Cell Injury and Repair

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Questions and Answers

What is the primary goal of cellular adaptation?

To increase the size of the organelles

To maintain viability and function (correct)

To promote apoptosis

To enhance the synthesis of proteins

Which term describes a decrease in cell size?

Hypertrophy

Metaplasia

Hyperplasia

Atrophy (correct)

What results from hypertrophy and hyperplasia occurring together?

A decrease in organ size

An enlarged organ (correct)

A stable organ size

A complete loss of organ function

Which cellular adaptation involves a change in cell type?

Metaplasia (C) Signup and view all the answers

What typically triggers cellular injury?

Exceeding adaptive capability (D) Signup and view all the answers

Hypertrophy primarily occurs in which type of cells?

Striated muscle cells (D) Signup and view all the answers

What is a characteristic of hyperplasia?

It involves the proliferation of cells (D) Signup and view all the answers

Which factor is NOT associated with homeostasis in cells?

Cellular injury (C) Signup and view all the answers

What is one of the major morphological features of reversible cellular injury?

Cellular swelling (B) Signup and view all the answers

Which process describes the lysosomal digestion of the cell’s own components?

Autophagy (D) Signup and view all the answers

What histological change is associated with necrosis?

Eosinophilia (D) Signup and view all the answers

What feature is associated with fatty change in reversible cellular injury?

Presence of lipid-filled vacuoles (C) Signup and view all the answers

Which condition results from the failure of ATP-dependent ion pumps?

Loss of ionic and fluid homeostasis (C) Signup and view all the answers

Which of the following represents a common effect of smooth endoplasmic reticulum hypertrophy?

Enhanced drug metabolism (D) Signup and view all the answers

What occurs to a cell’s nucleus during karyorrhexis?

Fragmentation of the nucleus (C) Signup and view all the answers

Which of the following is NOT a characteristic of necrosis?

Undamaged cell structure (C) Signup and view all the answers

What happens as a consequence of protracted drug use?

Increase in SER (C) Signup and view all the answers

Which of the following is NOT a type of cytoskeletal element?

Cytoplasmic vesicles (B) Signup and view all the answers

What role do mitochondria play in cellular adaptation following exercise?

Increase in number (A) Signup and view all the answers

What is a major consequence of failure in ATP-dependent calcium transporters?

Increased cytosolic calcium (A) Signup and view all the answers

Which type of drugs target microtubules to inhibit cell proliferation?

Anticancer drugs (C) Signup and view all the answers

Which of the following statements about reactive oxygen species (ROS) is TRUE?

ROS serve as physiological second messengers. (D) Signup and view all the answers

What are the effects of oxidative stress on cells?

Cellular injury (B) Signup and view all the answers

What is the purpose of the sodium-potassium pump in cells?

To maintain osmotic balance (C) Signup and view all the answers

What is compensatory hyperplasia primarily stimulated by?

Growth factors secreted by remnant hepatocytes (C) Signup and view all the answers

What type of hyperplasia is characterized by an overgrowth of endometrial tissue?

Pathologic hyperplasia (A) Signup and view all the answers

Which of the following is a possible physiological cause of atrophy?

Senile atrophy (B) Signup and view all the answers

What does metaplasia involve?

Replacement of one type of adult cell with another (B) Signup and view all the answers

Which term describes the increase in organ size due to increased workload?

Hypertrophy (C) Signup and view all the answers

What is a major characteristic of necrosis compared to apoptosis?

Results in cell lysis and inflammation (A) Signup and view all the answers

Which of the following accurately describes atrophy?

Decrease in cell size linked to loss of cell substance (A) Signup and view all the answers

Which condition results from an imbalance of estrogen and progesterone?

Endometrial hyperplasia (D) Signup and view all the answers

What primarily causes atrophy related to endocrine stimulation?

Hormonal deficiency due to menopause (B) Signup and view all the answers

What can chronic irritation in tissues lead to?

Metaplasia of differentiated cells (B) Signup and view all the answers

Study Notes

Cell Injury, Inflammation, and Repair (3 lecture hours)

Course: PHIDG 1501 - Integrated Sequence 1
Recommended Reading: Robbins Basic Pathology, 10th Edition (2018)
Learning Objectives:
- Describe the general principles of cell injury.
- Detail cell injury concepts: homeostasis, adaptation, hypertrophy, hyperplasia, atrophy, and metaplasia.
- Describe all possible mechanisms of cell injury.
- Detail morphological changes associated with cell injury.

Homeostasis

The intracellular milieu of cells is tightly regulated to remain fairly constant.
This state of cellular stability is called homeostasis.
Intracellular milieu components include anion and cation concentrations, enzyme concentration and activity, protein concentrations, and the pH of the cytosol and organelles.

Cellular Adaptation

Cells adapt to physiological stress (increased workload) or pathological stress (nutrient deprivation, injury).
The goal of cellular adaptation is to preserve cell viability and function.
Cellular injury develops if the adaptive capacity is exceeded.

Cell Injury Progression

Normal cell (homeostasis) → Injurious stimulus → Reversible injury → Severe, progressive injury → Irreversible injury → Cell death (necrosis or apoptosis)

Principal Adaptive Responses

Hypertrophy: Increased cell size (e.g., striated muscle cells). No new cells, only bigger cells enlarged by increased structural proteins and organelles. Could be physiological or pathological (e.g., in the heart due to hypertension).
- Physiological stimuli: chronic exercise, pregnancy
- Pathological stimuli: hypertension, myocardial infarction, endocrine disorders.
Hyperplasia: Increased cell number (e.g., smooth muscle cells). A response to hormones or other growth factors; occurs in tissue capable of cell division.
- Physiological hyperplasia: hormonal hyperplasia (e.g., female breast during puberty and pregnancy) and compensatory hyperplasia (e.g., growth of residual tissue after removal of part of liver).
- Pathological hyperplasia: excess hormones or growth factors (e.g., endometrial hyperplasia, papillomavirus wart).
Atrophy: Decreased cell/organ size due to loss of cell substance. Diminished function, but not dead. Possible causes include loss of innervation, decreased workload, reduced blood supply, inadequate nutrition, or loss of endocrine stimulation (e.g., menopause) and aging.
Metaplasia: Reversible change where one adult cell type is replaced by another. Cells sensitive to a stress are replaced by cells better able to withstand adverse environments. Example: squamous change in respiratory epithelium of smokers.

Overview of Cell Death

Necrosis: "chaotic," death of many cells, inflammation, lysosome breakdown, and cell swelling.
Apoptosis: "programmed," death of single cells, no inflammation, lysosomes intact.

Causes of Cell Injury

Oxygen deprivation: Interferes with oxidative phosphorylation (e.g., ischemia, commonly caused by reduced blood supply).
Chemical agents: Reactive oxygen species (ROS), O2, OH, other free radicals, various toxins.
Infectious agents: Viruses, bacteria, fungi, etc.
Immunologic reactions: Autoimmune and allergic reactions.
Genetic defects: Deficiency of functional proteins.
Physical agents: Trauma, radiation, extreme temperatures.

Morphology of Reversible Injury

Cellular swelling: ATP depletion leads to failure of ion pumps, loss of ionic and fluid homeostasis.
Fatty change (steatosis): Accumulation of lipids in cytoplasm, impairment of lipid metabolism.

Morphology of Necrosis

Increased eosinophilia (pink staining due to less RNA and increased denatured protein).
Myelin figures.
Calcification.
Nuclear changes:
- Karyolysis: DNA degradation
- Pyknosis: Shrinkage of nucleus
- Karyorrhexis: Fragmentation of the nucleus

Subcellular Responses to Injury

Autophagy: Lysosomal digestion of the cell's own components (survival mechanism during nutrient deprivation).
Residual bodies can contain undigested debris (e.g., pigments from tattoos)

Induction of Smooth ER

Drugs metabolized by the P450 enzyme system in the liver.
Protracted drug use leads to adaptive increase of SER (smooth endoplasmic reticulum).
Consequence: Need to increase drug dose.

Mitochondrial Alterations

Changes in size, shape, and number (e.g., exercise increases the number of mitochondria for energy production).

Cytoskeletal Abnormalities

Cytoskeleton: Elaborate array of protein fibers maintaining cell shape, strength, and chromosome separation.
3 types: Microtubules, actin filaments, and intermediate filaments.
- Cells constantly remodel their intracellular scaffolding in response to environmental stress.
- Membrane stability depends on cytoskeleton.
- Drugs binding to microtubules can prevent proliferation (e.g., anticancer drugs).

Mechanism of Cell Injury Overview

Injurious stimulus causes:
- Membrane damage
- Cytoskeletal damage
- DNA damage and accumulation of misfolded proteins.
These events lead to cell death (primarily by apoptosis).

ATP Depletion

Lack of oxygen and nutrients, direct mitochondrial damage, or toxins (e.g., cyanide) are the causes of ATP depletion.
Ichemia is a common cause of ATP depletion (e.g., reduced blood supply to the brain).
Consequences of ATP depletion include sodium pump dysfunction, osmotic gain of water, and subsequent cellular swelling.

Increased Cytosolic Calcium

When ATP-dependent calcium transporters fail in cells, cytosolic calcium increases significantly.
Increased cytosolic calcium leads to activation of enzymes.

Cellular Injury by Oxidative Stress

Oxidative stress occurs through the production of reactive oxygen species (ROS).
ROS damage cellular components, leading to cell injury and death.
ROS damage may include lipid peroxidation of fatty acids in cell membranes, protein oxidation, or DNA damage, producing mutations.
Cells have antioxidant mechanisms (e.g., superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase) for the removal of free radicals. However, prolonged oxidative stress will overwhelm cellular antioxidant mechanisms and result in injury.

Sources of ROS

NO synthase, NADPH oxidases, and xanthine oxidase are sources of ROS (reactive oxygen species).

ROS Paradigm Shift

Hydrogen peroxide and other ROS act as physiological second messengers for many biochemical pathways.
Excessive ROS production can damage cells.
Elevated ROS levels can cause cellular damage or dysregulation of cellular function.

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Description

This quiz covers vital concepts related to cell injury, inflammation, and repair as outlined in the PHIDG 1501 course material. It will test your understanding of homeostasis, cellular adaptation, and the mechanisms involved in cellular injury based on Robbins Basic Pathology. Prepare to explore important morphological changes and adaptive responses that cells undergo under stress.

Cell Injury and Repair - PHIDG 1501

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