01 Introduction

Contents
Table of

02 Special Pathology

03 Hematological tests

Bright medico
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IMPORTANT OF THE STUDY OF PATHOLOGY

INTRODUCTION

Pathology is a branch of medical science that investigates the causes, nature,

and effects of diseases. It plays a crucial role in understanding how and why
diseases develop, progress, and impact the human body. Pathologists, the
medical professionals who specialize in pathology, use their knowledge to
diagnose diseases, guide treatment decisions, and contribute to medical
research. Here's an introduction to the field of pathology:

1. The Study of Disease

● Pathology is the study of diseases, encompassing a wide range of medical

conditions, from infectious diseases like influenza to chronic conditions like
cancer.

2. Understanding Disease Processes:

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 ● Pathologists examine tissues, cells, organs, and bodily fluids to understand
the underlying mechanisms of diseases. They investigate how diseases
develop, spread, and affect the body's normal functions.

3. Diagnostic Role:

● Pathologists play a vital role in disease diagnosis. They examine tissue

samples (biopsies), blood, and other specimens to identify the presence of
diseases and provide information to healthcare providers for treatment
planning.

4. Subspecialties

Pathology has several subspecialties, including:

● Anatomic Pathology: Focuses on the examination of tissues and cells,

including surgical pathology and cytopathology.
● Clinical Pathology: Concentrates on laboratory testing of bodily fluids, such
as blood and urine, to diagnose diseases.
● Molecular Pathology: Involves the study of genes and genetic mutations to
understand and diagnose genetic diseases and cancer.

5. Research and Advancements:

● Pathologists are involved in medical research to advance our

understanding of diseases. Their work contributes to the development of
new treatments, therapies, and diagnostic tools.

6. Role in Healthcare Teams:

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 ● Pathologists collaborate with other healthcare professionals, including
clinicians, radiologists, and surgeons, to provide comprehensive patient
care.

7. Autopsy Examination:

● Forensic pathologists perform autopsies to determine the cause of death in

cases of suspicious or unexplained deaths. This helps in legal
investigations and understanding the epidemiology of diseases.

8. Role in Public Health:

● Pathology is essential in public health efforts to monitor disease trends,

investigate disease outbreaks, and ensure the safety of food and water
supplies.

9. Disease Prevention:

● Pathologists contribute to disease prevention by identifying risk factors and

recommending preventive measures, such as vaccinations and
screenings.

10. Education and Training:

● Pathologists often teach medical students, residents, and laboratory

personnel, sharing their expertise and knowledge with the next generation
of healthcare professionals.

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The study of pathology is of utmost importance in the field of medicine and
healthcare for several significant reasons:

Early Detection

● Pathological examinations can detect diseases at an early stage when

they may be asymptomatic. This early detection can lead to more effective
treatments and better outcomes.

Cancer Diagnosis and Staging

● Pathology is essential in diagnosing cancer and determining its stage. This

information is crucial for treatment planning and prognosis.

Infectious Disease Identification:

● Pathologists identify infectious agents like bacteria, viruses, and parasites,

aiding in the treatment of infectious diseases and the implementation of
infection control measures.

Genetic Disease Diagnosis:

● Molecular pathology investigates genetic mutations and disorders. This

helps diagnose genetic diseases and assess an individual's risk of
developing certain conditions.

DEFINITION OF TERMS IN PATHOLOGY

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Definition of Pathology

The word 'pathology' is derived from two Greek words-pathos meaning suffering
and logos meaning study. It is the study and diagnosis of disease through
examination of organs, tissues, body fluids, and whole bodies (autopsy).

Pathology is a scientific study of the structure and function of the body in disease
from molecular level to the effects on the individual.

Thus, pathology is the branch of medical science that studies the origin, cause,
nature, progression, course, and consequences of diseases. The ultimate goal of
pathology is the identification of the cause and nature of the disease, a
fundamental objective leading to successful therapy and to disease prevention.

Definition of Basic Terms in Pathology

It is essential to introduce the readers to common terminologies used in

pathology, so as to make the subsequent reading easy. Some of the commonly
used terminologies are:

● Patient is the person suffering from the disease.

● Lesions are pathological changes in cells and tissues, produced by the
disease.
● Etiology is the cause/causal factor of disease.
● Pathophysiology is the study of deranged (patho) bodily functions
(physiology), whichoccur as a consequence of the disease.
● Pathogenesis is the mechanism of disease evolution and progression.
● Morphology is the structural changes in cells and organs.

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 ● Gross or macroscopic examination refers to the structural changes in
organ systems or tissues observed by the naked eye.
● Microscopic findings refer to the morphological changes detected by the
use of light or electron microscopy.
● Clinical significance is the term used to explain the relationship of clinical
features tissue/cellular level changes occurring in the disease.
● Diagnosis is the final opinion on what is wrong with the patient.
● Prognosis refers to the fate of the patient suffering from the disease.
● Prevention refers to the steps that can be taken to avoid further
complications of the disease

SUBDIVISION OF PATHOLOGY

1. Pathology:

● Pathology is the medical specialty that focuses on the study of diseases. It

involves the examination of tissues, cells, organs, and bodily fluids to
understand the nature, causes, and effects of diseases.

2. Histopathology:

● Histopathology is the microscopic examination of tissue samples to

diagnose diseases. It involves the study of tissue structures and cellular
changes to identify abnormalities.

3. Cytopathology:

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 ● Cytopathology is the branch of pathology that focuses on the examination
of individual cells, often collected through techniques like fine-needle
aspiration, to diagnose diseases, especially cancer.

4. Clinical Pathology:

● Clinical pathology, also known as laboratory medicine, involves the

analysis of bodily fluids (e.g., blood, urine, cerebrospinal fluid) to diagnose
and monitor diseases.

5. Anatomic Pathology:

● Anatomic pathology involves the examination of tissues and organs

removed during surgery (surgical pathology) or during post-mortem
examinations (autopsy pathology) to diagnose diseases.

6.Molecular Pathology:

● Molecular pathology examines genetic and molecular changes within cells

and tissues to understand the molecular basis of diseases, especially
cancer and genetic disorders.

7. Gross Pathology:

● Gross pathology involves the macroscopic examination of tissues and

organs to identify visible abnormalities or lesions.

8.Necrosis:

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 ● Necrosis is the premature death of cells or tissues due to injury, infection,
or lack of blood supply. It often results in inflammation and tissue damage.

9. Apoptosis:

● Apoptosis is a programmed cell death process that occurs naturally to

remove old or damaged cells from the body without causing inflammation.

10. Metastasis:

● Metastasis refers to the spread of cancer cells from the primary tumor to
other parts of the body, where they can form secondary tumors.

11.Biopsy:

● A biopsy is the removal of a small sample of tissue or cells for examination

to diagnose or rule out diseases, such as cancer.

12.Tumor:

● A tumor is an abnormal growth of cells. Tumors can be benign

(non-cancerous) or malignant (cancerous).

13.Inflammation:

● Inflammation is the body's natural response to injury or infection,

characterized by redness, swelling, heat, pain, and loss of function.

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14.Autoimmunity:

● Autoimmunity occurs when the immune system mistakenly attacks and

damages the body's own tissues, as seen in autoimmune diseases like
rheumatoid arthritis and lupus.

15.Hematology:

● Hematology is the branch of clinical pathology that focuses on the study of

blood and blood-related disorders.

16.Immunohistochemistry (IHC):

● Immunohistochemistry is a technique used in pathology to identify

specific proteins or antigens in tissue sections, helping with diagnosis and
classification of diseases.

CELL INJURY

Cell Injury refers to the damage or abnormal changes that occur in cells when
they are exposed to harmful stimuli or conditions. These harmful factors can be
physical, chemical, biological, or immunological in nature. Cell injury can lead to
various outcomes, depending on the severity and duration of the injury, as well as
the ability of the cell to adapt or repair itself.

Here is a more detailed explanation and definition of cell injury:

Cell Injury

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Definition:

Cell injury is a process in which cells experience harmful changes or damage to

their structure and function due to various stressors or insults. These insults can
include physical trauma, toxic chemicals, infections, lack of oxygen (hypoxia),
immune reactions, and more.

Causes

Cell injury can be caused by a wide range of factors, including:

● Physical Agents: Such as mechanical trauma, radiation, extreme

temperatures, and pressure.
● Chemical Agents: Such as toxins, drugs, and environmental pollutants.
● Biological Agents: Such as bacteria, viruses, and parasites.

Hypoxia

nsufficient oxygen supply to cells, which can result from reduced blood flow or
respiratory problems.

● Immunological Reactions: In which the immune system mistakenly targets

and damages healthy cells.
● Outcomes: The outcome of cell injury can vary, and cells may respond in
different ways:
● Cells may adapt to the injury through mechanisms like hypertrophy
(increased cell size) or hyperplasia (increased cell number) to compensate
for lost function.

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 ● Cells may undergo reversible injury, where damage can be repaired, and
normal function can be restored if the harmful stimulus is removed.
● In cases of severe or prolonged injury, cells may undergo irreversible
injury, leading to cell death. Cell death can occur through different
pathways, such as necrosis or apoptosis.

Consequences:

Depending on the extent and type of cell injury,

● it can have various consequences, including:

● Tissue damage and dysfunction.

Organ failure.

● The initiation of inflammatory responses as the body attempts to repair the

damage.
● Implications for overall health, as cell injury can be a fundamental aspect of
many diseases, including cancer, infections, and degenerative disorders.

Etiological factors of cell injury:

The etiology of cell injury refers to the various causes or factors that can lead to
damage or harm to cells. These factors can be broadly categorized into physical,
chemical, biological, immunological, and genetic causes. Understanding the
etiology of cell injury is essential for diagnosing and treating diseases and
conditions.

1.Physical Agents:

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 ● Trauma: Physical injuries such as cuts, bruises, fractures, and contusions
can directly damage cells and tissues.
● Radiation: Exposure to ionizing radiation (e.g., X-rays) or ultraviolet (UV)
radiation can cause DNA damage and cellular injury.
● Temperature Extremes: Extreme heat (burns) and extreme cold (frostbite)
can lead to cellular damage.

2.Chemical Agents:

● Toxins: Exposure to toxic chemicals, whether environmental pollutants,

industrial chemicals, or drugs, can cause cellular injury. For example,
alcohol can damage liver cells, and some drugs can harm kidney cells.
● Heavy Metals: Heavy metals like lead, mercury, and arsenic can
accumulate in tissues and cause cellular toxicity.
● Chemical Burns: Strong acids or bases can cause chemical burns and
damage to skin and mucous membrane cells.

3. Biological Agents:

● Infections: Pathogenic microorganisms such as bacteria, viruses, fungi,

and parasites can invade and damage host cells. The cellular injury is
often a result of microbial replication and the host's immune response to
infection.
● Biological Toxins: Toxins produced by certain bacteria (e.g., botulinum
toxin) can cause cellular damage.

4.Immunological Factors:

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 ● Autoimmunity: In autoimmune diseases, the immune system mistakenly
targets and damages the body's own cells and tissues.
● Inflammatory Responses: Chronic inflammation, whether due to
autoimmune reactions or chronic infections, can lead to ongoing cellular
injury.

5.Hypoxia and Ischemia:

● Hypoxia: Reduced oxygen supply to cells (hypoxia) or complete lack of

oxygen (anoxia) can result from conditions like inadequate blood flow,
respiratory problems, or high altitudes. Hypoxia can lead to cellular injury.
● Ischemia- Ischemia is a more severe form of hypoxia caused by reduced
blood flow to tissues, often due to blood vessel blockage. Ischemia can
result in cell injury or death in affected areas.

6. Genetic Factors:

● Genetic Mutations: Inherited genetic mutations can lead to cellular

dysfunction and injury, as seen in various genetic disorders.

7.Metabolic Disturbances:

● Nutritional Deficiencies: Inadequate intake of essential nutrients can lead

to metabolic imbalances and cellular injury.
● Electrolyte Imbalances: Abnormal levels of electrolytes like sodium,
potassium, and calcium can disrupt cellular function.

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8. Iatrogenic Factors:

● Medical Procedures: Some medical treatments or interventions, if not

performed correctly, can result in cellular injury. For example, surgical
errors or complications from medical procedures.

PATHOGENESIS OF REVERSIBLE AND IRREVERSIBLE

Cell injury can have different outcomes depending on its severity, duration, and
the ability of the cell to adapt or repair itself. Two main outcomes of cell injury are
reversible injury and irreversible injury.

Reversible Cell Injury:

Reversible cell injury refers to cellular damage that can be repaired if the harmful
stimulus is removed promptly. Here is the pathogenesis of reversible cell injury:

1.Cellular Stress: Reversible injury often begins with exposure to a stressor,

which can be physical (e.g., mild trauma), chemical (e.g., exposure to toxins), or
physiological (e.g., decreased blood flow).

2.Cellular Response: Cells respond to stress by activating protective

mechanisms. These mechanisms include:

● Cellular Swelling: Cells may swell due to an influx of water, a common

response to injury.

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 ● Mitochondrial Dysfunction: Mitochondria may become dysfunctional,
affecting energy production.
● Endoplasmic Reticulum Stress: Stress in the endoplasmic reticulum can
lead to protein misfolding.

3.Cellular Adaptation: Cells attempt to adapt to the stressor by activating various

cellular pathways, such as the unfolded protein response (UPR) and autophagy.

4.Restoration of Homeostasis: If the stressor is removed or the adaptive

mechanisms are successful, the cell can return to its normal state, and injury is
reversible. This involves:

● Repair of damaged organelles and cellular structures.

● Removal of accumulated toxins or waste products.
● Restoration of normal cellular function.

5.Clinical Outcome: In clinical terms, reversible cell injury is often associated with
temporary dysfunction or mild, transient tissue damage. Common examples
include mild infections, short-term exposure to toxins, and ischemic events with
brief periods of reduced blood flow.

Irreversible Cell Injury:

Irreversible cell injury occurs when the cellular damage is severe, prolonged, or
beyond the point of recovery. Here is the pathogenesis of irreversible cell injury:

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1. Severe Stress: Irreversible injury typically results from exposure to severe and
sustained stressors. This may include prolonged ischemia (lack of blood flow),
severe toxins, or extensive trauma.

2.Progressive Damage: The stressor causes progressive and extensive damage

to cellular structures and organelles. Mitochondrial damage and cell membrane
disruption are common.

3.Point of No Return: As cellular damage accumulates, the cell reaches a "point

of no return," where it can no longer recover or repair itself. This is often
characterized by:

● Severe mitochondrial dysfunction and depletion of ATP (cellular energy).

● Irreversible membrane damage, leading to cell lysis (cell rupture).

4.Cell Death: Irreversible injury leads to cell death. There are two main forms of
cell death associated with irreversible injury:

● optosis: The cell undergoes programmed self-destruction without causing

inflammation.

5. Clinical Outcome: Irreversible cell injury often results in significant tissue

damage, organ failure, and clinical symptoms. Common examples include
advanced stages of cancer, extensive heart attacks, and severe brain injuries.

Morphology of Reversible Cell Injury:

1.Cellular Swelling:

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 ● Cellular swelling is a hallmark of reversible cell injury. It occurs due to the
influx of water into the cell, leading to an increase in cell volume.
● Microscopically, the cell appears larger than usual, and the cytoplasm
becomes more translucent.
● Organelles within the cell, such as the endoplasmic reticulum and
mitochondria, may also appear swollen and altered.

2.Glycogen Accumulation:

● In some cases, reversible injury may lead to the accumulation of glycogen

granules within the cell. This can be observed microscopically as increased
cytoplasmic granularity.

3.Fatty Change (Steatosis):

● In specific types of reversible injury, such as in the liver, there can be an

accumulation of fat droplets (steatosis) within hepatocytes. This is
commonly seen in conditions like fatty liver disease.

4.Membrane Integrity:

● The cell membrane remains intact during reversible injury, preventing the
leakage of cellular contents into the surrounding tissue.

5.Nuclear Changes:

● The nucleus typically remains structurally intact during reversible injury,

and chromatin (genetic material) retains its normal pattern.

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Morphology of Irreversible Cell Injury:

1.Cellular Lysis:

● Irreversible cell injury may progress to the point where the cell membrane
ruptures, leading to cellular lysis.
● This results in the release of cellular contents, including enzymes and
other intracellular components, into the surrounding tissue.

2.Nuclear Changes:

● In cases of irreversible injury, nuclear changes become prominent. The

chromatin may undergo condensation and fragmentation.
● The nucleus may become pyknotic (shrunken and dense) or karyorrhectic
(fragmented).

3. Membrane Damage:

● Irreversible injury often leads to damage to the cell membrane, causing

disruption and loss of membrane integrity.
● This allows the release of cellular contents into the extracellular space and
can trigger inflammatory responses.

4.Loss of Organelle Integrity:

● Mitochondrial damage becomes extensive, leading to a loss of

mitochondrial integrity. Mitochondria may swell and rupture.
● Endoplasmic reticulum and other organelles may also become damaged
beyond repair.

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5.Inflammatory Response:

● Irreversible cell injury results in the release of cellular debris and

pro-inflammatory molecules, leading to an inflammatory response in the
surrounding tissue.

Necrosis

It is a type of cell death that occurs as a result of pathological processes and is

typically associated with tissue damage and inflammation. Unlike apoptosis,
which is a programmed and controlled form of cell death, necrosis is uncontrolled
and often occurs in response to external factors or severe injury. Necrosis can
manifest in various forms, each with distinct morphological characteristics. Here
are the five main types of necrosis:

1.Coagulative Necrosis:

● Coagulative necrosis is the most common type of necrosis. It typically

occurs in response to ischemia (reduced blood flow) and is characterized
by the preservation of the tissue architecture for a short period.
● Morphology: Under the microscope, coagulative necrosis appears as pale
and homogenous tissue with a preserved outline of cell structures. Cell
nuclei may disappear, and the tissue takes on a firm, coagulated
appearance. This type of necrosis is commonly seen in infarctions (tissue
death due to lack of blood supply), such as myocardial infarction (heart
attack).

2.Liquefactive Necrosis:

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 ● Liquefactive necrosis is characterized by the rapid dissolution of dead
cells and the transformation of tissue into a liquid, often due to enzymatic
digestion. It is commonly associated with bacterial infections and the brain.
● Morphology: Under the microscope, liquefactive necrosis appears as a
viscous, liquid-filled space surrounded by a "liquefied" border. Cellular
debris and inflammatory cells are often visible within the liquid area. This
type of necrosis is typical in abscess formation, where immune cells
attempt to contain and eliminate infections.

3. Caseous Necrosis:

● Caseous necrosis is a specific form of coagulative necrosis often seen in

granulomatous infections, such as tuberculosis. It is characterized by the
formation of a cheese-like, friable (crumbly) material.
● Morphology: Under the microscope, caseous necrosis appears as an
amorphous, eosinophilic (pink) and granular material. It lacks the cellular
and tissue architecture seen in coagulative necrosis.

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4.Fat Necrosis:

● Fat necrosis typically occurs in adipose (fat) tissue and is often associated
with trauma or inflammation. It results from the release of lipases, which
break down triglycerides in fat cells.
● Morphology: Microscopically, fat necrosis appears as chalky-white areas
surrounded by inflammatory cells. The released fatty acids can bind with
calcium ions, forming calcium soaps. This type of necrosis is often seen in
breast tissue after trauma.

5.Gangrenous Necrosis:

● Gangrenous necrosis is a term used to describe necrosis that occurs in a

body part that has lost its blood supply and becomes infected. It can be dry
or wet.

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 ● Morphology: Dry gangrene appears as coagulative necrosis with a dry,
shrunken, and darkened appearance. Wet gangrene, on the other hand, is
associated with liquefactive necrosis due to bacterial infection and appears
as a moist, foul-smelling tissue.

Gangreneis

Is term used to describe the death and decay of body tissues, often caused by a
lack of blood supply (ischemia) or severe infection. It is a serious medical
condition that requires prompt attention and treatment. There are three major
forms of gangrene, each with distinct characteristics:

1.Dry Gangrene:

Dry gangrene is typically a result of reduced blood flow (ischemia) without

infection. It commonly occurs in extremities like fingers, toes, and limbs.

Characteristics:

● Affected tissue becomes dry, shriveled, and discolored (dark brown or

black).

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 ● There is little to no bacterial growth, and the tissue remains relatively
intact.
● Dry gangrene often progresses slowly.
● Causes: Dry gangrene can be caused by conditions like atherosclerosis
(narrowing of blood vessels), diabetes, or frostbite.

2. Wet Gangrene:

Wet gangrene is characterized by tissue decay resulting from both ischemia and
bacterial infection. It is a medical emergency.

Characteristics

● The affected tissue is moist, swollen, and often emits a foul odor due to
bacterial growth.
● Tissue appears black or greenish.
● Wet gangrene spreads rapidly and can be life-threatening.
● Causes- Wet gangrene can develop when an infection enters an area with
poor blood circulation. This can occur as a complication of injuries, diabetic
foot ulcers, or certain infections.

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3. Gas Gangrene (Clostridial Myonecrosis):

Gas gangrene is a severe form of wet gangrene caused by bacterial infection

with gas-producing bacteria, such as Clostridium perfringens. It is a medical
emergency and progresses rapidly.

Characteristics:

● The tissue is swollen and emits gas bubbles, which can be felt under the
skin (crepitus).
● The affected area has a foul odor and appears discolored, often with a
greenish tint.
● Gas gangrene can lead to systemic toxicity and septic shock.
● Causes: Gas gangrene usually results from contamination of wounds,
especially puncture wounds or injuries that introduce bacteria deep into the
body, away from oxygen-rich environments.

These three major forms of gangrene represent different stages and

manifestations of tissue death, with distinct clinical and pathological features.
Immediate medical attention is crucial in cases of gangrene, as it can lead to
severe complications if left untreated. Treatment often involves surgical removal

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of the dead tissue (debridement) and appropriate antibiotics to manage
infections.

Cellular adaptation

● It is a fundamental biological process that allows cells to adjust and

respond to changes in their environment or physiological demands.
● Cells are constantly exposed to various internal and external factors that
can challenge their normal functioning.
● In order to survive and maintain homeostasis, cells can undergo adaptive
changes that alter their structure, function, or behavior. These adaptations
help cells cope with stress, injury, or changing requirements without
necessarily resorting to cell death.

There are several types of cellular adaptation, including:

1.Hypertrophy:

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Hypertrophy is the increase in the size of individual cells. It typically occurs in
response to increased workload or functional demands. For example, when
someone engages in regular strength training, the muscle cells undergo
hypertrophy to generate more force. This adaptation allows cells to perform their
functions more efficiently.

2. Hyperplasia:

Hyperplasia involves an increase in the number of cells within a tissue or organ.

It is often seen in tissues with the capacity for cell division. An example is the
thickening of the uterine lining during the menstrual cycle in response to
hormonal changes.

3. Atrophy:

Atrophy is the opposite of hypertrophy and refers to a decrease in cell size or the
number of cells. This can result from disuse, aging, decreased blood supply, or
other factors. Muscle wasting due to immobility is a common example of atrophy.

4. Metaplasia:

Metaplasia is a reversible change in which one type of mature cell is replaced by

another type of mature cell. This often occurs in response to chronic irritation or
inflammation and is a protective mechanism. For example, in response to
cigarette smoke, the normal ciliated columnar epithelial cells in the bronchial
lining can change into squamous epithelial cells, which are better equipped to
handle the stress.

5.Dysplasia:

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Dysplasia refers to the abnormal development or growth of cells. It is often
considered a pre-cancerous change and can involve changes in cell size, shape,
and organization. Cervical dysplasia, for instance, is a precursor to cervical
cancer.

6.Autophagy:

Autophagy is a cellular process in which cells break down and remove damaged
or dysfunctional components, such as organelles or proteins. It is a vital adaptive
response to maintain cellular health and prevent the accumulation of harmful
substances.

Cellular adaptation is a dynamic and essential aspect of cell biology. These

adaptive changes allow cells to maintain their functionality and integrity when
faced with various challenges, ensuring the overall health and survival of the
organism. It's important to note that while these adaptations can be protective,
they can also have pathological consequences if they occur excessively or
persistently, leading to diseases or abnormal tissue changes.

Cellular atrophy

● It is a process in which cells shrink in size and decrease in functional

capacity due to a reduction in their workload or the demand placed on
them.
● It is one of the types of cellular adaptation and is typically associated with
a decrease in cell size rather than cell number.
● Atrophy can occur in various tissues and organs of the body in response to
a variety of physiological or pathological conditions.

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Definition of Cellular Atrophy:

Cellular atrophy is a morphological and functional response of cells to a decrease

in the demand for their specific functions or a reduction in the available resources
necessary for their maintenance. This adaptive process results in a reduction in
cell size, which helps conserve energy and resources in situations where the
cell's function is no longer required or sustainable.

Causes of Cellular Atrophy:

1. Disuse Atrophy: This is a common cause of cellular atrophy and occurs when
cells are not subjected to their usual workload or activity. For example, when
muscles are not regularly used due to immobilization, the muscle cells undergo
atrophy.

2.Nutrient Deprivation: When cells are deprived of essential nutrients, such as in

cases of malnutrition or reduced blood supply (ischemia), they can undergo
atrophy because they lack the necessary resources to maintain their normal size
and function.

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3. Aging: Cellular atrophy is a natural part of the aging process, particularly in
tissues and organs that are less active with age. For instance, brain cells may
undergo atrophy as a person ages.

4. Hormonal Changes: Changes in hormone levels can influence cellular atrophy.

For example, the decline in estrogen levels during menopause can lead to
atrophy in the vaginal and breast tissues.

Consequences of Cellular Atrophy:

The consequences of cellular atrophy can vary depending on the tissue or organ
affected and the underlying cause. However, in general, cellular atrophy can lead
to a decrease in tissue mass, functional impairment, and decreased metabolic
activity. For example, muscle atrophy can result in weakness and reduced
muscle strength, while brain atrophy can contribute to cognitive decline.

Reversibility:

● Cellular atrophy is often reversible if the underlying cause is addressed.

For example, if muscle atrophy is due to disuse, regular exercise and
physical therapy can help restore muscle size and function. However, if
atrophy is a result of irreversible damage or a chronic disease, the degree
of recovery may be limited.
● cellular atrophy is a process in which cells reduce in size and function due
to decreased demand or available resources. It is an adaptive response
that allows cells to conserve energy and adapt to changing conditions, but
it can also have adverse effects on tissue and organ function if it becomes
excessive or chronic.

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Morphological features of atrophy

It refer to the observable structural changes that occur in cells, tissues, or

organs when they undergo atrophy. These changes can be identified through
microscopic examination. The specific morphological features of atrophy include:

1. Decreased Cell Size: The most prominent morphological feature of atrophy is

a reduction in the size of individual cells. Cells that were once normal or
hypertrophic (enlarged) may become smaller.

2.Decreased Cytoplasmic Volume: Atrophic cells often have reduced cytoplasm,

which is the gel-like substance that fills the cell between the nucleus and the cell
membrane. This reduction in cytoplasm contributes to the overall shrinkage of
the cell.

3. Increased Nuclear-Cytoplasmic Ratio: As the cytoplasm decreases in volume,

the nuclear-cytoplasmic ratio increases. This means that the nucleus, which
contains genetic material and controls cell activities, becomes relatively larger in
relation to the shrinking cytoplasm.

4.Increased Chromatin Condensation: The chromatin within the nucleus may

become more condensed and darker under microscopic examination. This
indicates increased genetic material compaction.

5.Loss of Organelles: Atrophic cells may lose some of their organelles, such as
mitochondria and endoplasmic reticulum, which are responsible for energy
production and protein synthesis. The reduction in organelles reflects the cell's
decreased metabolic activity.

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6.Loss of Myofibrils (in Muscle Atrophy): In the case of muscle atrophy, there is a
reduction in myofibrils, which are the contractile fibers responsible for muscle
contraction. This leads to a loss of muscle mass and strength.

7.Thinning of Tissues: In organs or tissues undergoing atrophy, there can be a

noticeable thinning of the tissue layers. For example, the lining of the digestive
tract may become thinner when atrophy occurs.

8.Loss of Functional Structures: In addition to structural changes, atrophy can

also lead to the loss of functional structures. For example, in the brain, atrophy
can result in a decrease in the number of neurons and synapses, which can
impact cognitive function.

9.Fatty Infiltration (Fatty Atrophy): In some cases, especially in long-term or

severe atrophy, there may be a replacement of normal tissue with fat. This is
referred to as fatty infiltration and is commonly seen in conditions like fatty liver
disease.

10.Degeneration of Tissues: Atrophy can be accompanied by cellular

degeneration, where cells may appear abnormal and undergo degenerative
changes that reflect their reduced function.

It's important to note that the specific morphological features of atrophy can vary
depending on the tissue or organ affected and the underlying cause of atrophy.
Additionally, these changes can be reversible to some extent if the cause of
atrophy is addressed and the tissue is allowed to recover.

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Hyperplasia

It is a cellular adaptation characterized by an increase in the number of cells

within a tissue or organ. This response occurs in response to various stimuli,
such as increased demand for a particular function or as a compensatory
mechanism for tissue damage or loss. Hyperplasia is a controlled and regulated
process that allows an organ or tissue to adapt to changing conditions while
maintaining its structural and functional integrity.

Definition of Hyperplasia:

Hyperplasia is a physiological process characterized by an increase in the

number of cells in a specific tissue or organ, resulting in an enlargement of that
tissue or organ. This increase in cell number is typically controlled by tightly
regulated mechanisms, including cell signaling pathways and growth factors, to
maintain tissue homeostasis.

Causes of Hyperplasia:

Hyperplasia can be triggered by a variety of factors, including:

1.Hormonal Stimulation: Hormones play a crucial role in regulating cell growth

and division. For example, during puberty, the breast tissue undergoes
hyperplasia under the influence of estrogen.

2.Compensatory Hyperplasia: When a portion of an organ is removed or

damaged, the remaining cells can undergo hyperplasia to compensate for the
loss. For instance, the liver can regenerate and undergo hyperplasia after
surgical resection.

32
3. Chronic Irritation or Injury: Tissues subjected to chronic irritation or injury may
experience hyperplasia as a protective response. For example, the formation of
calluses on the skin is a result of hyperplasia in response to friction.

4.Infection or Inflammation: Inflammatory responses to infections or injuries can

stimulate hyperplasia in various tissues, such as the enlargement of lymph nodes
during an infection.

Types of Hyperplasia:

Hyperplasia can be classified into two main types:

1.Physiological Hyperplasia: This is a normal, controlled process that occurs in

response to a physiological need. Examples include the growth of breast tissue
during pregnancy and the expansion of the uterine lining during the menstrual
cycle.

2.Pathological Hyperplasia: This type of hyperplasia occurs as a response to

abnormal stimuli, such as hormonal imbalances or chronic irritation. Pathological
hyperplasia may be associated with an increased risk of developing diseases,
including cancer.

Consequences of Hyperplasia:

● Hyperplasia results in an enlargement of the affected tissue or organ.

While it can be a beneficial adaptation in some cases, such as tissue repair
or compensation for loss, it may also have clinical implications.

33
 ● For example, if hormonal hyperplasia is uncontrolled, it can lead to benign
tumor formation (e.g., benign prostatic hyperplasia) or increase the risk of
cancer if genetic mutations occur during the hyperplastic process.
● hyperplasia is a regulated cellular response characterized by an increase
in the number of cells within a tissue or organ.
● It serves as an adaptive mechanism in various physiological and
pathological situations to meet the body's demands, but it must be carefully
regulated to prevent uncontrolled cell growth and potential health issues.

Metaplasia

● It is a type of cellular adaptation in which one mature type of cell is

replaced by another mature type of cell in response to chronic irritation,
inflammation, or changes in the cellular environment.
● It represents a reversible change in cell differentiation and is often
considered a protective mechanism, as the new cell type may be better
suited to withstand the altered conditions.
● Metaplasia is typically seen in epithelial tissues and can occur in various
organs and systems of the body.

Definition of Metaplasia:

● Metaplasia is a cellular adaptation characterized by the transformation of

one type of fully differentiated cell into another type of mature cell.
● This change involves a shift in the cellular phenotype, where one cell type
is replaced by another that is better adapted to withstand the local
microenvironmental changes or chronic stressors.

Causes of Metaplasia

34
Metaplasia usually occurs in response to chronic irritation, inflammation, or other
persistent changes in the cellular environment.

Common causes of metaplasia include:

1. Irritation or Injury: Repeated exposure to irritants or injury can trigger

metaplasia as a protective response. For example, cigarette smoke can lead to
metaplasia in the bronchial lining, where ciliated columnar epithelial cells are
replaced by squamous epithelial cells, which are better able to withstand the
stress.

2. Chronic Inflammation: Prolonged inflammation can stimulate metaplastic

changes in affected tissues. In the gastrointestinal tract, for instance, chronic acid
reflux can lead to metaplasia in the esophageal lining, known as Barrett's
esophagus.

3. Hormonal Changes: Hormonal imbalances can also contribute to metaplastic

changes. For example, during pregnancy, the cervical epithelium may undergo
metaplasia to form a mucus-secreting epithelium in response to hormonal
fluctuations.

Types of Metaplasia

There are different types of metaplasia depending on the specific cell

transformations that occur.

Some common types include:

35
1. Squamous Metaplasia: This is one of the most frequently observed types of
metaplasia. It involves the replacement of one cell type with squamous epithelial
cells, which are flat and protective in nature. Squamous metaplasia is often seen
in the respiratory and reproductive tracts.

2. Columnar Metaplasia: In this type, one cell type is replaced by columnar

epithelial cells. This can occur in various organs, including the stomach and the
esophagus.

3. Glandular Metaplasia: Glandular metaplasia involves the transformation of one

cell type into a glandular epithelial cell. It is commonly observed in the respiratory
and gastrointestinal tracts.

Consequences of Metaplasia:

● Metaplasia can be a protective adaptation that allows tissues to better

withstand chronic stressors. However, it can also have clinical implications.
● In some cases, metaplastic changes may increase the risk of developing
diseases, such as cancer, especially if the metaplastic tissue continues to
be exposed to harmful stimuli.
● metaplasia is a reversible cellular adaptation characterized by the
replacement of one mature cell type with another in response to chronic
irritation or environmental changes.
● It represents a protective response but should be monitored, as persistent
metaplasia may be associated with increased disease risk.

Dysplasia

36
 ● It is a term used in pathology to describe an abnormality or disordered
growth of cells within a tissue or organ. It is considered a pre-cancerous
condition because it represents a change in cell appearance, organization,
or function that can potentially progress to cancer if left untreated.
● Dysplasia is typically characterized by an irregular and abnormal
arrangement of cells, loss of uniformity, and changes in cell size and
shape.

Definition of Dysplasia

Dysplasia is an abnormal cellular development or growth pattern within a tissue

or organ. It involves a loss of the normal structural and functional organization of
cells. Dysplastic cells often appear different from their normal counterparts in
terms of size, shape, and organization, and they may exhibit an increased rate of
mitosis (cell division).

Causes of Dysplasia:

Dysplasia usually arises in response to chronic irritation, inflammation, or other

long-term cellular stressors.

Some common causes and risk factors for dysplasia include:

1. Chronic Inflammation: Prolonged inflammation in a tissue can lead to

dysplastic changes. Chronic inflammatory conditions, such as ulcerative colitis,
can increase the risk of dysplasia in the colon.

37
2. Viral Infection: Certain viruses, such as human papillomavirus (HPV) and
hepatitis B and C viruses, are associated with dysplastic changes in tissues they
infect.

3. Environmental Factors: Exposure to environmental carcinogens, such as

tobacco smoke and asbestos, can lead to dysplasia in the affected tissues.

Grades of Dysplasia:

Dysplasia is often graded to assess its severity and potential for progression to
cancer. The grades of dysplasia are typically categorized as follows:

1.Low-Grade Dysplasia -Cells exhibit mild to moderate abnormalities in size,

shape, and organization. The risk of progression to cancer is relatively lower
compared to high-grade dysplasia.

2. High-Grade Dysplasia: Cells show marked and severe abnormalities, and

there is a higher risk of progression to cancer. High-grade dysplasia is
considered a more advanced pre-cancerous stage.

Consequences of Dysplasia:

● The main concern with dysplasia is its potential to progress to cancer over
time if not treated.
● Therefore, it is considered a pre-cancerous condition. The likelihood of
progression depends on factors such as the tissue involved, the extent of
dysplasia, and the underlying causes.

38
 ● Dysplasia can be detected through medical screenings, such as Pap
smears for cervical dysplasia or endoscopic procedures for gastrointestinal
dysplasia.
● If detected, dysplasia is often closely monitored, and interventions may be
recommended to prevent its progression.
● dysplasia is an abnormal cellular growth pattern characterized by changes
in cell size, shape, and organization within a tissue or organ.
● It is considered a pre-cancerous condition because it has the potential to
develop into cancer if not treated or managed appropriately.
● Regular medical screenings and interventions are essential for detecting
and addressing dysplasia early to reduce the risk of cancer development.

Apoptosis,

● It Is referred to as programmed cell death or cell suicide, is a highly

regulated and controlled process by which cells in multicellular organisms
self-destruct in a planned and orderly manner.
● Apoptosis plays a crucial role in various physiological processes, including
tissue development, maintenance of tissue homeostasis, and the removal
of damaged or unnecessary cells.
● It is a fundamental aspect of biology that helps maintain the overall health
and functionality of an organism.

Definition of Apoptosis:

Apoptosis is a genetically programmed and highly orchestrated process of cell

death that occurs in multicellular organisms. It is characterized by a series of
biochemical and morphological changes within the cell, ultimately leading to its
controlled self-destruction. Apoptosis is a fundamental mechanism for removing
unwanted, damaged, or infected cells while minimizing harm to neighboring cells
and maintaining tissue integrity.

39
Key Features of Apoptosis

Apoptosis involves several distinctive features:

1. Cell Shrinkage: Apoptotic cells undergo a reduction in size, causing them to

become smaller and denser.

2. Chromatin Condensation: The cell's chromatin (DNA and associated proteins)

undergoes condensation, leading to the formation of dense, compact structures.

3.Blebbing- The cell's membrane begins to form irregular, bubble-like protrusions

called blebs.

4. Fragmentation: The cell's nucleus fragments into smaller, discrete bodies

known as apoptotic bodies, each containing a portion of the cell's DNA.

5. Phagocytosis-: Apoptotic bodies are recognized and engulfed by neighboring

cells or specialized immune cells, such as macrophages, preventing the release
of potentially harmful cellular contents into the surrounding tissue.

6. Lack of Inflammatory Response: Apoptosis typically occurs without causing

inflammation, in contrast to necrosis, another form of cell death that is often
associated with inflammation.

Functions of Apoptosis-

Apoptosis serves several critical functions in the body:

40
1. Tissue Development-: During embryonic development, apoptosis helps shape
and sculpt tissues and organs by eliminating unwanted or excessive cells. For
example, apoptosis in the formation of fingers and toes separates initially
webbed digits.

2. Tissue Homeostasis-: Throughout an organism's life, apoptosis helps maintain

tissue balance by eliminating aged or damaged cells and replacing them with
healthy ones. This process is essential for the maintenance of overall tissue
health and function.

3. immune System Regulation-: Apoptosis helps regulate the immune system by

removing immune cells that are no longer needed or that may have become
harmful, preventing autoimmune responses.

4. Defense Against Infections-: Apoptosis can be induced in infected cells as a

defense mechanism against viruses or intracellular pathogens, limiting the
spread of infection.

5. Tumor Suppression-: Apoptosis can prevent the formation and growth of

tumors by eliminating cells with DNA damage or genetic mutations.

apoptosis is a programmed and controlled form of cell death that plays a

fundamental role in various biological processes, including development, tissue
maintenance, immune regulation, and defense against infections. It is a critical
mechanism for preserving the overall health and integrity of multicellular
organisms.

INFLAMMATION

41
Inflammation is a complex biological response that occurs in the body's tissues
as a reaction to injury, infection, or other harmful stimuli. It is a fundamental part
of the body's immune system and is designed to protect and repair tissues.
Inflammation is characterized by a combination of physiological responses,
including increased blood flow, immune cell activation, and the release of
chemical mediators. These responses help to isolate and remove the injurious
agents and promote tissue healing.

Definition of Inflammation:

● Inflammation is a localized, protective response of the body's tissues to

injury, infection, or irritants, characterized by increased blood flow, immune
cell recruitment, and the release of chemical signals. It aims to eliminate
harmful agents and promote tissue repair and healing.
● Inflammation can manifest as redness, heat, swelling, pain, and loss of
function in the affected area. It is a crucial defense mechanism that allows
the body to combat infections and repair damaged tissues. However, when
inflammation becomes chronic or excessive, it can contribute to various
diseases and health conditions.

42
Acute Inflammation

Acute inflammation is the initial reaction of tissue to injury. The process begins
rapidly, gets severe in a short period, and lasts for a few days, e.g., cellulitis or
acute pneumonia.

● Changes in the caliber of blood vessels, vasodilation resulting in an

increase in the blood flow.
● Structural changes in microvasculature that allow leakage of plasma
proteins and leukocytes.
● Emigration and accumulation of neutrophils and macrophages at the site
of injury.

Etiology

● Bacterial, viral, parasites, and other infections.

● Physical injuries due to trauma, and exposure to ionizing radiation, heat,
and cold. Due to tissue necrosis caused due to ischemia or infarction.

Cardinal Signs of Acute Inflammation

● Swelling (tumor) due to increased vascular permeability.

● Redness (rubor) due to vascular congestion/ arteriolar dilatation.
● Pain (dolor) due to release of a mediator.

Pathological Changes in Acute Inflammation

● The components of acute inflammation, are described under two broad

headings-vascular events and cellular events.

43
Vascular Events

The sequence of the hemodynamic changes in acute inflammation is as follows:

● Vasoconstriction: This is the earliest change seen in acute inflammation.

● Vasodilation: There is a dilation of the blood vessels, which begins with the
arteriole followed by the capillaries and venules. This leads to a local
increase in vascular flow, which manifests as redness and warmth. The
primary mediator for vasodilation is histamine Increased permeability of the
microvasculature elevates the local hydrostatic pressure Leads to escape
of protein-rich fluid (exudate) into the interstitium.

Cellular Events

The main function of inflammation is the delivery of leukocytes to the site of

injury. Leukocytes ingest the offending agent, kill microbes and degrade foreign
antigens and necrotic tiss The most important leukocytes involved are
neutrophils and macrophages. Cellular events of acute inflammation can be
divided into two phases-extravasation and phagocytosis.

Extravasation of Neutrophils

● The migration of neutrophils from the vascular lumen to the interstitial

tissue is called extravasation and involves the following sequence of
events:
● Margination: Vascular stasis leads to a peripheral orientation of the
leukocytes, i leukocytes, which normally flow in the central column of the
bloodstream, accum towards the endothelial surface of the vascular lumen.
This, process is called margination

44
 ● Rolling and adhesion: The accumulated leukocytes (mainly neutrophils) roll
over endothelial cells lining the vessel wall, and adhere transiently to the
endothelial cells (adhesion).
● Diapedesis: Transmigration of leukocytes from the vascular lumen to the
interstitial tissot in the venules.

Phagocytosis

Phagocytosis is a process of engulfment of solid particulate material by the cells.

There are No types of phagocytic cells-polymorphonuclear neutrophils, also
known as macrophages, and monocytes, also known as macrophages,
Phagocytosis involves three distinct steps which re-recognition and attachment,
engulfment, and killing.

1. Recognition and attachment: There is recognition and attachment of the

particle/microbe be ingested by the leukocyte. Many microbes are coated
with a naturally occurring factor the serum called opsonins,. The two
important opsonins are-Fc fragment of immunoglobulin G and complement
component C3b.
2. Engulfment: The leukocytes/phagocytic cells extend pseudopods around
the particle to be engulfed, and subsequently form a phagocytic vacuole or
phagosome.
3. Killing or degradation: This stage involves the killing of bacteria by a
number of bactericidal mechanisms, such as oxygen-dependent
bactericidal mechanism, oxygen-independent bactericidal mechanism, and
nitric oxide mechanism.

Effects of Acute Inflammation

Acute inflammation has local and systemic effects, which may be both beneficial
and harm

45
Beneficial Effects of Inflammation to be carried a

● Dilution of toxins, such as those produced by bacteria and allows them by

lymphatics thereby stimulating an immune response.
● Entry of antibodies, due to increased vascular permeability.
● Transport of drugs, such as antibiotics to the site where bacteria are
multiplying
● Fibrin formation from exuded fibrinogen, which serves formation. as a
matrix for granulation t
● Delivery of nutrients and oxygen, which are essential for repair and
healing, by incre
● blood flow through the area.

Harmful Effects of Inflammation

● Digestion of normal tissues: Enzymes, such as collagenases and

proteases may digesnormal tissues, resulting in their destruction; for
example, in type III hypersensiti reactions, in some types of
glomerulonephritis, and in abscess cavities.
● Swelling. The swelling of acutely inflamed tissues may be harmful; for
example, the swelling of epiglottis due to Haemophilus influenzae in
children may obstruct the airway resulting in death.
● Inappropriate inflammatory response: Such as those which occur in type I
hypersensitivi

Morphological Forms of Acute Inflammation

Acute inflammation may manifest in varied morphological forms. An inflamed

organ is referrel to by adding the suffix 'itis' to its name; for example, acute

46
appendicitis, acute salpingitis and acute pancreatitis. Few morphological varieties
of acute inflammation are as listed below

● Ulcer: It is a localized breach in the surface epithelium of an organ due to

inflammation Common sites of ulceration are the skin and mucosa of the
gastrointestinal tract.
● Abscess formation-An abscess is formed when there is tissue necrosis due
to inte neutrophilic infiltration in the inflamed tissue. A cavity is formed,
which is called an abscess
● Bacterial infection of blood: There are mainly three conditions-bacteremia
wher there is the presence of a small number of bacteria in the blood,
which do not multip significantly,
● Cellulitis: It is an inflammation of soft tissues caused by the release of
substances, such as hyaluronidases by bacteria.
● Pseudomembranous inflammation: It is an inflammatory response of
mucosal surfaces,

Result of Acute Inflammation

● Resolution: It refers to the complete restoration of the inflamed tissue back

to its normal state. Resolution is usually the end result of minor injuries,
which are short-lived and involve minimal tissue damage and infection, and
wherein the tissue has the capacity to regenerate. Resolution involves a
complete reversal of the inflammatory response.
● Fibrosis: Healing by connective tissue replacement or scarring/fibrosis
occurs when the injury involves substantial amounts of tissue destruction,
or when the damaged tissue is unable to regenerate.

Chronic Inflammation

47
 ● Chronic inflammation is an inflammation of prolonged duration, which can
extend over a long period of time. Chronic inflammation usually follows
recurrent acute inflammation; however, may begin insidiously as a
low-grade, gradual process. In this type of inflammation, acute
inflammation, tissue destruction and attempts at healing and repair go
hand in hand.
● Chronic inflammation arises in the following three settings-prolonged
exposure to potentially toxic agents, which may be endogenous or
exogenous, persistent infections with a certain type of microorganisms,
and autoimmunity. Granulomatous inflammation is a specific type of
chronic inflammation.

Etiology of Chronic Inflammation

● Failure to eradicate infectious organisms, such as Mycobacterium, fungi,

protozoa, and other viruses that can withstand host defenses. Persistent
acute inflammation by such toxic agents may also lead to chronic
inflammation. However, in some cases, chronic Inflammation itself can be
an independent response, e.g., tuberculosis and rheumatoid arthritis.

Cells Involved in Chronic Inflammation

Macrophages

● Macrophages are phagocytic cells (which eliminates microbes and

damaged tissues) derived from blood monocytes during embryonic
development and are the key cellular component of a chronic inflammatory
response.
● Lymphocytes (T and B) get activated in chronic inflammatory conditions by
contact with an antigen or by exposure to bacterial toxins. Once activated,

48
 the lymphocytes produce lymphokines, which in turn stimulate monocytes
and macrophages. The involvement of these cells leads to persistent and
severe inflammation, such as granulomatous inflammation.
● Plasma Cells Plasma cells produce antibodies directed either against
foreign antigens or against altered self-antigens.
● Mast Cells Mast cells are scattered in connective tissues and play a role in
acute as well as persistent inflammatory reactions. They are major
mediators of anaphylactic reactions and certain responses to types of
parasitic infections.
● Eosinophils are characteristically seen in immune reactions mediated by
IgE and parasitic Eosinophils infections.

Morphological Patterns of Chronic Inflammation

Chronic inflammation can be of two types non-specific inflammation and

granulomatous inflammation.

Chronic Non-specific Inflammation

● Chronic non-specific inflammation is characterized by non-specific

mononuclear nflammatory cell infiltrate of macrophages, lymphocytes, and
plasma cells.
● This type of inflammation is seen in a variety of conditions, such as
chronic peptic ulcer of the stomach, osteomyelitis, empyema thoracis,
Crohn's disease, and chronic cholecystitis.
● Fibrosis is a common feature of chronic inflammatory reactions, and
becomes prominent once the active inflammation and tissue destruction
has subsided and is superseded by repair and healing.

Chronic granulomatous inflammation

49
 ● is a distinctive type of chronic inflammation where the predominant cell
type is an activated macrophage, which has a modified, epithelial-like
(epithelioid) appearance.
● The characteristic feature is the formation of granulomas. Granuloma aa
focal aggregate of activated macrophages, which are surrounded by a rim
of lymphocytes and a few plasma cells.
● Sometimes epithelioid cells fuse to form multinucleate giant cells. Some of
the granulomas may show central areas of necrosis.
● Few examples of granulomatous inflammation are tuberculosis
(characterized by central caseous necrosis), sarcoidosis, foreign body
granulomas, fungal infections, cat scratch disease, parasitic infections, and
leprosy.

WOUND HEALING

● Wound healing is a complex, but a well-coordinated process, which

attempts to restore the normal structure and function of the injured
tissue/organ.

50
 ● It is an orderly and timely reparative process that results in a durable
restoration of anatomic and functional integrity.
● Wound healing involves an intricate blend of a series of events, which are
as follows:
● the initial injury followed by the introduction of an acute inflammatory
process, regeneration of parenchymal cells, migration and proliferation of
parenchymal as well as connective tissue cells, synthesis of tracellular
matrix proteins, remodeling of connective tissue and parenchymal
components and finally collagenization and attainment of wound strength.

Types of Wound Healing

Wound healing is a complex and highly regulated biological process that aims to
repair damaged tissues and restore normal structure and function. There are
three primary types of wound healing, each with its own characteristics and
mechanisms:

1. Primary Intention Healing:

● Characteristics: Primary intention healing occurs when the wound edges

are closely approximated, such as in surgical incisions or clean,
well-approximated traumatic wounds. The wound is typically clean and free
of infection.
● Mechanism: In this type of healing, there is minimal tissue loss, and the
wound edges are brought together with sutures, staples, or adhesive
strips. This promotes rapid healing with minimal scar formation.
● Phases: Primary intention healing generally follows the three typical
phases of wound healing: inflammation, proliferation, and remodeling.
However, the process is more rapid and results in less scar tissue
compared to the other types of healing.

51
2. Secondary Intention Healing:

● Characteristics: Secondary intention healing occurs when a wound has a

significant tissue loss, irregular wound edges, or a higher risk of infection.
Examples include open wounds, pressure ulcers, and large burns.
● Mechanism: In this type of healing, the wound is left open to heal naturally.
Granulation tissue forms from the base of the wound, and wound
contraction occurs as myofibroblasts pull the wound edges together.
Epithelialization also takes place from the wound edges toward the center.
● Phases: Secondary intention healing follows the same three phases as
primary intention healing but typically takes longer. It often results in more
significant scar formation and may require specialized wound care.

3. Tertiary Intention Healing (Delayed Primary Closure):

● Characteristics: Tertiary intention healing, also known as delayed primary

closure, is a combination of primary and secondary intention healing. It is
often used in contaminated or infected wounds that are initially left open
and then closed surgically once the risk of infection is reduced.
● Mechanism: Initially, the wound is managed as an open wound to allow
for adequate drainage and control of infection. After a period of
observation and treatment, the wound may be surgically closed using
techniques similar to primary intention healing.
● Phases: Tertiary intention healing involves the same wound healing
phases but combines the strategies of both primary and secondary
intention healing. It may result in variable scar formation, depending on the
extent of tissue damage and infection control.

Factors Affecting Wound Healing

52
Factors, which affect wound healing are broadly divided into two categories:

Local Factors

● Infection: It is the most important local cause for delay in healing.

● Size or extent of wound: Small wound due to surgical incision or other
injuries heals quickly with less scar formation than large wound.
● Apposition of edges of wound: The wound edges, which are appropriately
approximated heals faster than which do not have adequate apposition of
the edges.
● Blood supply: Wound in areas with good blood supply, such as the face,
heals faster than those with poor blood supply, such as the foot. For
example, varicose veins of the legs decrease the venous drainage and can
cause non-healing of ulcers.
● Mobility, if the wounded part: Excess movement of the wounded area can
result in delayed healing.

Systemic Factors

● Nutritional status: Protein deficiency, vitamin C deficiency, inhibits collagen

synthesis and diminished healing process.
● Metabolic status: Diabetes mellitus (DM) is associated with delayed
healing.
● Immune status: Poor immunity of an individual contributes to the increased
susceptibility for infections and delayed wound healing.
● Systemic circulation: Inadequate blood supply, such as atherosclerosis or
venous abnormalities, such as varicose veins that leads to delayed wound
healing
● Hormones: Steroids inhibit collagen synthesis, thereby impairing wound
healing.

53
Factors Accelerating Wound Healing

● Ultraviolet light, steroids, growth hormone, and hyperbaric oxygen helps in

faster healing

Wound Strength

By the end of 7 days, 10% of strength is regained. By 3 months maximum

strength is gained (70-80% of normal skin). A wound will never get back 100% of
normal strength.

Complications of Wound Healing

Some of the common complications of wound healing are as follows:

● Secondary infections, which may lead to delayed wound healing and

chronic non-healing ulcers.
● Deficient scar formation, which may lead to ulceration or wound
dehiscence.
● Excessive formation of granulation tissue and fibrous scar leading to
raised swollen scars referred to as keloids.

NOMENCLATURE

54
Benign tumors are usually designated by adding the suffix -oma to the cell from
which the tumor has developed. For example, lipoma is a benign tumor of the
adipocytes, chondroma originates from cartilage (chondrocytes),

Malignant tumors are commonly called cancers. They invade and destroy the
surroun ding tissue, may spread to distant organs (metastasis), and eventually
kill the host Malignancies are also named according to the cell of origin.

NORMAL CELLS AND CANCER CELLS

Biological Properties of Cancer Cells

● Acquisition of self-sufficiency in growth signals and loss of sensitivity to

antigrowth signals, leading to unchecked growth.
● Loss of capacity of apoptosis (programmed cell death), in order to allow
growth despite genetic errors and external antigrowth signals.
● Loss of capacity for senescence, leading to limitless replicative potential
(immortality

Neoplasia is a term used in medicine to describe the abnormal and uncontrolled

growth of cells that results in the formation of a new, often solid, mass or lump of
tissue. These abnormal growths, known as neoplasms or tumors, can be benign
or malignant. Neoplasia is a key concept in the field of oncology, which focuses
on the study and treatment of cancer.

Definition of Neoplasia:

● Neoplasia refers to the process of abnormal and uncontrolled cell growth

that leads to the formation of neoplastic tissue or a neoplasm (tumor).

55
 Neoplasms can be characterized as either benign or malignant based on
their behavior and potential for invasion and metastasis.
● Benign Neoplasm- Benign neoplasms are non-cancerous growths that
typically grow slowly, do not invade nearby tissues, and do not spread to
other parts of the body. They are usually encapsulated and remain
localized.
● Malignant Neoplasm (Cancer): Malignant neoplasms, commonly referred
to as cancer, are characterized by uncontrolled and aggressive growth.
They can invade surrounding tissues and have the potential to
metastasize, meaning cancer cells can spread to distant sites in the body
through the bloodstream or lymphatic system.
● Neoplasia arises from genetic alterations or mutations in a cell's DNA,
which disrupt normal cellular control mechanisms and result in unregulated
cell division. These genetic changes can be caused by various factors,
including exposure to carcinogens (cancer-causing agents), genetic
predisposition, and other unknown factors.

It's important to note that not all neoplasms are cancerous, and many benign
neoplasms can be successfully treated with surgical removal or other
interventions.

However, malignant neoplasms require more aggressive treatment approaches,

including surgery, radiation therapy, chemotherapy, immunotherapy, and targeted
therapy, to control their growth and prevent metastasis. Early detection and
diagnosis of neoplasms are crucial for effective management and treatment.

BENIGN AND MALIGNANT TUMORS

● Benign tumors are slow-growing, well-circumscribed or encapsulated, and

remain localized to one site.

56
 ● They do not spread to distant organs and do not possess any malignant
potential.
● Malignant tumors on the other hand proliferate rapidly, are locally invasive,
and spread to distant organs.
● The majority of the tumors can be clinically and morphologically
categorized into benign and malignant on the basis of certain properties.

Degree of Cellular Differentiation

● Differentiation refers to the extent to which the tumor cell resembles its
normal counterpart or cell of origin.
● Benign tumors are very well differentiated and closely resemble their
normal counterparts.
● Malignant cells on the other hand show a wide range of differentiation.
● They can be very well differentiated to absolutely undifferentiated, wherein
determining their lineage becomes a challenging task for the
histopathologist.
● These undifferentiated tumors are often referred to as anaplastic.
● Malignant cells often show the following morphological features
● Pleomorphism: Variation in shape and size of cells and nuclei
● Hyperchromatic: Nuclei contain an abundance of dark staining chromatin
● Nuclear enlargement or nucleomegaly Increased mitosis with abnormal
mitotic figures
● Formation of tumor giant cells

Rate of Growth

Benign tumors are slow-growing and grow gradually over a period of time. Most
malignan neoplasms grow very rapidly. The growth rate of a tumor usually
correlates with the level of differentiation of the tumor cells.

57
Circumscription

● Most of the benign tumors are very well circumscribed and are usually
surrounded by a fibrous capsule, e.g., lipoma, fibroadenoma, or by a
compressed rim of surrounding normal tissue (e.g., leiomyoma).
● The tumors, which are surrounded by a fibrous capsule are called
'encapsulated'.

Metastasis

● Metastasis refers to the spread of tumor cells from one part of the body to
another. The tumor cells may spread via the bloodstream or through the
lymphatic channels.
● Metastasis is a hallmark of malignancy because benign tumors do not
metastasize.

Implantation

● Refers to transfer of neoplastic cells from one serous or mucous surface to

another by direct contact. Body cavities are commonly involved. Because
of their lack of cohesiveness, neoplastic cells growing on epithelial
surfaces are prone to shed into the surrounding spaces.
● Implantation is a feature of some malignant neoplasms.

CARCINOMA IN SITU

1. Definition:

58
 CIS, also known as intraepithelial neoplasia, signifies cancer in place. It
represents a transformation of epithelial cells within a tissue, where cells become
disordered and show cancer-like changes but have not invaded neighboring
tissues.

2. Characteristics:

In CIS, cells lose their normal maturation process and revert to a more primitive,
rapidly dividing state. However, they remain confined to their original location
within the tissue.

3. Lack of Invasion:

The defining characteristic of CIS is the absence of invasion into surrounding

tissues. It's a localized stage of cancer.

4. Potential Progression:

While CIS itself is not highly invasive or destructive, it has the potential to
progress to invasive malignancy if left untreated over time. Therefore, it is often
treated as a serious condition.

5. Treatment:

Doctors often recommend complete removal of the CIS lesion because of its
potential to progress to invasive carcinoma. Treatment approaches may be
similar to those used for malignant tumors, such as surgery, radiation therapy, or
other interventions.

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6. Examples: CIS can occur in various organs and tissues. Examples include CIS
in the bladder (which can lead to bladder carcinoma), squamous intraepithelial
lesions (SIL) in the uterine cervix, ductal carcinoma in situ (DCIS) of the breast,
Bowen's disease of the skin, and prostatic intraepithelial neoplasia in the
prostate.

TUMOR METASTASIS

1. Metastasis in Malignant Tumors: Malignant tumors have the ability to invade

nearby tissues and gain access to blood vessels, lymphatic vessels, or body
cavities. Once they enter these circulation pathways, cancer cells can travel to
distant parts of the body. This is where they may establish new tumors, a process
known as metastasis.

2. Exceptions: While metastasis is a defining characteristic of most malignant

tumors, as you mentioned, there are exceptions. Some cancers are less prone to
metastasis, and a few, like basal cell carcinoma and certain brain tumors (e.g.,
glioblastoma multiforme), have a low propensity for metastasis. Nevertheless,
these exceptions are relatively rare.

3. Mechanisms of Metastasis: The process of metastasis involves several steps,

including local invasion of nearby tissues, intravasation (entry into blood or
lymphatic vessels), circulation through the bloodstream or lymphatic system,
extravasation (exit from vessels), and colonization at a distant site. This process
is highly complex and depends on numerous factors, including interactions
between cancer cells and the surrounding microenvironment.

4. Clinical Significance: Metastasis is a critical aspect of cancer progression and

is often associated with a worse prognosis. Once cancer has metastasized to

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distant sites, it can be more challenging to treat, as multiple tumor sites may
need to be addressed.

5. Treatment Implications: Understanding the potential for metastasis is crucial

for cancer staging and treatment planning. It may influence decisions regarding
surgery, radiation therapy, chemotherapy, targeted therapy, immunotherapy, and
other treatments. The goal is often to prevent or delay metastasis and to control
existing metastatic disease.

The three routes of metastasis are as follows:

Metastasis is the process by which cancer cells spread from the primary tumor
site to distant parts of the body. This can occur through several routes or
pathways, and the three primary routes of metastasis are as follows:

1. Hematogenous Metastasis (Bloodborne Metastasis):

● Route: In hematogenous metastasis, cancer cells enter the bloodstream

(through nearby blood vessels) and are carried to distant organs or tissues.
Once in circulation, cancer cells can be transported to various parts of the
body.
● Common Target Organs: Some cancers have a tendency to spread to
specific organs through the bloodstream. For example, breast cancer can
metastasize to the bones, lungs, liver, or brain.

2. Lymphatic Metastasis (Lymphatic Spread):

● Route: Lymphatic metastasis involves the spread of cancer cells through

the lymphatic system. Cancer cells can enter the lymphatic vessels, which

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 are part of the body's immune system, and travel to regional lymph nodes
and beyond.
● Common Target Locations: Lymphatic metastasis often starts with
regional lymph nodes near the primary tumor site. From there, cancer cells
may progress to more distant lymph nodes and tissues.

3. Direct Extension or Invasion (Local Spread):

● Route: Some cancers can spread directly by invading and infiltrating

nearby tissues and organs. Instead of traveling through the bloodstream or
lymphatic system, cancer cells move locally to adjacent structures.
● Common Scenarios: Direct extension is common in certain cancers, such
as head and neck cancers, where tumors can invade neighboring
structures like the jawbone or nearby lymph nodes.

Thrombosis

is a medical term that refers to the formation of a blood clot, known as a

thrombus, within a blood vessel. Thrombosis can occur in both arteries and veins
and has distinct pathophysiology, morphological features, and clinical
consequences depending on the location and size of the clot.

Pathophysiology of Thrombosis:

● Thrombosis occurs when there is an imbalance between the factors that

promote blood clotting (coagulation) and the factors that inhibit it
(anticoagulation).
● Several factors can contribute to the development of thrombosis:

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1. Endothelial Injury: Damage to the inner lining of blood vessels, called the
endothelium, can trigger the activation of platelets and the coagulation cascade,
leading to clot formation.

2. Stasis or Sluggish Blood Flow: Slow or stagnant blood flow can promote clot
formation, as it allows blood components, particularly platelets and clotting
factors, to accumulate and initiate clotting.

3. Hypercoagulability: Certain medical conditions, such as inherited or acquired

clotting disorders, cancer, and pregnancy, can increase the tendency of the blood
to clot excessively.

4. Venous Stasis: In the veins, the accumulation of blood due to impaired venous
return (as seen in conditions like deep vein thrombosis or DVT) can lead to
venous thrombosis.

5. Arterial Wall Changes: In arteries, atherosclerosis (narrowing and hardening of

the arteries) can create a prothrombotic environment, promoting arterial
thrombosis.

Formation of Thrombi at Different Sites

1. Venous Thrombosis (Deep Vein Thrombosis - DVT:

● In DVT, a thrombus typically forms in the deep veins of the legs, pelvis, or
arms.
● It can partially or completely obstruct the affected vein, leading to swelling,
pain, and potentially severe complications.

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 ● If a portion of the thrombus breaks off and travels to the lungs, it can cause
a pulmonary embolism (PE), a life-threatening condition.

2. Arterial Thrombosis:

● Arterial thrombosis can occur in arteries affected by atherosclerosis.

● These thrombi are often rich in platelets and can lead to the sudden
occlusion of the artery, causing conditions like myocardial infarction (heart
attack) or ischemic stroke.

Morphological Features of Thrombi

● Thrombi are composed of platelets, fibrin (a protein involved in clot

formation), and trapped red and white blood cells.
● They can vary in size, from small and localized to large and extending
along the length of a vessel.
● Thrombi can adhere to the vessel wall, partially or completely obstruct
blood flow, and may be organized (remodeled) over time.

Clinical Features:

The clinical features of thrombosis depend on its location:

1. Deep Vein Thrombosis (DVT):

● Pain, swelling, and warmth in the affected limb.

● Redness and tenderness in the area.
● In severe cases, DVT can lead to complications like post-thrombotic
syndrome or pulmonary embolism.

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2. Arterial Thrombosis:

● Myocardial Infarction (Heart Attack): Chest pain, shortness of breath, and

other signs of cardiac distress.
● Ischemic Stroke: Sudden weakness, numbness, or difficulty speaking,
depending on the affected brain area.

EMBOLISM

Embolism is the process of partial or complete obstruction of some part of the

cardiovascular system by any mass carried in the circulation; the transported
intravascular mass detached from its site of origin is called an embolus. Most
usual forms of emboli (90%) are thromboemboli I.e., originating from thrombi or
their parts detached from the vessel wall.

Emboli may be of various types: .

Depending upon the matter in the emboli:

● Solid
● Liquid
● Gaseous

Depending upon whether infected or not:

● Bland
● Septic

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Depending upon the source of the emboli:

● Cardiac emboli
● Arterial emboli
● Venous emboli
● Lymphatic emboli

Depending upon the flow of blood, two special types of emboli are mentioned:

1. Paradoxical embolus: An embolus which is carried from the venous side of

circulation to the arterial side or vice versa, is called paradoxical or crossed
embolus.

2. Retrograde embolus: An embolus which travels against the flow of blood is

called retrograde embolus.

Thromboembolism

A detached thrombus or part of thrombus constitutes the most common type of

embolism.

Arterial (Systemic) Thromboembolism

● Courses within the heart (80-85% ): These are mural thrombi in the left
atrium or left ventricle. vegetation on the mitral or aortic valves, prosthetic
heart valves and cardiomyopathy.
● Causes within the arteries: These include emboli developing in relation to
atherosclerotic plaques. Aortic aneurysms, pulmonary veins and
paradoxical arterial emboli from the systemic venous circulation.

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Venous Thromboembolism

● Deep vein thrombosis (DVT) of the lower legs, the most com of venous
thrombi
● Thrombi in the pelvic veins
● Thrombi in the veins of the upper limbs Thrombosis in cavernous sinus of
the brain
● Thrombi in the right side of heart

The most significant effect of venous embolism is obstruction of pulmonary

circulation leading to pulmonary embolism.

Pulmonary Thromboembolism

Definition:

Pulmonary embolism is the most common and fatal form of venous

thromboembolism in which there is occlusion of pulmonary arterial tree by
thromboemboli. In and pulmonary hypertension. contrast, pulmonary thrombosis
is uncommon and may occur in pulmonary atherosclerosis

Etiology:

Pulmonary emboli are more common in hospitalized or bedridden

patients,though they can occur in ambulatory patients as well.

The causes are as follows:

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 ● Thrombi originating from large veins of lower legs (such as popliteal,
femoral and iliac) are the cause in 95% of pulmonary emboli.
● Less common sources include thrombi in varicosities of superficial veins of
the legs,and pelvic veins, such as periprostatic, periovarian, uterine and
broad ligament veins.

Pathogenesis:

● The risk factors for pulmonary thromboembolism are stasis of venous

blood and hypercoagulable states.
● If the thrombus is large, it is impacted at the bifurcation of the main
pulmonary artery (saddle embolus), or may be found in the right ventricle
or its outflow tract.
● More commonly, there are multiple emboli, or a large embolus may be
fragmented into many smaller emboli which are then impacted in a name
of vessels.
● Rarely, paradoxical embolism may occur by passage of an embryo from
right heart into the left heart through atrial or ventricular septal defect. In
this way, pulmonary emboli may reach systemic circulation.

Consequences of pulmonary embolism:

Pulmonary embolism occurs more commonly as a complication in patients of

acute or chronic debilitating diseases who are immobilized for a long duration.
Women in their reproductive period are at higher risk, such as in late pregnancy,
follow delivery and with use of contraceptive pills.

Natural history of pulmonary embolism may have following consequences:

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 ● Sudden death
● Acute cor pulmonale Pulmonary infarction
● Pulmonary hemorrhage
● Resolution
● Pulmonary hypertension, chronic cor pulmonale and pulmonary
arteriosclerosis.

Systemic Embolism

This is the type of arterial embolism that originates commonly from thrombi in the
left ventricle, These heart diseases include myocardial infarction,
cardiomyopathy, rheumatic heart disease (RHD), congenital heart disease,
infective endocarditis and prosthetic cardiac valves.

Fat Embolism

● It is an obstruction of arterioles and capillaries by fat globules constitutes

fat embolism.

Etiology

● It may occur from following causes:

Traumatic causes

● Trauma to bones is the most common cause of fat embolism, e.g., in

fractures of long bones leading to passage of fatty marrow in circulation,
concussions of bones, after orthopedic surgical procedures, etc.

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 ● Trauma to soft tissue, e.g., laceration of adipose tissue and in puerperium
due to injury to pelvic fatty tissue.

Non-traumatic causes

● Extensive burns Diabetes mellitus

● Fatty liver
● Pancreatitis
● Sickle cell anemia
● Decompression sickness
● Inflammation of bones and soft tissues
● Extrinsic fat or oils introduced into the body
● Hyperlipidemia
● Cardiopulmonary bypass surgery

Pathogenesis

Pathogenesis of fat embolism is explained by following mechanisms:

● Mechanical theory: Mobilization of fluid fat may occur following trauma to

the bone of soft tissues.
● Emulsion instability theory: This theory explains the pathogenesis of fat
embolism in non- traumatic cases. According to this theory, fat emboli are
formed by aggregation of plasma lipids (chylomicrons and fatty acids) due
to disturbance in natural emulsification of fat.
● Intravascular coagulation theory: In stress, release of some factor activates
disseminated intravascular coagulation (DIC) and aggregation of fat
emboli.
● Toxic injury theory: According to this theory, the small blood vessels of
lungs are chemically injured by high plasma levels of free fatty acid.

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Consequences of Fat Embolism

The effects of fat embolism depend upon the size and quantity of fat globules.

Pulmonary fat embolism in patients dying after fractures of bones, presence of

numerous fat emboli in the capillaries of the lung is a frequent autopsy finding.
Systemic fat embolism: Some of the fat globules may pass through the
pulmonary circulation.

Air Embolism

● Air embolism occurs when air is introduced into venous circulation

Venous Air Embolism

● Ar may be sucked into systemic veins under the following circumstances:

● Operation on the head and neck, and trauma
● Obstetrical operation and trauma
● Intravenous infusion of blood and fluid
● Angiography

The effects of venous air embolism depend upon the following factors:

● Amount of air
● Rapidly of entry
● Position of the patient
● General condition of the patient
● The mechanism of death is by entrapment of air emboli in the pulmonary
arterial trunk in the right heart.

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Shock

It is a critical medical condition characterized by a circulatory disturbance

resulting in inadequate tissue perfusion, which can lead to cellular hypoxia and
organ dysfunction. Here's a comprehensive overview:

Define:

Shock is a life-threatening condition where there is an insufficient supply of

oxygen and nutrients to body tissues and organs due to impaired circulatory
function.

Classification:

Shock can be classified into several types based on its underlying causes:

1. Hypovolemic Shock: Caused by a decrease in blood volume, often due to

severe bleeding or fluid loss.

2. Cardiogenic Shock: Stemming from a primary cardiac disorder, such as a

heart attack or heart failure, leading to inadequate pumping of blood by the heart.

3. Distributive Shock: Results from widespread vasodilation and decreased

systemic vascular resistance,including subtypes:

● Septic Shock: Due to severe infection leading to systemic inflammation.

● Anaphylactic Shock: An extreme allergic reaction causing systemic
vasodilation and bronchoconstriction.

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 4. Obstructive Shock: Arises from mechanical obstruction of blood flow, often
due to conditions like pulmonary embolism or cardiac tamponade.

Etiology:

Etiology varies depending on the shock type but can include factors like trauma,
severe infection, heart disease, allergic reactions, and more.

Pathophysiology:

Shock leads to cellular and tissue hypoxia due to reduced oxygen delivery. It
triggers a cascade of events, including activation of the sympathetic nervous
system and release of inflammatory mediators.

Pathophysiology in Specific Types of Shock:

● In septic shock, maldistribution of blood flow and microcirculation

disturbances contribute to hypoxia.
● In cardiogenic shock, impaired cardiac contractility leads to decreased
stroke volume and cardiac output.

Morphologic Features:

● Morphologic changes in shock include cellular injury, organ dysfunction,

and tissue damage. Specific features vary based on the type of shock.

Clinical Features:

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 ● Clinical manifestations encompass tachycardia, hypotension, altered
mental status, cold and clammy skin, and reduced urine output, among
others.

Complications:

● Untreated shock can lead to multi-organ failure, including damage to the

heart, lungs, kidneys, and liver, with the potential for long-term
consequences or death.

EDEMA

The accumulation of fluids in the body cavities is known as effusion and is named
according to the body cavity involved. Hydrothorax is the accumulation of fluid in
the pleural cavity hydroperitoneum of ascites is in the peritoneal cavity and
hydropericardium is a collection of fluid in the pericardial cavity

Depending upon the constituents of the accumulated fluid, edema fluid may be
categorized as exudates or transudate:

● Exudate: It is typically seen in inflammatory edema, where the fluid

escapes due toM increased vascular permeability. The protein and cellular
content of exudates are high and the specific gravity is above 1.018.
● Transudate: It is the edema fluid that accumulates as a result of
hydrodynamic imbalances It is essentially a filtrate of plasma and has
low-protein content, very low cellularity, and a specific gravity of less than
1.015. Transudate is seen in edema due to renal and candiac diseases

Pathogenesis of Edema

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 ● Decreased plasma oncotic pressure: The plasma oncotic pressure
decreases as a result of excessive loss of albumin. This results in an
increased outward movement of fluid from capillaries and decreased
inward movement from interstitial spaces, resulting in edema, eg. nephrotic
syndrome
● Increased capillary hydrostatic pressure: Usually hydrostatic pressure is
lower at the vemular end, but if it rises to a level more than the plasma
oncotic pressure it leads to accumulation of fluid in the interstitial space,
e.g., ascites of liver disease . Lymphatic obstruction: Leads to impaired
lymphatic drainage and causes localized edema, eg, filarial lymphedema.

Morphology of Different Types of Edema

● Pulmonary edema: Grossly, the lungs appear boggy and heavy. The cut
section reveals oozing of frothy pinkish blood-tinged fluid, which is an
admixture of edema fluid, air, and blood. Microscopically, the alveoli and
interstitial space of the lungs are filled with a pale pink proteinaceous.
● Cerebral edema: The brain is swollen, soft with flattened gyrl and narrowed
sulci.
● Cytotoxic edema - the cell are swollen and vacuolated microscopically.

TRANSUDATES

● Transudates are colorless or pale yellow, clear fluids of alkaline reaction

containing a varying amount of proteins, extractives and salts.
● A transudate is a filtrate of blood caused by increased pressure in veins
and capillaries that force fluid through vessel walls or for low levels of
protein in the blood serum. Transudates accumulate in the tissues outside
the blood vessels and cause edema.

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 ● Transudate contains low protein content, little or no cellular material and a
low specific gravity.
● They are the ultrafiltrate of blood plasma resulting from osmotic and
hydrostatic Imbalance in vessel without an increase of vascular
permeability which may be seen in left ventricular failure, cirrhosis and
nephrosis Transudates are non-inflammatory and a transudative effusion,
e.g., in pleural effusion is characterized by the following
● Pleural fluid/serum protein ratio: 0.5 or absolute value <3 g/dL.
● Pleural fluid/serum LDH ratio: <0.6 or absolute value <0.45 upper normal
serum limit.
● Pleural fluid specific gravity: <1.018.

Pathology

● Increased hydrostatic pressure, e.g., in congestive heart failure,

constrictive pericarditis, superior vena cava syndrome.
● Decreased osmotic pressure, e.g., in nephrotic syndrome,
hypoalbuminemia, hepatic cirrhosis.
● Increased intrapleural negative pressure, e.g., in atelectasis and
pulmonary embolism.

EXUDATE

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A fluid rich in proteins and cellular elements that leaks out of the blood vessels
due to inflammation and accumulates in the surrounding tissues. An exudate is
formed in inflam- mation, because of increased vascular permeability due to
increased inter-endothelial spaces.

Pathology

● Inflammation or malignancy due to increased vascular permeability of

vessels of parietal pleura.
● Infections of the lung, such as tuberculosis, pneumonia, lung abscess and
infarcts. Malignancies, such as lymphoma, metastasis from cancer of lung,
breast, and ovaries Carcinomatosis, surgery or trauma that may result in
decreased lymphatic drainage.
● Autoimmune diseases, such as rheumatoid arthritis and systemic lupus
erythematosus.

Types of Inflammatory Exudates

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 Hemorrhagic; sanguineous: It appears to be red with presence of red blood cells
(RBCs) Small amounts of this type are expected after surgery or trauma. A large
amount may indicate hemorrhage. If there is sudden large amount of dark, red
blood; it is an indication of draining hematoma.

Serosanguineous: This type of exudate is blood-tinged or yellow or pink with

presence of RBCs. This is expected to appear 48-72 hours after injury or trauma
to the microvasculature Serous: Serous exudate is thin, clear yellow, or straw
colored with albumin, immuno globulins and is expected to be appear for 1 week
after any trauma or surgery. It appears

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 UNIT - 2
Special Pathology

Pathological changes in disease conditions of selected systems:

Respiratory system

In pathology, the respiratory system refers to the complex network of organs and
structures involved in the process of breathing and gas exchange. It
encompasses the upper and lower respiratory tracts, from the nasal passages to
the lungs, and plays a vital role in maintaining the body's oxygen balance and
eliminating carbon dioxide. The primary components of the respiratory system
involved in pathology include:

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1. Upper Respiratory Tract:

● Nasal Passages: The air enters the respiratory system through the nasal
passages, where it is filtered, humidified, and warmed before reaching the
lower respiratory tract.
● Pharynx (Throat): The pharynx serves as a common pathway for both air
and food. It is divided into nasopharynx, oropharynx, and laryngopharynx.

2. Lower Respiratory Tract:

● Larynx (Voice Box): The larynx contains the vocal cords and is essential for
phonation. It also protects the lower airways during swallowing.

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 ● Trachea (Windpipe): The trachea is a tubular structure that connects the
larynx to the bronchi. It is supported by C-shaped cartilage rings.
● Bronchi and Bronchioles: The trachea branches into bronchi, which further
divide into smaller bronchioles. These structures conduct air into the lungs.
● Alveoli: The bronchioles terminate in tiny air sacs called alveoli. This is
where gas exchange occurs, with oxygen entering the bloodstream and
carbon dioxide being expelled.

3. Lungs:

● Pleura: The lungs are enclosed by a double-layered membrane called the

pleura. The visceral pleura covers the lung surface, while the parietal
pleura lines the chest cavity.
● Pulmonary Vasculature: Blood vessels in the lungs facilitate the exchange
of gases. The pulmonary arteries carry deoxygenated blood to the lungs,
while the pulmonary veins return oxygenated blood to the heart.

In pathology, the respiratory system is subject to various disorders and diseases,

including infections (pneumonia, bronchitis), chronic obstructive pulmonary
disease (COPD), lung cancer, and interstitial lung diseases. Pathological
changes may involve inflammation, fibrosis, structural abnormalities, and
impaired gas exchange, leading to respiratory symptoms and compromised lung
function. Understanding respiratory pathology is crucial for healthcare
professionals in diagnosing, treating, and managing respiratory diseases.

Pulmonary Infections:

Pneumonia:

Pathogenesis:

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 ● Pneumonia is initiated by the invasion of pathogens (bacteria, viruses, or
fungi) into the lungs, triggering inflammation in the lung parenchyma.
● The inflammatory response leads to increased vascular permeability,
exudate formation, and impairment of normal gas exchange in the alveoli.
● Alveoli become filled with inflammatory cells, fluid, and debris, resulting in
consolidation and decreased lung compliance.

Clinical Features:

● Patients typically present with symptoms such as fever, cough, chest pain,
dyspnea, and the production of purulent or blood-tinged sputum.
● Physical examination may reveal crackles, decreased breath sounds, and
signs of respiratory distress.
● Severe cases can lead to complications such as pleural effusion, abscess
formation, and respiratory failure.

Interventions:

● Treatment involves administering appropriate antibiotics based on the

identified pathogen.
● Oxygen therapy is provided to maintain adequate oxygenation.
● Supportive care includes hydration, rest, and monitoring vital signs.

Lung Abscess:-

Pathogenesis:

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 ● Lung abscesses result from the formation of a localized collection of pus
within the lung parenchyma, often arising from aspiration or secondary to
an existing infection.
● Aspiration of oral or gastric contents introduces bacteria into the lower
respiratory tract, leading to necrosis and abscess formation.
● Predisposing factors include conditions that compromise the cough reflex,
such as altered consciousness or underlying lung diseases.

Clinical Features:

● Common symptoms include cough, fever, weight loss, and the production
of foul-smelling sputum.
● Physical examination may reveal signs of consolidation, and diagnostic
imaging (chest X-ray or CT scan) confirms the presence of a cavity.
● Systemic signs of infection, such as leukocytosis, may be evident.

Interventions:

● Treatment involves a combination of antibiotics effective against anaerobic

and aerobic bacteria.
● Percutaneous or surgical drainage may be necessary for large abscesses.
● Supportive care includes pain management, nutritional support, and
monitoring for complications.

Pulmonary Tuberculosis (TB):

Pathogenesis:

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 ● Pulmonary TB is caused by Mycobacterium tuberculosis and is primarily
transmitted through inhalation of airborne droplets containing the
bacterium.
● The initial infection triggers an immune response, leading to the formation
of granulomas containing the bacteria.
● Progressive disease involves caseous necrosis, fibrosis, and cavitation in
the lung tissue.

Clinical Features:

● Chronic cough, hemoptysis (coughing up blood), night sweats, weight loss,

and fatigue are common symptoms.
● Reactivation of TB may occur in individuals with weakened immune
systems.
● Diagnostic tests include sputum culture, chest X-ray, and tuberculin skin
test.

Interventions:

● Treatment requires a combination of antibiotics for an extended duration.

● Directly observed therapy (DOT) ensures medication adherence.
● Isolation precautions are implemented during the infectious period.

Key Points

● Regular assessment of respiratory status is critical for early detection of

worsening symptoms.
● Administration of prescribed antibiotics on schedule is crucial for
successful treatment.
● Oxygen therapy is provided as needed to maintain optimal oxygen levels.

84
 ● Patient education emphasizes the importance of completing the full
antibiotic course.
● Strict adherence to infection control measures prevents the spread of
infectious agents.
● Supportive care includes maintaining adequate hydration and nutrition.

Chronic Obstructive Pulmonary Disease (COPD):

1. Chronic Bronchitis:

● Definition:- Chronic bronchitis is a type of COPD characterized by

persistent inflammation of the bronchial tubes, leading to increased mucus
production.
● Pathogenesis:-Prolonged exposure to irritants (such as smoking) causes
chronic inflammation and hyperplasia of mucus-secreting cells.
● Clinical Features:-Persistent cough with sputum production, wheezing,
shortness of breath, and frequent respiratory infections.
● Pathological Changes:-Thickening of bronchial walls, increased mucus
production, and compromised airflow.
● Interventions:-Smoking cessation, bronchodilators, inhaled
corticosteroids, and pulmonary rehabilitation.

2. Emphysema:

● Definition:-Emphysema is a COPD subtype characterized by the

destruction of alveolar walls, reducing the surface area for gas exchange.
● Pathogenesis:-Chronic exposure to irritants, particularly smoking, triggers
inflammation and the breakdown of alveolar walls.
● Clinical Features:-Progressive dyspnea, barrel chest, prolonged
expiration, and decreased exercise tolerance.

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 ● Pathological Changes:- Loss of alveolar elasticity, airspace enlargement,
and reduced gas exchange efficiency.
● Interventions:-Smoking cessation, bronchodilators, oxygen therapy, and
lung volume reduction surgery in severe cases.

3. Bronchial Asthma:

● Definition:- Bronchial asthma is a chronic inflammatory disorder of the

airways characterized by recurrent episodes of reversible airflow
obstruction.
● Pathogenesis:-Triggered by allergens, irritants, or infections, leading to
bronchial hyperreactivity and inflammation.
● Clinical Features:-Recurrent episodes of wheezing, coughing, chest
tightness, and shortness of breath.
● Pathological Changes:-Airway inflammation, bronchoconstriction, and
increased mucus production during exacerbations.
● Interventions:-Inhaled bronchodilators, corticosteroids, leukotriene
modifiers, and allergen avoidance.

4. Bronchiectasis:

● Definition:- Bronchiectasis involves the abnormal and permanent dilation

of the bronchi due to chronic inflammation and recurrent infections.
● Pathogenesis:-Chronic infections damage the bronchial walls, leading to
the loss of elasticity and bronchial dilation.
● Clinical Features:-Chronic cough, copious sputum production, recurrent
respiratory infections, and hemoptysis.
● Pathological Changes:-Dilated bronchi filled with thick mucus, impaired
mucociliary clearance, and risk of bronchial wall destruction.
● Interventions:-Antibiotics for infections, airway clearance techniques,
bronchodilators, and, in severe cases, surgical intervention.

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 Tumors of the Lungs:

1. Non-Small Cell Lung Cancer (NSCLC):

● Types:-NSCLC includes adenocarcinoma, squamous cell carcinoma, and

large cell carcinoma, each with distinct histological features and prognosis.
● Pathogenesis:-Frequently associated with cigarette smoking, exposure to
environmental carcinogens, and genetic factors influencing cell mutations.
● Clinical Features:-Symptoms may include persistent cough, hemoptysis,
chest pain, weight loss, and respiratory difficulties.
● Diagnostic Methods:-Diagnosis involves imaging studies like CT scans,
PET scans, bronchoscopy, and histological examination through biopsy.
● Treatment:-Strategies include surgical resection, chemotherapy, radiation
therapy, targeted therapies (for specific mutations), and immunotherapy.

2. Small Cell Lung Cancer (SCLC):

● Pathogenesis:-Strongly associated with cigarette smoking, characterized

by rapid growth, early metastasis, and paraneoplastic syndromes.
● Clinical Features:-Presents with aggressive features, such as rapid
growth, early dissemination, and potential paraneoplastic syndromes like
SIADH or Cushing's syndrome.
● Diagnostic Methods: -Imaging studies and biopsy play a crucial role in
diagnosis.
● Treatment:-Mainstay is chemotherapy due to its high responsiveness,
often complemented by radiation therapy.

3. Carcinoid Tumors:

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 ● Type: Divided into typical and atypical carcinoids based on cellular
characteristics.
● Pathogenesis:-Originates from neuroendocrine cells and tends to grow
slowly.
● Clinical Features:-Frequently asymptomatic; symptoms, if present, may
include bronchial obstruction or carcinoid syndrome.
● Diagnostic Methods:-Diagnosis involves imaging, bronchoscopy, and
confirmation through biopsy.
● Treatment:-Surgical resection is the primary treatment, while somatostatin
analogs may be used for carcinoid syndrome.

Cardiovascular System:

Definition:

The cardiovascular system, also known as the circulatory system, comprises the
heart and blood vessels. It is a vital organ system responsible for circulating
blood, oxygen, nutrients, and hormones throughout the body. The system
ensures the delivery of oxygenated blood to tissues and organs and the removal
of waste products, playing a crucial role in maintaining homeostasis.

Components:

1. Heart:

● The muscular organ acts as a pump, propelling blood throughout the

circulatory system.
● Divided into four chambers: left and right atria (upper chambers) and left
and right ventricles (lower chambers).

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2. Blood Vessels:

● Arteries: Carry oxygenated blood away from the heart to the body's
tissues.
● Veins: Transport deoxygenated blood from the body back to the heart.
● Capillaries: Tiny vessels where oxygen and nutrients are exchanged with
tissues.

3. Blood:

● A fluid connective tissue containing red and white blood cells, platelets,
and plasma.

Functions:

● Transportation:-Oxygen and nutrients are transported to cells, and waste

products are carried away.
● Oxygenation:-Oxygen is supplied to tissues, and carbon dioxide is
removed.
● Nutrient Delivery:-Nutrients from the digestive system are distributed to
cells.
● Hormone Circulation:-Hormones are carried to target organs and tissues.

1. Atherosclerosis:

Pathogenesis:

● Atherosclerosis is a chronic inflammatory condition characterized by the

buildup of plaques within arterial walls.

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 ● The process begins with the accumulation of cholesterol, fatty substances,
cellular debris, and inflammatory cells on the inner lining of arteries
(endothelium).
● Over time, plaques may calcify, leading to the hardening and narrowing of
arterial walls.

Clinical Features:

● Atherosclerosis often progresses asymptomatically for years.

● Symptoms may manifest when blood flow is significantly reduced, resulting
in conditions such as angina (chest pain) or claudication (pain in the legs
during walking).

Complications:

● Atherosclerosis is a major contributor to cardiovascular diseases, including

coronary artery disease (CAD), peripheral artery disease (PAD), and
cerebrovascular disease.
● Plaque rupture can lead to thrombosis, causing acute events like
myocardial infarction (heart attack) or stroke.

Interventions:

● Lifestyle modifications, including a heart-healthy diet and regular exercise,

are essential.
● Medications such as statins, antiplatelet agents, and antihypertensives
may be prescribed.
● Invasive procedures like angioplasty and stent placement or surgical
interventions like bypass surgery may be necessary in advanced cases.

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2. Ischemia and Infarction:

Ischemia:

● Ischemia refers to inadequate blood supply to a specific organ or tissue,

often due to reduced blood flow through arteries.
● In the context of the cardiovascular system, myocardial ischemia occurs
when the blood supply to the heart muscle is insufficient, leading to
reduced oxygen delivery.

Infarction:

● Infarction is the irreversible damage or death of tissue due to prolonged

ischemia.
● Myocardial infarction (MI) occurs when a coronary artery is blocked,
resulting in the death of heart muscle cells.

Clinical Features:

● Ischemia may present with symptoms like chest pain or discomfort

(angina) during physical exertion or stress.
● Infarction manifests as severe and persistent chest pain, shortness of
breath, nausea, and sweating in the case of MI.

Complications:

● Ischemia can progress to infarction if blood flow is not restored promptly.

● Infarction can lead to heart failure, arrhythmias, or structural damage to the
affected organ.

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Interventions:

● Ischemia may be managed with medications that improve blood flow or

reduce the heart's oxygen demand.
● Infarction requires urgent medical attention, often involving reperfusion
therapy such as thrombolytic drugs or percutaneous coronary intervention
(PCI).

3. Rheumatic Heart Disease:

Pathogenesis:

● Rheumatic heart disease is a consequence of rheumatic fever, an

inflammatory condition caused by untreated streptococcal infections.
● The immune response to the bacterial infection can lead to damage to
heart valves, particularly the mitral valve.

Clinical Features:

● Rheumatic heart disease may manifest with symptoms such as chest pain,
shortness of breath, and fatigue.
● Valvular involvement can lead to murmurs and complications like heart
failure.

Complications:

● Valve damage, leading to stenosis (narrowing) or regurgitation (leakage),

can result in impaired cardiac function.
● Long-term complications may include infective endocarditis.

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Interventions:

● Treatment involves antibiotics to eradicate the streptococcal infection.

● Valve repair or replacement surgery may be necessary for severe valve
damage.

Infective Endocarditis:

Pathogenesis:

● Bacteria gain access to the bloodstream through various routes, such as

dental procedures, invasive medical interventions, or skin infections.
● Once in the bloodstream, bacteria can adhere to damaged heart valves or
other areas of the endocardium, forming vegetation.

Clinical Features:

● Symptoms can be nonspecific and may include fever, chills, fatigue, and
weight loss.
● Specific signs depend on the involvement of heart valves and may include
new or changing murmurs, embolic phenomena (e.g., stroke), and
evidence of systemic septic emboli.

Microorganisms:

● Common causative organisms include Staphylococcus aureus,

Streptococcus viridans, and Enterococcus species.

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 ● In individuals with predisposing conditions like intravenous drug use,
infections may be caused by Staphylococcus aureus, including
methicillin-resistant strains (MRSA).

Complications:

● Untreated infective endocarditis can lead to severe complications,

including heart valve destruction, heart failure, and systemic emboli
affecting various organs.

Prevention:

● Prophylactic antibiotics may be recommended for individuals with certain

high-risk conditions before dental or surgical procedures to prevent the
development of infective endocarditis.

Gastrointestinal Tract:

Definition:

The gastrointestinal (GI) tract, also known as the digestive tract or alimentary
canal, is a continuous and hollow tube that extends from the mouth to the anus. It
is responsible for the digestion and absorption of food, as well as the elimination
of waste. The GI tract includes various organs, each with specific functions in the
digestive process.

Components of the Gastrointestinal Tract:

● Mouth:- Ingestion and initial mechanical and chemical digestion of food.

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 ● Esophagus:-Transport of food from the mouth to the stomach via
peristalsis.
● Stomach:-Storage of food, mixing with gastric juices, and the initial
breakdown of proteins.
● Small Intestine:-Further digestion and absorption of nutrients (duodenum,
jejunum, ileum).
● Large Intestine (Colon):-Absorption of water and electrolytes, formation
and storage of feces.
● Rectum:- Storage of feces before elimination.
● Anus:-Opening through which feces are expelled from the body.

Peptic Ulcer Disease (Gastric and Duodenal Ulcer):

Pathogenesis:

➔ Peptic ulcer disease involves the formation of open sores (ulcers) in

the lining of the stomach (gastric ulcer) or the upper part of the small
intestine (duodenal ulcer).
➔ Common causes include Helicobacter pylori infection, prolonged use
of nonsteroidal anti-inflammatory drugs (NSAIDs), and excessive
stomach acid production.
● Clinical Features: - Epigastric pain or discomfort, bloating, nausea,
vomiting, and in some cases, bleeding leading to dark stools or vomiting
blood.
● Complications:-Bleeding ulcers can cause anemia; perforated ulcers can
lead to a life-threatening infection in the abdominal cavity.
● Diagnosis:-Endoscopy, barium contrast studies, and H. pylori testing.
● Treatment:-Antibiotics for H. pylori eradication, proton pump inhibitors
(PPIs) to reduce stomach acid, and avoidance of NSAIDs.

Gastritis - H. pylori Infection:

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 ● Pathogenesis:- Gastritis is inflammation of the stomach lining, often
associated with H. pylori infection, long-term use of NSAIDs, or
autoimmune disorders.
● Clinical Features:-Epigastric pain, nausea, vomiting, bloating, and loss of
appetite.
● Complications:-Chronic gastritis can lead to the development of peptic
ulcers and, in severe cases, stomach cancer.
● Diagnosis:-Endoscopy with biopsy, breath test for H. pylori, blood tests.
● Treatment:-Antibiotics for H. pylori, medications to reduce stomach acid,
and management of underlying causes.

Oral Mucosa: Oral Leukoplakia, Squamous Cell Carcinoma:

Oral Leukoplakia:

● Pathogenesis:-Oral leukoplakia is a white patch or plaque that cannot be

rubbed off, associated with chronic irritation or tobacco use.
● Clinical Features:- White or grayish patches on the oral mucosa, typically
painless.
● Complications:-Some cases may progress to squamous cell carcinoma.

Squamous Cell Carcinoma:

● Pathogenesis:- Squamous cell carcinoma is a type of oral cancer that

arises from the squamous cells lining the oral cavity.
● Clinical Features:-Persistent mouth ulcers, red or white patches, difficulty
swallowing, and swelling.
● Complications:-Local invasion, metastasis, and potential mortality if not
treated early.

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 ● Diagnosis:-Biopsy of suspicious lesions, imaging studies for cancer
staging.
● Treatment:-Surgical excision, radiation therapy, chemotherapy for
squamous cell carcinoma.Management of risk factors and monitoring for
oral leukoplakia.

Esophageal Cancer:

● Pathogenesis:-Esophageal cancer develops in the cells lining the

esophagus and is often associated with chronic irritation, such as chronic
acid reflux (gastroesophageal reflux disease or GERD), smoking, and
excessive alcohol consumption.

There are two main types: squamous cell carcinoma and adenocarcinoma.

● Clinical Features:-Dysphagia (difficulty swallowing), weight loss, chest

pain, and regurgitation.
● Complications:-Esophageal obstruction, metastasis to other organs.
● Diagnosis:-Endoscopy with biopsy, imaging studies (CT scan, PET scan).
● Treatment:-Surgical resection, chemotherapy, radiation therapy.

Gastric Cancer:

● Pathogenesis:- Gastric cancer, also known as stomach cancer, originates

in the lining of the stomach and is often associated with chronic H. pylori
infection, certain dietary factors, and genetic predisposition.
● Clinical Features:-Early stages may be asymptomatic; later stages may
present with abdominal pain, weight loss, nausea, and vomiting.
● Complications:-Metastasis to lymph nodes and other organs.

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 ● Diagnosis:-Endoscopy with biopsy, imaging studies (CT scan, endoscopic
ultrasound).
● Treatment:-Surgical resection, chemotherapy, radiation therapy.

Intestinal Disorders:

Typhoid Ulcer:

● Pathogenesis:-Typhoid ulcer is associated with systemic infection by

Salmonella typhi, causing ulcers in the small intestine.
● Clinical Features:-High fever, abdominal pain, diarrhea, and the
development of characteristic rose-colored spots on the trunk.
● Complications: -Perforation of the intestine, systemic complications.

Inflammatory Bowel Disease (Crohn's Disease and Ulcerative

Colitis):

● Pathogenesis:-Chronic inflammatory conditions of the gastrointestinal

tract with an autoimmune component.
● Clinical Features: -Diarrhea, abdominal pain, weight loss, and fatigue.
● Complications:-Bowel strictures, fistulas, increased risk of colorectal
cancer.

Colorectal Cancer:

● Pathogenesis:- Colorectal cancer originates in the colon or rectum and is

often associated with genetic factors, age, and lifestyle factors.
● Clinical Features:-Changes in bowel habits, blood in stools, abdominal
pain, and unintended weight loss.
● Complications:-Metastasis to other organs, bowel obstruction.

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 ● Diagnosis:-Colonoscopy with biopsy, imaging studies (CT scan, MRI).
● Treatment:-Surgical resection, chemotherapy, radiation therapy.

Liver:

Definition:-

The liver is a vital organ located in the upper right side of the abdomen. It plays a
crucial role in metabolism, detoxification, storage of nutrients, and the production
of proteins necessary for blood clotting.

Liver Hepatitis:

Pathogenesis:

➔ Hepatitis refers to inflammation of the liver, and it can be caused by

viral infections (Hepatitis A, B, C, D, E) or non-viral factors such as
alcohol, drugs, or autoimmune reactions.
➔ The viruses primarily target liver cells, leading to inflammation and
potential liver damage.
● Clinical Features:-Jaundice (yellowing of the skin and eyes), fatigue,
abdominal pain, nausea, vomiting, and dark urine.
● Complications:-Chronic hepatitis can progress to cirrhosis or liver cancer.
● Diagnosis:-Blood tests for liver enzymes and viral markers, imaging
studies (ultrasound).
● Treatment:-Supportive care, antiviral medications for viral hepatitis, and
lifestyle modifications.

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 Amoebic Liver Abscess:

Pathogenesis:

➔ Amoebic liver abscess is caused by the protozoan parasite

Entamoeba histolytica.
➔ The parasite typically infects the intestines and can travel to the liver,
forming abscesses.
● Clinical Features:-Fever, right upper abdominal pain, hepatomegaly
(enlarged liver), and in severe cases, jaundice.
● Complications:-Rupture of the abscess, leading to peritonitis or lung
involvement.
● Diagnosis:-Serologic tests, imaging studies (ultrasound, CT scan).

Antiparasitic medications, sometimes drainage of the abscess may be

required.

Cirrhosis of Liver:

Pathogenesis:

➔ Cirrhosis is the advanced scarring of the liver tissue, often a result of

chronic liver diseases such as chronic hepatitis or long-term alcohol
abuse.
➔ The scar tissue replaces healthy liver tissue, leading to impaired liver
function.
● Clinical Features:-Fatigue, weakness, ascites (fluid accumulation in the
abdomen), jaundice, and confusion (hepatic encephalopathy).

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 ● Complications:-Portal hypertension, esophageal varices, liver failure,
increased risk of liver cancer.
● Diagnosis:-Liver function tests, imaging studies (CT scan, MRI), liver
biopsy.
● Management of underlying causes (e.g., treatment of viral hepatitis,
alcohol cessation), supportive care, and in some cases, liver
transplantation.

Gall Bladder:

Definition:-

The gallbladder is a small organ located beneath the liver. Its primary function is
to store and concentrate bile produced by the liver, releasing it into the small
intestine to aid in the digestion of fats.

Gall Bladder: Cholecystitis:

Pathogenesis:

➔ Cholecystitis refers to inflammation of the gallbladder, often

associated with the presence of gallstones blocking the cystic duct.
➔ The blockage leads to the accumulation of bile and inflammation of
the gallbladder wall.
● Clinical Features:-Severe abdominal pain (typically in the right upper
quadrant), nausea, vomiting, fever.
● Complications:-Gallbladder perforation, abscess formation, and
sometimes progression to gangrenous cholecystitis.
● Diagnosis:-Ultrasound, blood tests (elevated liver enzymes), and
sometimes a HIDA scan.

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 ● Treatment:-Antibiotics for infection, pain management, and in severe
cases, surgical removal of the gallbladder (cholecystectomy).

Pancreas:

● The pancreas is a gland located behind the stomach that plays a crucial
role in digestion and blood sugar regulation. It produces digestive enzymes
and insulin.

Pancreas: Pancreatitis:

Pathogenesis:-

➔ Pancreatitis is inflammation of the pancreas, and it can be acute or

chronic.
➔ Acute pancreatitis is often caused by gallstones or excessive alcohol
consumption, while chronic pancreatitis may result from long-term
alcohol use or other conditions.
● Clinical Features:-Severe abdominal pain, nausea, vomiting, and
elevated levels of pancreatic enzymes in the blood.
● Complications:-Pancreatic necrosis, pseudocysts, and in chronic cases,
diabetes.
● Diagnosis tests (elevated amylase and lipase), imaging studies (CT scan,
MRI), and sometimes endoscopy.
● Treatment:-Supportive care (hydration, pain management), addressing
underlying causes (e.g., gallstone removal), and in severe cases, surgery.

Tumors of the Liver, Gall Bladder, and Pancreas:

Liver Tumors:

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 ● Hepatocellular Carcinoma:
● Primary liver cancer often associated with chronic liver disease (cirrhosis),
viral hepatitis, or alcohol abuse.
● Clinical features include abdominal pain, weight loss, and jaundice.
● Diagnosis involves imaging studies (CT scan, MRI) and biopsy.
● Treatment includes surgery, chemotherapy, or liver transplantation.

Gall Bladder Tumors:

Gallbladder Carcinoma:

● Cancer originating in the gallbladder, often associated with gallstones.

● Clinical features include abdominal pain, jaundice, and weight loss.
● Diagnosis involves imaging studies (ultrasound, CT scan) and biopsy.
● Treatment may involve surgery, chemotherapy, and sometimes radiation.

Pancreatic Tumors:

● Pancreatic Cancer (Pancreatic Adenocarcinoma):**

● Cancer of the pancreas, often diagnosed in advanced stages.
● Clinical features include abdominal pain, weight loss, and jaundice.
● Diagnosis involves imaging studies (CT scan, MRI) and biopsy.
● Treatment may include surgery, chemotherapy, and radiation.

Skeletal System:

Definition:

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The skeletal system, also known as the musculoskeletal system, is a complex
structure composed of bones, cartilage, joints, ligaments, and tendons. It
provides structural support, and protection for internal organs, facilitates
movement, and serves as a reservoir for minerals such as calcium and
phosphorus. The human skeleton is divided into the axial skeleton (skull,
vertebral column, ribcage) and the appendicular skeleton (limbs and girdles).

Bone:

Bone Healing:

Process:

● Bone healing, also known as bone regeneration or ossification, involves a

series of stages: hematoma formation, inflammation, soft callus formation,
hard callus formation, and remodeling.
● Hematoma formation occurs at the fracture site, followed by the influx of
inflammatory cells and the creation of a soft callus, which is gradually
replaced by a hard callus made of woven bone.
● The final stage involves remodeling, where the bone is reshaped to its
original form.
● Clinical Significance:-Adequate nutrition, immobilization, and proper
alignment of fractured bones support effective bone healing.

Osteoporosis:

Pathogenesis:-

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 ➔ Osteoporosis is characterized by the loss of bone density and
microarchitectural deterioration, leading to fragile bones.
➔ It often results from an imbalance between bone resorption and formation,
with aging, hormonal changes, and nutritional factors playing significant
roles.
● Clinical Features:-Increased susceptibility to fractures, particularly in the
spine, hip, and wrists.
● Diagnosis:-Bone density scans (DEXA scan).
● Treatment:-Calcium and vitamin D supplementation, weight-bearing
exercises, and medications to improve bone density.

Osteomyelitis:

Pathogenesis:-

➔ Osteomyelitis is an infection of the bone, often caused by bacteria

entering the bone tissue through open wounds, surgical procedures,
or the bloodstream.
● Clinical Features:-Localized pain, swelling, redness, and in severe cases,
systemic symptoms like fever.
● Diagnosis:-Blood cultures, imaging studies (X-rays, MRI), bone biopsy.
● Treatment:-Antibiotic therapy, drainage of abscesses, and sometimes
surgical debridement.

Bone Tumors:

Types:

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 ● Benign tumors (e.g., osteoma, osteochondroma) and malignant tumors
(e.g., osteosarcoma, chondrosarcoma).
● Clinical Features:-Pain, swelling, and sometimes pathological fractures.
● Diagnosis:-Imaging studies (X-rays, CT scans, MRI), biopsy.
● Treatment:-Surgical removal, chemotherapy, radiation therapy depending
on the type and stage of the tumor.

Joints:

Rheumatoid Arthritis:

Pathogenesis:

➔ Rheumatoid arthritis is an autoimmune disorder characterized by

chronic inflammation of synovial joints.
➔ The immune system attacks the synovium, leading to joint
inflammation, cartilage damage, and bone erosion.
● Clinical Features:- Symmetrical joint pain, swelling, morning stiffness, and
systemic symptoms like fatigue.
● Diagnosis: - Blood tests (rheumatoid factor, anti-CCP antibodies), imaging
studies (X-rays, MRI).
● Treatment: - Disease-modifying antirheumatic drugs (DMARDs),
nonsteroidal anti-inflammatory drugs (NSAIDs), and physical therapy.

Osteoarthritis:

Pathogenesis:-

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 ➔ Osteoarthritis is a degenerative joint disease resulting from the wear
and tear of joint cartilage over time.
➔ Cartilage breakdown leads to pain, swelling, and decreased joint
mobility.
● Clinical Features:-Joint pain, stiffness, and decreased range of motion.
● Diagnosis:-Clinical evaluation, imaging studies (X-rays, MRI).
● Treatment:-Pain management, physical therapy, lifestyle modifications,
joint replacement in severe cases.

Endocrine System:

Definition

The endocrine system is a complex network of glands and organs that produce
and release hormones, and chemical messengers that regulate various
physiological processes in the body. These hormones travel through the
bloodstream to target organs and tissues, where they play crucial roles in
maintaining homeostasis, growth and development, metabolism, and
reproductive functions.

Diabetes Mellitus:

● Pathogenesis Mellitus is a chronic metabolic disorder characterized by

elevated blood glucose levels due to either insufficient insulin production
(Type 1) or ineffective use of insulin (Type 2).
● Clinical Features:-Polyuria (excessive urination), polydipsia (excessive
thirst), polyphagia (excessive hunger), fatigue.
● Diagnosis:-Blood glucose tests (fasting glucose, oral glucose tolerance
test), HbA1c levels.

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● Treatment:-Insulin therapy, oral antidiabetic medications, lifestyle
modifications (diet, exercise).

Goiter:

● Pathogenesis refers to the enlargement of the thyroid gland, often due to

iodine deficiency, autoimmune disorders (like Hashimoto's thyroiditis), or
nodular growths (nodular goiter).
● Clinical Features:-Swelling or lump in the front of the neck, difficulty
swallowing or breathing, and in some cases, overproduction or
underproduction of thyroid hormones.
● Diagnosis:-Physical examination, ultrasound, blood tests measuring
thyroid hormone levels, and sometimes a thyroid scan.
● Treatment:-Depends on the underlying cause – iodine supplementation,
thyroid hormone replacement therapy, or surgery in certain cases.

Carcinoma Thyroid:

● Pathogenesis-Carcinoma thyroid refers to cancer of the thyroid gland. The

most common types include papillary and follicular thyroid cancer.
● Clinical Features:-Nodule or lump in the thyroid, difficulty swallowing,
changes in voice, advanced stages, symptoms related to metastasis.
● Diagnosis:-Fine needle aspiration (FNA) biopsy, ultrasound, CT scan, and
radioactive iodine scan.
● Treatment (thyroidectomy), radioactive iodine therapy, and in some cases,
external beam radiation therapy or targeted drug therapy.

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 UNIT - 3
Hematological tests for the diagnosis of
blood disorders

Hematological tests for the diagnosis of blood disorders

Hematological tests play a crucial role in diagnosing various blood disorders.

These tests provide valuable information about the composition, function, and
overall health of blood components. Here are some common hematological tests
used for the diagnosis of blood disorders:

1. Complete Blood Count (CBC):

➔ Purpose: To assess overall blood composition and identify abnormalities.

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 Components measured:

● Red Blood Cell (RBC) count

● Hemoglobin (Hb) concentration
● Hematocrit (Hct) levels
● White Blood Cell (WBC) count
● Platelet count
➔ Mean Corpuscular Volume (MCV),
➔ Mean Corpuscular Hemoglobin (MCH),
➔ Mean Corpuscular Hemoglobin Concentration (MCHC)

2. Peripheral Blood Smear:

➔ Purpose: To examine blood cells under a microscope for abnormalities in size,

shape, and structure.

Components examined:

● Red blood cells

● White blood cells
● Platelets

3. Blood Smear for Malaria Parasites:

➔ Purpose: To detect the presence of malaria parasites in red blood cells.

Components examined:

● Identification of Plasmodium species

(e.g., Plasmodium falciparum, Plasmodium vivax) in blood smears.

4. Coagulation Profile:

➔ Purpose: To assess the blood's ability to clot properly.

Components measured:

● Prothrombin Time (PT)

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 ● Partial Thromboplastin Time (PTT)
● International Normalized Ratio (INR)
● Fibrinogen levels

5. Blood Chemistry Tests:

Purpose: To evaluate the levels of various substances in the blood, providing

information about organ function and metabolic processes.

Components measured:

● Liver function tests (e.g., ALT, AST, bilirubin)

● Kidney function tests (e.g., creatinine, blood urea nitrogen)
● Electrolyte levels (e.g., sodium, potassium)
● Blood glucose levels

6. Bone Marrow Aspiration and Biopsy:

➔ Purpose: To examine the bone marrow for abnormalities in cell production.

Components examined:

● Cellular composition of the bone marrow

● Presence of abnormal cells (e.g., leukemia cells)

7. Hemoglobin Electrophoresis:

➔ Purpose: To identify and quantify different types of hemoglobin in the blood,

particularly useful in diagnosing hemoglobinopathies.

Components examined:

● Different forms of hemoglobin (e.g., HbA, HbS)

8. Flow Cytometry:

➔ Purpose: To analyze the characteristics of individual cells in a blood sample, often

used for immunophenotyping in leukemia and lymphoma.

Components examined:

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 ● Surface markers on blood cells

These hematological tests, when interpreted collectively, aid in the diagnosis and
monitoring of various blood disorders, including anemia, leukemia,
thrombocytopenia, clotting disorders, and hemoglobinopathies. Interpretation of
results often requires collaboration between hematologists, pathologists, and
other healthcare professionals.

Blood tests

include Hemoglobin (Hb), White Blood Cell (WBC) count, Platelet count, Packed
Cell Volume (PCV), and Erythrocyte Sedimentation Rate (ESR), provide
essential information about the composition and characteristics of the blood.
Here's an overview of each test:

1. Hemoglobin (Hb):

Purpose: Measures the concentration of hemoglobin, the oxygen-carrying protein

in red blood cells.

Clinical Significance:

● Low Hb levels may indicate anemia.

● High Hb levels may occur in conditions like polycythemia.

2. White Blood Cell (WBC) Count:

● Purpose: Determines the number of white blood cells in a specified volume

of blood.

Clinical Significance:

● An elevated WBC count may indicate infection, inflammation, or leukemia.

● Low WBC count may be seen in certain viral infections or bone marrow
disorders.

3. Platelet Count:

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Purpose: Measures the number of platelets in the blood.

Clinical Significance:

● Low platelet count (thrombocytopenia) may lead to bleeding disorders.

● High platelet count (thrombocytosis) may be associated with inflammatory
conditions or myeloproliferative disorders.

4. Packed Cell Volume (PCV) or Hematocrit (Hct):

Purpose: Indicates the proportion of blood that is composed of red blood cells.

Clinical Significance:

● Low PCV may indicate anemia.

● High PCV may be seen in conditions like polycythemia.

5. Erythrocyte Sedimentation Rate (ESR):

Purpose: Measures the rate at which red blood cells settle in a tube of blood over
time.

Clinical Significance:

● Elevated ESR is a non-specific indicator of inflammation in the body.

● It may be increased in conditions such as infections, autoimmune
diseases, and certain cancers.

Interpreting these blood tests is essential for diagnosing and monitoring various
health conditions. Abnormalities in these parameters may prompt further
investigations, such as blood smears, bone marrow examinations, or additional
specialized tests, to determine the underlying cause of the abnormalities.
Healthcare professionals use these results in conjunction with the patient's
medical history and physical examination to make accurate diagnoses and
formulate appropriate treatment plans.

Coagulation tests

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play a crucial role in assessing the blood's ability to clot properly. Here's an
overview of three common coagulation tests: Bleeding Time (BT), Prothrombin
Time (PT), and Activated Partial Thromboplastin Time (APTT):

1. Bleeding Time (BT):

Purpose: Measures the time for small blood vessels to stop bleeding after a
standardized skin incision.

Procedure:

● A blood pressure cuff is inflated on the upper arm, and a small incision is
made on the lower arm.
● The time it takes for bleeding to stop is recorded.

Clinical Significance:

● Prolonged bleeding time may indicate platelet dysfunction or disorders.

2. Prothrombin Time (PT):

Purpose: Evaluate the extrinsic and common pathways of the coagulation

cascade.

Procedure:

● Blood is mixed with a reagent that triggers clotting, and the time taken for
clot formation is measured.

Clinical Significance:

● Monitors the effects of warfarin (coumarin) anticoagulant therapy.

● Assess the integrity of the extrinsic pathway.
● Elevated PT may indicate liver dysfunction or vitamin K deficiency.

3. Activated Partial Thromboplastin Time (APTT):

Purpose: Evaluate the intrinsic and common pathways of the coagulation

cascade.

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Procedure:

● Blood is mixed with a reagent that activates the intrinsic pathway, and the
time taken for clot formation is measured.

Clinical Significance:

● Monitors the effects of heparin anticoagulant therapy.

● Assess the integrity of the intrinsic pathway.
● Prolonged APTT may indicate hemophilia or other clotting factor
deficiencies.

Blood chemistry

also known as blood tests or blood panels, involves analyzing the chemical
components present in the blood to assess various aspects of health and
diagnose medical conditions. Blood chemistry tests provide valuable information
about organ function, metabolic processes, and overall health. Here are some
common components measured in blood chemistry:

1. Liver Function Tests:

Components measured:

● Alanine aminotransferase (ALT)

● Aspartate aminotransferase (AST)
● Alkaline phosphatase (ALP)
● Bilirubin

Clinical Significance:

● Assess liver function and detect liver diseases.

2. Kidney Function Tests:

Components measured:

● Blood urea nitrogen (BUN)

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 ● Creatinine
● Glomerular filtration rate (GFR)

Clinical Significance:

● Evaluate kidney function and detect renal disorders.

3. Electrolytes:

Components measured:

● Sodium (Na)
● Potassium (K)
● Chloride (Cl)
● Bicarbonate (HCO3)

Clinical Significance:

● Assess electrolyte balance and detect imbalances that can affect various
bodily functions.

4. Blood Glucose:

Components measured:

● Fasting blood glucose

● Hemoglobin A1c (HbA1c)

Clinical Significance:

● Diagnose and monitor diabetes mellitus.

5. Lipid Profile:

Components measured:

● Total cholesterol
● Low-density lipoprotein (LDL) cholesterol
● High-density lipoprotein (HDL) cholesterol
● Triglycerides

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Clinical Significance:

● Assess cardiovascular risk and monitor lipid metabolism.

6. Blood Proteins:

Components measured:

● Albumin
● Total protein
● Globulins

Clinical Significance:

● Evaluate nutritional status and liver function.

7. Thyroid Function Tests:

Components measured:

● Thyroid-stimulating hormone (TSH)

● Free thyroxine (T4)
● Triiodothyronine (T3)

Clinical Significance:

● Assess thyroid function and diagnose thyroid disorders.

8. Markers of Inflammation:

Components measured:

● C-reactive protein (CRP)

● Erythrocyte Sedimentation Rate (ESR)

Clinical Significance:

● Indicate the presence of inflammation in the body.

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Blood chemistry tests are valuable tools for healthcare professionals in
diagnosing and monitoring various medical conditions. The interpretation of
results is often done in conjunction with other diagnostic tests, medical history,
and physical examination findings to comprehensively assess a patient's health.

Blood Bank:

1. Blood Grouping and Cross-Matching:

Blood Grouping:

Identifying the ABO and RhD blood group of an individual (A, B, AB, O, and
Rh-positive or Rh-negative).

Cross-Matching:

● Testing compatibility between donor and recipient blood to prevent

transfusion reactions.
● Mixing donor red blood cells with recipient plasma (major cross-match) and
vice versa (minor cross-match) to ensure compatibility.

2. Blood Components:

Red Blood Cells (RBCs):

● Used to treat anemia, surgery, and trauma.

Platelets:

● Essential for blood clotting; used in treating bleeding disorders or cancer

patients.

Plasma:

● The liquid component of blood contains water, electrolytes, proteins, and

clotting factors.

Cryoprecipitate:

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 ● Rich in clotting factors; used to manage bleeding disorders.

3. Plasmapheresis:

Purpose:

● A medical procedure involving the removal, treatment, and return of blood

plasma.
● Used to treat autoimmune disorders, remove harmful substances, or
collect plasma for donation.

Procedure:

● Blood is drawn, plasma is separated, and the remaining components are

returned to the donor or patient.

4. Transfusion Reactions:

Hemolytic Reaction:

● Occurs when there is an ABO or Rh incompatibility between donor and

recipient blood.
● Symptoms include fever, chills, back pain, hemoglobinuria, and renal
failure.

Febrile Non-Hemolytic Reaction:

● Caused by antibodies to donor white blood cells.

● Symptoms include fever, chills, and headache.

Allergic Reaction:

● Caused by sensitivity to plasma proteins.

● Symptoms include itching, hives, and respiratory distress.

Graft-versus-Host Disease (GVHD):

● Rare but serious; occurs when donor T cells attack the recipient's tissues.
● Symptoms include rash, diarrhea, and liver dysfunction.

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Blood Bank Safety Measures:

● Stringent screening of donors for infectious diseases.

● Accurate labeling and documentation of blood units.
● Use of advanced testing methods to ensure compatibility.
● Immediate recognition and management of transfusion reactions.

The Blood Bank plays a critical role in providing safe and compatible blood
products for transfusions. Adhering to strict protocols and safety measures is
crucial to prevent adverse reactions and ensure the well-being of both donors
and recipients.

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