.
Cells can adapt to increased demands/stress to maintain homeostasis, a steady state that is a reversible response involving structural or functional modifications to accommodate physiological and pathological conditions.
Example of physiological adaptation: Uterus enlarges during pregnancy.
Example of pathological adaptation: Myocardial cells enlarge under conditions of hypertension.
Common sources of stress include structural damage, neoplasia, fluid/solute accumulations, genetic influences, and aging.

Atrophy: Decrease in cell size (e.g., skeletal muscle, heart, brain).
- Physiological atrophy occurs with normal development (e.g., thymus gland involution).
- Pathological atrophy results from decreased workload, blood supply, nutrition, hormonal, or neural stimulation.
Hypertrophy: Compensatory increase in cell size in response to mechanical stress (e.g., heart or kidney).
- Physiological hypertrophy occurs due to increased demand or hormonal stimulation (e.g., runner's heart).
- Pathological hypertrophy occurs from chronic overload (e.g., hypertension, heart failure).
Hyperplasia: Increase in cell number due to increased cellular division.
- Mechanisms include hormones or growth factors stimulating remaining cells or tissue stem cells.
- Compensatory hyperplasia enhances regeneration following loss of tissue.
- Hormonal hyperplasia occurs in estrogen-dependent organs (e.g., uterus during pregnancy).
Dysplasia: Abnormal changes in size, shape, and organization of cells, often not a true adaptation and can lead to precancerous conditions.
Metaplasia: Reversible replacement of one mature cell type with another, typically in response to an adverse environment.
- Example: Ciliated columnar epithelium replacing with stratified squamous cells due to smoking.

Injury occurs from any factor disrupting cellular structures or depriving the cell of essential nutrients.
Cellular injury may be sublethal (reversible) or lethal (irreversible).
Classifications of injury sources include ischemic-hypoxic, ischemia-reperfusion, free radical, immunologic, infectious, intentional/unintentional, and inflammatory.

Table summarizing protections and adaptations.
Prolonged stress leads to cell injury detailed in mechanisms of ATP depletion, oxidative stress, and calcium overload.

Hypoxia: Most common cause of cellular injury.
- Caused by: lowered oxygen in blood, loss of hemoglobin, decreased RBC production.
- Ischemia: Lacks sufficient blood supply causing severe damage.
- Oxygen deprivation can cause cell swelling and death in various tissues.

Restoration of blood flow post-ischemia can paradoxically cause oxidative stress leading to additional cell damage.
- Mechanisms include oxidative stress, increased intracellular calcium, inflammation, and complement activation.

Free radicals cause cell damage by oxidizing proteins, lipids, and nucleic acids.
- Generated from mitochondrial respiration, environmental toxins, or inflammatory processes.
- Depletion of antioxidants can lead to cell injuries linked with aging and various diseases.

Covers exposure to xenobiotics and resultant cellular stress mechanisms.
- Chemical agents can produce acute or chronic toxicity depending on concentration and duration of exposure.
- Liver is a primary site for chemical detoxification and often affected by xenobiotics.

Impact of air pollution and household pollutants on global health.
Risks to children and vulnerable populations from substances like lead, mercury, and toxins in consumer products.

Include various causes such as motor vehicle accidents, falls, and firearms.
- Reported death rates from unintentional injuries are high, calling for preventive measures.

Specific exposure scenarios and associated health outcomes for individuals in various professions.
- Regular assessment and mitigation strategies are effective in reducing overall injury and illness rates.

Suffocation: Resulting from a lack of oxygen or blockage of airways.
Choking: Obstruction of the pulmonary airways that may require immediate intervention (Heimlich maneuver, bronchoscopy).

External pressure on the neck preventing airflow can lead to death within seconds.
Mechanisms include mechanical compression of blood vessels and respiration pathways.

Carbon Monoxide: A major gas asphyxiant with high affinity to hemoglobin; can cause unconsciousness and death without warning.