INTRODUCTION TO PATHOLOGY

Term Definition Key Aspects/Mnemonic

Study of disease using scientific methods; focuses on cellular

Pathology Pathology = Cellular & Tissue Changes (due to injury)
& tissue changes due to injury.

Abnormality in body structure or function (physiological or

Disease Disease = Abnormality in Structure or Function
psychological).

Parts of Pathology

Aspect of Pathology Description Mnemonic/Memory Aid

Epidemiology Study of disease distribution in populations. Epidemio = Population

Etiology Study of disease causes. Etiology = Cause

Pathogenesis Study of disease development and progression. Pathogenesis = Progress

Morphologic Changes Structural changes in cells and tissues due to disease. Morpho = Structural

Clinical Features Signs and symptoms of disease. Clinical = Signs & Symptoms
 Mnemonic/Memory
Concept Description Examples/Illustrative Points Why We Study It
Aid

Study of disease occurrence &

distribution in populations; uses this Studies patterns, causes, effects of EPI = Population Disease To understand and improve
Epidemiology
knowledge to improve health disease in populations. Study public health.
systems.

Demographics (sex, age, race)

Occupation (asbestos workers, aniline

To identify high-risk groups,
dye workers),
Characteristics influencing disease predict disease trends, and
Factors Studied DOGS
patterns. target interventions
Geography (developed vs.
effectively.
underdeveloped countries),

Socioeconomic strata.

Prevalence (total cases),

Incidence (new cases),

To track disease burden,

Sequelae (complications),
Quantitative measures of disease in assess intervention
Key Metrics PISPMM
a population. effectiveness, and guide
Prognosis (expected outcome),
resource allocation.

Morbidity (illness),

Mortality (death rate).

Disease Classification Type Description Examples Mnemonic/Memory Aid

Idiopathic/Cryptogenic/Ess Many diseases fall into this

Etiology (Cause) Cause is unknown. Idon't Know (IDK)
ential category.

Disease Classification Present at birth or develops within the

Congenital Congenital = Birth
(by Onset) first month of life.

Caused by genetic or chromosomal

Genetic/Chromosomal Hemophilia, Down syndrome Genetic = Chromosomal
abnormalities.

Birth defects not caused by genetic or

Non-Genetic chromosomal abnormalities. (cleft lip, Cleft lip, spina bifida Non-Genetic = Birth defects
spina bifida)

Acquired Develops after birth. Acquired = After birth

Rheumatoid arthritis,
Inflammatory Caused by inflammation. Inflammation
dermatitis

Caused by infectious agents (bacteria, Pneumonia, influenza, fungal

Infective Infection
viruses, fungi). infections

Vascular Caused by blood vessel problems. Atherosclerosis, vasculitis Vascular = Blood vessels

Caused by progressive tissue or organ Alzheimer's disease,

Degenerative Degeneration
deterioration. Parkinson's disease

Neoplastic Involves abnormal cell growth (cancer). Various cancers Neoplastic = Cancer

Caused by therapeutic or recreational Drug-induced liver damage,

Drug-Associated Drug-related
drug use. medication side effects

Metabolic Caused by metabolic dysfunction. Diabetes Metabolic

Caused by nutritional deficiencies or

Nutritional Scurvy, obesity Nutritional
excesses.
 Radiation Caused by radiation exposure. Radiation-induced cancers Radiation

Mechanical Caused by physical trauma or injury. Fractures, lacerations Mechanical

Pathogenetic Mechanism Description Example(s) Morphologic Changes Mnemonic

The body's response to injury or Swelling, redness, heat, pain,

Infection, trauma, autoimmune
Inflammatory Process infection, involving immune cells loss of function, pus Inflammation Fights Injury
diseases
and mediators. formation

Degeneration Destroys Tissue

Gradual deterioration of cells and Aging, wear and tear, genetic Cell death, tissue atrophy,
Degenerative Process
tissues over time. disorders fibrosis, organ dysfunction

Development of cancer, involving Genetic mutations,

Tumor formation, metastasis,
Carcinogenesis uncontrolled cell growth and environmental factors, viral Cancer Grows Uncontrollably
tissue destruction
spread. infections

Dysregulation of the immune Autoimmune diseases, Tissue damage from immune

Immunological Process system, leading to either over- or allergies, immunodeficiency response, organ failure, Immune Reaction Goes Astray
under-reactivity. disorders infections

Aspect of Disease Description Examples Memorization Tip

Structural alterations in cells or tissues due Cell swelling, tissue atrophy, Think "Morphing" – the structure is
Morphologic Changes
to disease. inflammation, tumor formation, fibrosis changing shape.
Aspect of Disease Description Examples Memorization Tip

Manifestations of disease affecting organ Think "Clinically apparent" – observable

Clinical Features These are divided into signs and symptoms.
function. or reported changes.

Subjective experiences reported by the Think "Symptoms are what the

Symptoms Fatigue, headache, abdominal pain, nausea
patient. patient says."

Objective findings detected by the Swelling, enlarged organs (liver, spleen), Think "Signs are what the
Signs
physician during examination. fever, rash, abnormal heart sounds doctor sees or measures."

Incubation period, prodromal phase, acute

Stages of disease progression without Think of a timeline or a graph showing
Course of the Disease phase, convalescence, chronic phase,
intervention. the disease's progression.
remission, exacerbation
THE DIAGNOSTIC PROCESS AND THE ROLE OF PATHOLOGIST

Stage Description Key Players/Tests Mnemonic/Memory Aid

Patient visits clinician, providing history and

Patient Presentation Clinician, patient History & Physical Examination (HPE)
undergoing physical examination.

Clinician orders tests to further investigate Blood, Urine, Stool (BUS) + other
Diagnostic Testing Clinician, lab technicians, pathologist
the patient's condition. specialized tests

Think of routine, readily available

Common Pathology Tests Basic tests often ordered initially. Blood, urine, stool analysis
tests.

More complex tests used for specific Cytopathology (cells), Histopathology

Specialized Pathology Tests Cytology, Histopathology (CH) + others
diagnoses. (tissue), other specialized tests

Analyzes test results to provide crucial

Diagnosis, Management, Treatment
Pathologist's Role information for diagnosis and treatment Pathologist
(DMT)
planning.

Clinical Pathology: Lab tests & cross-

Different areas of pathology focus on sectional analysisExperimental Clinical (lab work) vs. Experimental
Types of Pathology
different aspects of the disease process. Pathology: Animal models & cell (research)
cultures
Procedure Description Methods/Techniques Advantages/Uses Mnemonic/Memory Aid

Biopsies (endoscopic, Gold standard for diagnosis;

Histopathology Microscopic study of tissues. Histo = Tissue (study of tissue)
incisional) detailed tissue analysis

Faster, cheaper, less invasive

Scraping (exfoliative),
Microscopic study of than histopathology; useful Cyto = Cell (study of cells), less
Cytopathology aspiration (fine-needle),
individual cells. for cancer screening and invasive
washing, fluid cytology
diagnosis.

External examination, internal Determines cause of death

Examination of a deceased
organ examination, (homicide, suicide, accident); Autopsy = Death investigation
Autopsy (Forensic Pathology) body to determine cause of
microscopic analysis of tissues identifies diseases; aids (study of death)
death and identify diseases.
and fluids. research and education.
DIAGNOSTIC TOOLS IN PATHOLOGY

Tool Description Key Features/Applications Mnemonic/Memory Aid

Standard microscope using Visualizes basic tissue components

Light Microscope transmitted light; requires thin (nuclei, cytoplasm, collagen); H&E Light = Basic tissue structure
sections and staining. staining is common.

Diagnoses immunological diseases;

Uses fluorescent dyes and antibodies
Immunofluorescent Microscope uses special filters and fluorescent Immuno = Antigen detection
to identify specific antigens in tissue.
dyes.

High-resolution microscope using Visualizes organelles (mitochondria,

Electron Microscope electron beams; allows visualization of ER, viral particles); high magnification Electron = Organelle detail
subcellular structures. and resolution.

Uses antibodies labeled with enzymes Localizes specific proteins within

Immunohistochemistry or dyes to detect specific proteins in tissues; uses a light microscope to Immuno = Protein localization
tissue. visualize the labeled proteins.

Diagnoses and studies blood disorders;

Methods used to study blood cells and
Hematologic Techniques includes various staining and counting Hemato = Blood analysis
components.
techniques.

Used for cytogenetic analysis

Growing cells in a controlled
(chromosome spreads); allows study
Cell Cultures environment; allows manipulation and Culture = Cell manipulation
of cell behavior and responses to
observation of cellular responses.
various treatments.
CHAPTER 2
Cellular Response Description Reversibility Key Features Example Outcome

Reversible functional
Myocardial hypertrophy
and structural response New, altered steady
(increased heart muscle Cell survival and
Adaptation to changes in physiologic Reversible state achieved; cell
size due to high blood continued function
states or some survives and functions.
pressure)
pathologic stimuli.

Increased protein
synthesis and organelle
Increase in cell size and Muscle growth with Increased functional
Hypertrophy Reversible (usually) size.
functional activity. exercise capacity

Increased cell division. Callus formation on skin

Hyperplasia Increase in cell number. Reversible (usually) Increased tissue mass

Decreased protein
Decrease in cell size and Muscle wasting due to Reduced tissue mass and
Atrophy Reversible (usually) synthesis and increased
metabolic activity. disuse function
protein degradation.

Columnar to squamous
Replacement of one Altered tissue function;
Change in cell epithelium in the
Metaplasia Usually reversible differentiated cell type increased risk of cancer
phenotype. respiratory tract due to
with another. (sometimes)
smoking.

Functional alterations;
Cell damage that can be may have subtle Myocardial injury with
Cell recovery and return
Reversible Cell Injury repaired if the injurious Reversible cytoplasmic changes temporary reduced
to normal function
stimulus is removed. (e.g., swelling, fat blood flow
accumulation).

Loss of membrane
integrity; organelle
Irreversible cell damage Myocardial infarction Loss of cell function;
Cell Death Irreversible dysfunction.
leading to cell demise. (heart attack) tissue damage

Cellular swelling,
Unregulated cell death; Inflammation, tissue
membrane rupture, and Tissue damage from
Necrosis often associated with Irreversible damage, and potential
release of cellular infection or trauma
inflammation organ failure
contents.

Cellular shrinkage, DNA

fragmentation, and
 Apoptosis Programmed cell death; Irreversible formation of apoptotic Immune cell elimination Controlled cell removal
usually doesn't cause bodies. of infected cells without inflammation
inflammation.

Cell survival or cell

Cellular self-digestion; Degradation of cellular
Can be adaptive or lead Response to nutrient death, depending on the
Autophagy can be adaptive or lead components through
to irreversible cell death deprivation extent and duration of
to cell death. lysosomes.
stress.

Variable; may be Proteins, lipids,

reversible or irreversible carbohydrates, or
Intracellular Buildup of substances Impaired cell function;
depending on the pigments. Fatty liver disease
Accumulations within cells. potential tissue damage
substance and extent of
accumulation

Deposition of calcium
Calcium deposition in Tissue damage and
Pathologic Calcification salts at sites of cell Irreversible Atherosclerosis
damaged tissues. impaired function
death.

Accumulation of cellular
Gradual deterioration of Gradual decline in
damage; reduced Wrinkles and age-related
Cell Aging cellular structure and Irreversible function and increased
capacity for repair and decline in organ function
function with time. vulnerability to disease
replication.

KEY DIFFERENCES SUMMARIZED:

Adaptation Injury:

Adaptations are reversible responses to stress that allow cells to survive Injury can be reversible or irreversible, leading to cell death.

Necrosis Apoptosis

Necrosis is unregulated and inflammatory apoptosis is programmed and non-inflammatory.

Reversible Irreversible

Reversible changes can be repaired irreversible changes lead to cell death or permanent damage.

CAUSES OF CELL INJURY

 Morphologic Changes
Category of Cause Specific Causes Mechanisms of Injury Reversibility
(Timing)

Reduced blood flow

(ischemia), inadequate Reversible (early stages);
Reduced aerobic Cell swelling (minutes),
Oxygen Deprivation (Hypoxia) oxygenation, decreased irreversible
respiration, ATP depletion necrosis (hours to days)
oxygen-carrying capacity (severe/prolonged)
(anemia, CO poisoning)

Mechanical trauma, Depends on the agent and

Direct cellular damage,
temperature extremes, severity; can range from
Physical Agents disruption of cellular Variable
pressure changes, radiation, immediate damage to delayed
structures
electric shock effects

Simple chemicals (glucose,

Depends on the agent and
salt), poisons (arsenic, Direct toxicity, disruption of
concentration; can range from
Chemical Agents & Drugs cyanide), pollutants, cellular metabolism, Variable
subtle changes to immediate
insecticides, recreational electrolyte imbalance
necrosis
drugs, therapeutic drugs

Depends on the agent and the

Viruses, bacteria, fungi, Infection, inflammation, toxin host's immune response; can
Infectious Agents Variable
parasites production range from subtle changes to
massive necrosis

Autoimmune diseases, allergic Immune system attacks own

Immunologic Reactions Variable Inflammation, tissue damage
reactions cells or foreign substances

Varies greatly depending on

Chromosomal abnormalities, Defective protein function,
the specific defect; can range
Genetic Abnormalities single-gene mutations, DNA accumulation of damaged Usually irreversible
from subtle changes to severe
damage DNA or misfolded proteins
malformations

Depends on the type and

Protein-calorie deficiencies, Metabolic derangements, severity of imbalance; can
Nutritional Imbalances Variable
vitamin deficiencies, obesity nutrient deficiencies range from subtle changes to
severe organ damage

NOTES:

Progression of Cell Injury:

Biochemical Alterations (Early): These are subtle and often detectable only with sensitive techniques (minutes to hours).
Ultrastructural Changes: Changes visible at the electron microscopic level (hours).
Light Microscopic Changes: Changes visible with a light microscope (hours to days).
 Grossly Visible Changes: Changes visible to the naked eye (days)

Key Points:

The time lag between the initial insult and the appearance of morphologic changes is important. Early biochemical changes may be present before any visible
changes are apparent.
Reversible injury can be repaired if the stimulus is removed; irreversible injury leads to cell death (necrosis or apoptosis).
The type of cell death (necrosis or apoptosis) depends on the nature and severity of the injury.

REVERSIBLE CELL INJURY

Feature of Reversible Cell Injury Description Mechanism Reversibility

Failure of ATP-dependent Na+/K+ pump;

Generalized swelling of the cell and its influx of water. Often due to oxygen Reversible if the damaging stimulus is
Cellular Swelling
organelles. deficiency, mitochondrial damage removed.
(radiation, toxins), etc.

Formation of small, balloon-like Disruption of the cell membrane's Reversible if the damaging stimulus is
Plasma Membrane Blebbing
protrusions on the cell surface. cytoskeleton. removed.

Reduced protein synthesis due to ATP

Ribosomes detach from the Reversible if the damaging stimulus is
Ribosomal Detachment depletion or direct damage to
endoplasmic reticulum (ER). removed and ATP levels are restored.
ribosomes.

Condensation of chromatin within the Altered gene expression and DNA Reversible in early stages; irreversible in
Nuclear Chromatin Clumping
nucleus. damage. severe cases.

Accumulation of triglyceride-filled lipid

vacuoles in the cytoplasm. Primarily in Disruption of lipid metabolism due to Reversible in early stages; irreversible in
Fatty Change (Steatosis)
organs involved in lipid metabolism toxic injury. severe cases.
(e.g., liver).

KEY POINTS:

Reversible cell injury represents early stages of cellular damage.

The features listed above are often seen together, but the severity can vary.
The ability to reverse the injury depends on the severity and duration of the damaging stimulus. Removal of the stimulus is crucial for recovery.

CELL DEATH
I. Comparison of Necrosis and Apoptosis:

Feature NECROSIS APOPTOSIS

Mechanism Unregulated, accidental cell death; severe cellular damage Regulated, programmed cell death; specific molecular pathways

Stimulus Ischemia, toxins, infections, trauma Physiologic processes, DNA damage, etc.

Morphology Cellular swelling, membrane rupture, inflammation Cellular shrinkage, apoptotic bodies, no inflammation

Inflammation Present Absent

ATP Depletion Typically present Usually not significantly depleted

DNA Fragmentation Usually late or absent Characteristic feature

Membrane Integrity Lost Maintained initially; then fragmented

Cellular Contents Released into extracellular space Remains contained within apoptotic bodies
 II. Patterns of Tissue Necrosis:

Type of Necrosis Description Appearance Associated Conditions

Architecture preserved; cells are eosinophilic; Firm texture; pale or slightly reddened
Coagulative Ischemia (except in brain), infarcts
protein denaturation. tissue

Creamy yellow pus (if leukocytes Bacterial or fungal infections, brain

Liquefactive Digestion of dead cells; tissue becomes liquid.
present) infarcts

Friable, white, cheese-like appearance; fragmented Granular debris enclosed within

Caseous Tuberculosis
cells. inflammatory border (granuloma)

Fat Focal areas of fat destruction; saponification. Chalky-white areas (calcium soaps) Acute pancreatitis

Bright pink, amorphous appearance Immune reactions involving blood

Fibrinoid Vascular damage; immune complex deposition.
(H&E stain) vessels

KEY POINTS:

Necrosis is generally considered accidental cell death due to overwhelming injury.

Apoptosis is a regulated process of programmed cell death.
Different patterns of necrosis reflect the underlying cause of tissue damage.
The presence of inflammation is a key distinguishing feature between necrosis and apoptosis.
I. Cell Injury and Necrosis:

Concept Description Key Features Reversibility

Functional and structural alterations that Cellular swelling, fatty change, plasma membrane
Cell Injury (Reversible) are correctable if the damaging stimulus is blebbing, mitochondrial swelling, ER dilation, Reversible
removed. decreased cytoplasmic RNA (eosinophilia)

Pathologic cell death; cellular membranes Eosinophilia, nuclear changes (pyknosis,

Necrosis are destroyed, contents leak out, karyorrhexis, karyolysis), membrane breakdown, Irreversible
inflammation ensues. myelin figures, enzymatic digestion of contents

Coagulative (preserved architecture), liquefactive

Different morphologic patterns of necrosis (liquid), gangrenous (limb ischemia), caseous
Patterns of Necrosis Irreversible
in tissues, reflecting the underlying cause. (cheese-like, TB), fat (pancreatitis), fibrinoid
(immune vascular damage)

II. Apoptosis:

Concept Description Key Features Reversibility

Programmed cell death; tightly

Cell shrinkage, chromatin condensation,
regulated suicide program; cells activate
Apoptosis formation of apoptotic bodies, phagocytosis of Irreversible
enzymes that degrade DNA and
apoptotic bodies (no inflammation)
proteins.

Removal of supernumerary cells during

development, involution of hormone-
Normal process; eliminates cells no
Physiologic Apoptosis dependent tissues, cell turnover in Irreversible
longer needed; maintains homeostasis.
proliferating populations, elimination of self-
reactive lymphocytes

DNA damage, accumulation of misfolded

Cell death in response to injury beyond
Pathologic Apoptosis proteins, certain infections, pathologic atrophy Irreversible
repair; prevents collateral damage.
after duct obstruction
 III. Key Differences (Necrosis vs. Apoptosis):

Feature Necrosis Apoptosis

Inflammation Present Absent

Cell Size Swelling Shrinkage

Membrane Integrity Lost Maintained (initially); then fragmented

Cellular Contents Released into extracellular space Remains contained within apoptotic bodies

MECHANISMS OF APOPTOSIS

I. Overview of Apoptosis:

Feature Description

Definition Programmed cell death; eliminates unwanted or damaged cells with minimal host reaction.

Key Enzyme Caspases (cysteine proteases that cleave proteins after aspartic acid residues).

Phases Initiation (caspase activation) and execution (cellular fragmentation).

Regulation Balance between pro-apoptotic and anti-apoptotic proteins.

Initiation Pathways Mitochondrial (intrinsic) and death receptor (extrinsic).

Outcome Enzymatic degradation of proteins and DNA; formation of apoptotic bodies; phagocytosis by macrophages (no inflammation).
II. Mitochondrial (Intrinsic) Pathway:

Step Description Key Players

Outer mitochondrial membrane becomes permeable; pro- BCL2 family proteins (BAX, BAK, BH3-only proteins,
Increased Mitochondrial Permeability
apoptotic proteins leak into the cytoplasm. BCL2, BCL-XL, MCL1)

Cytochrome c (and other proteins) released from the

Cytochrome c Release
intermembrane space into the cytoplasm.

Cytochrome c binds to APAF-1, forming the apoptosome,

Apoptosome Formation APAF-1, caspase-9
which activates caspase-9 (initiator caspase).

Caspase-9 activates executioner caspases (e.g., caspase-

Caspase Cascade Caspase-3, caspase-6
3, caspase-6), leading to cellular fragmentation.

Smac/DIABLO neutralizes inhibitors of apoptosis proteins

IAP Inhibition Smac/DIABLO, IAPs
(IAPs), allowing caspase activation.
III. Death Receptor (Extrinsic) Pathway:

Step Description Key Players

Death Receptor Engagement Death receptors (e.g., Fas) bind to their ligands (e.g., FasL). Fas, FasL

FADD Recruitment Death domains of Fas recruit the adaptor protein FADD. FADD

Caspase-8 Activation FADD binds and activates caspase-8 (initiator caspase). Caspase-8

Caspase-8 activates executioner caspases (e.g., caspase-3,

Caspase Cascade Caspase-3, caspase-6
caspase-6), leading to cellular fragmentation.

FLIP Inhibition FLIP can inhibit caspase-8 activation. FLIP

Caspase-8 can cleave BID (BH3-only protein), activating the

Cross-talk with Intrinsic Pathway BID
mitochondrial pathway.

IV. Execution Phase:

Step Description Key Players

Caspases cleave an inhibitor of DNase, activating it and causing

DNase Activation Caspase-3, caspase-6, DNase
DNA degradation.

Caspases degrade structural components of the nuclear matrix,

Nuclear Matrix Degradation Caspase-3, caspase-6
leading to nuclear fragmentation.

Apoptotic Body Formation Cell fragments into membrane-bound apoptotic bodies.

V. Removal of Dead Cells (Efferocytosis):

Feature Description Key Players

Phosphatidylserine externalization; secretion of soluble factors; coating with Phosphatidylserine, soluble factors, natural
"Eat Me" Signals
natural antibodies and complement proteins (C1q). antibodies, C1q

Phagocytosis Macrophages recognize and engulf apoptotic bodies. Macrophages

I. Other Mechanisms of Cell Death:

Type of Cell Death Description Key Features Caspase Dependence Inflammation Associated Diseases

Loss of ATP, cell swelling,

Hybrid of necrosis and ROS generation,
Steatohepatitis,
apoptosis; lysosomal enzyme
pancreatitis, ischemia-
morphologically release, membrane
Necroptosis No Yes reperfusion injury,
resembles necrosis but is rupture; caspase-
neurodegenerative
triggered by signaling independent;
diseases
pathways. RIPK1/RIPK3/MLKL
pathway involved

Activation of caspase-1
Form of programmed (and related caspases 4
necrosis accompanied by & 5); inflammasome
Pyroptosis Yes (caspase-1) Yes Microbial infections
release of IL-1 (fever- activation; release of
inducing cytokine). inflammatory
mediators.

Iron-dependent cell death Lipid peroxidation;

triggered by excessive iron mitochondrial cristae Cancer,
Ferroptosis or ROS overwhelming loss; membrane No Variable neurodegenerative
antioxidant defenses, rupture; regulated by diseases, stroke
causing lipid peroxidation. specific signals.
 II. Autophagy:

Feature Description Key Players

Cellular self-digestion; cytoplasmic materials delivered to lysosomes for

Definition
degradation.

Survival mechanism (nutrient deprivation); organelle turnover; clearance of

Purpose
intracellular aggregates.

1. Isolation membrane (phagophore) formation;

2. Autophagosome formation (encloses cargo);

ATG proteins; LC3 (microtubule-associated protein
Process
light chain 3); lysosomal enzymes
3. Fusion with lysosomes (autophagolysosome);

4. Degradation.

Initiated by cellular stress (nutrient deprivation, growth factor depletion);

Regulation
regulated by ATG proteins.

Can promote or suppress cancer; implicated in neurodegenerative disorders,

Role in Disease
infectious diseases, and inflammatory bowel diseases.

MECHANISMS OF CELL INJURY

II. Intracellular Targets of Injurious Stimuli:

Target Mechanisms of Damage Consequences

ATP depletion (leading to cell swelling, altered

Increased cytosolic Ca2+, ROS, oxygen deprivation; mutations in metabolism, decreased protein synthesis); ROS
Mitochondria
mitochondrial genes. formation; release of pro-apoptotic proteins
(intrinsic apoptosis pathway).

Loss of osmotic balance; influx of fluids and ions;

ROS (lipid peroxidation); decreased phospholipid synthesis; increased loss of cellular contents; leakage of lysosomal
Cell Membranes
phospholipid breakdown; cytoskeletal abnormalities. enzymes (necrosis); mitochondrial dysfunction;
plasma membrane damage.

Activation of p53; cell cycle arrest; DNA repair;

DNA Radiation, chemotherapeutic drugs, ROS; spontaneous damage (aging).
apoptosis (if repair fails).

Decreased protein synthesis due to ATP depletion, ribosomal detachment, Accumulation of misfolded proteins leading to ER
Protein Synthesis
and protein misfolding. stress and apoptosis.
IV. Key Biochemical Mechanisms:

ATP Depletion: Widespread effects on cellular processes; leads to cell swelling, metabolic dysfunction, and ultimately necrosis.
Membrane Damage: Disrupts cellular function and integrity, leading to necrosis.
DNA Damage: Triggers cell cycle arrest, DNA repair, or apoptosis (if repair fails).
Oxidative Stress: Damage to lipids, proteins, and DNA; contributes to various pathologies.

Disturbance in Calcium homeostasis

Endoplasmic reticulum (ER) stress and the unfolded protein response

CLINICOPATHOLOGIC CORRELATIONS: SELECTED EXAMPLES OF CELL INJURY AND DEATH