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Course Overview

• Title: Altered Cellular and Tissue Biology

• Instructor: Dr. Kelley McGuire, PhD, RN, CNE

Learning Outcomes

• Understand the basic principles of cellular adaptation and injury.

• Relate the pathophysiology of cellular injury to clinical manifestations and complications.

• Describe the stages of cellular death.

• Explain the difference between cellular death and somatic death.

• Describe the physiologic changes that occur after somatic death.

Cellular Adaptation

Types of Cellular Adaptation

• Atrophy: Decrease in cell size. Common in skeletal muscle, heart, brain. Physiologic (e.g., thymus in childhood) vs. Pathologic (e.g., due to workload, blood supply, hormonal changes).

• Hypertrophy: Increase in cell size due to mechanical load/stress. Physiologic (increased demand) vs. Pathologic (e.g., hypertension related changes).

• Hyperplasia: Increase in the number of cells due to increased division rate. Can be physiologic (adaptive regeneration) or pathologic (excess hormonal stimulation).

• Dysplasia: Abnormal changes in cell size, shape, organization (not true adaptive change); linked to precancerous conditions.

• Metaplasia: Reversible replacement of one cell type with another, often found in response to damage (e.g., cigarette smoke changes in respiratory epithelium).

Cellular Injury

Types of Progressive Cell Injury and Responses

• Adaptation: Atrophy, hypertrophy, hyperplasia, metaplasia.

• Active cell injury: Immediate cell response; reversible.

• Irreversible injury: Point of no return, severe structural damage (e.g., mitochondrial vacuolization).

• Necrosis: Common cell death type; severe cell swelling and breakdown.

• Apoptosis: Programmed cell death; eliminates unwanted cells.

• Autophagy: Cell recycling and self-digestion processes.

• Chronic cell injury: Specific organelle changes under persistent stimuli.

Mechanisms of Cell Injury

• Ischemic and Hypoxic Injury:

  • Hypoxia = lack of oxygen (most common cause of cell injury).

  • Ischemia = reduced blood supply; causes rapid ATP depletion leading to cellular swelling.

• Ischemia-Reperfusion Injury: Restoration of blood flow causing additional cell death via oxidative stress and inflammation.

• Oxidative Stress: Reactive oxygen species cause lipid peroxidation, protein alterations, DNA damage.

• Chemical Injury: Caused by xenobiotics; may induce oxidative stress and cellular damage.

Specific Chemical Agents

• Lead: Toxic metal exposure leads to neurological, reproductive, and systemic issues; mainly through inhalation, ingestion.

• Alcohol (Ethanol): Commonly abused substance; metabolized to toxic acetaldehyde; impacts CNS, liver, and cardiovascular health.

Common Injuries and Their Classification

Unintentional and Intentional Injuries

• Statistics: 231,991 injury deaths noted in 2016; major causes include poisoning, vehicle accidents, and firearm-related incidents.

Types of Injuries

• Blunt Force Injuries: Include contusions, lacerations, fractures.

• Sharp Force Injuries: Include incised wounds, stab wounds, puncture wounds.

• Gunshot Injuries: Classified as penetrating (bullet retains) vs. perforating (bullet exits).

• Asphyxiation Types: Includes suffocation, strangulation, drowning.

Somatic Death and Postmortem Changes

• Pallor mortis: Skin becomes pale.

• Algor mortis: Decrease in body temperature.

• Rigor mortis: Muscle stiffening within hours.

• Livor mortis: Blood settles in dependent areas.

• Putrefaction & Decompensation: Breakdown of body tissues.

Aging and Cellular Biology

• Aging is a universal process involving gradual loss of homeostatic mechanisms.

• Changes include cellular atrophy and reduced function; contributes to tissue dysfunction and increased susceptibility to diseases.

Systemic Manifestations of Cellular Injury

• Fever, increased heart rate, leukocytosis, pain due to injury.

• Release of cellular enzymes indicates tissue damage (e.g., LDH, CK, AST, ALT).

Necrosis Types

• Coagulative, liquefactive, caseous, fatty, and gangrenous necrosis indicating varying paths/pathology of cellular injury.

Apoptosis

• Active self-destruction mechanism; occurs in response to various stimuli including severe injury or infections.

Autophagy

• Process initiated during nutrient deprivation or stress; recycles damaged organelles to maintain metabolism.

Conclusion

• Understanding the mechanisms and pathways of cellular adaptations and injuries is crucial for recognizing and treating associated pathophysiological conditions.