Puviyarasi MSC Nursing,PATHOLOGY UNIT-1.pptx

Definition
 Pathology is the scientific study (logos) of
disease (pathos). It mainly focuses on the
study of the structural and functional changes
in cells, tissues, and organs in disease.

Study of Pathology
Etiology: The etiology of a disease is its cause.
The causative factors of a disease can be
divided into two major categories: genetic and
acquired (e.g. infectious, chemical, hypoxia,
nutritional, physical). Most common diseases
are multifactorial due to combination of causes
(genetic and acquired).

Pathogenesis: It refers to the mechanism by
which the causative factor/s produces
structural and functional abnormalities. In
infectious disorders (due to bacteria, viruses,
etc.), the period between exposure to the
causative agent and the development of
disease is called the incubation period.

Morphologic changes: All diseases start with
structural changes in cells. The morphologic
changes refer to the gross and microscopic
structural changes in cells or tissues affected
by the disease. Rudolf Virchow (known as the
Father of modern pathology) proposed that
injury to the cell is the basis of all disease. If
the structural changes are characteristic of a
disease or diagnostic of an etiologic process it
is called as pathognomonic.

Clinical manifestations: The structural changes
in cells and tissues produce functional
abnormalities. These functional derangements
give rise to clinical manifestations (symptoms
and signs) of disease. Diseases characterized
by multiple abnormalities are called
syndromes.

 Prognosis: The prognosis forecasts or
predicts the likely outcome of the disease and
therefore, the fate of the patient.
 Complications: It is a negative pathologic
process or event occurring during the course
of a disease and usually aggravating the
illness.
For example, perforation and hemorrhage are
complications which may develop in typhoid
ulcer of intestine.

IMPORTANCE OF THE STUDY
OF PATHOLOGY
Pathology is a vital (extremely important) component of medical
education for all doctors, nurses and other health care
practitioners.
 Pathology knowledge is fundamental to modern medical
practice and health care.
 Pathology is the basic foundation for clinical medicine and is
used in the diagnosis, treatment and management of a
disease condition.
 Pathology investigations are an integral part of the clinical
consultation. Most of the health care decisions affecting
diagnosis or treatment involve pathology.
 Knowledge of pathology is essential for the prevention, early
detection, diagnosis and treatment of many of the disease.

CELLULAR RESPONSES TO
STRESS AND INJURIOUS
STIMULI
Types of Cellular Responses to Injury
Depending on the nature of stimulus/injury, the
cellular responses may be mainly divided into four
types.
 1. Cellular adaptations
 2. Cell injury
 Reversible cell injury: Cellular swelling, fatty change
 Irreversible cell injury: Necrosis,apoptosis
 3. Intracellular accumulations
 4. Pathologic calcification

1.CELLULAR ADAPTATIONS
 When the cell is exposed to pathological
stimuli, it undergoes a series of
metabolicchanges known as cell stress. The
cells can undergo adaptation to damaging
stimuli, and achieve a new, steady altered
state that allows the cells to survive and
continue to function in an abnormal
environment.
 Cells can adapt to certain pathologic stimuli
by changes in size, number or differentiation of
cells in affected tissue. These are reversible
changes and constitute cellular adaptations.

Types of Adaptations
The types adaptations include:
 hypertrophy,
 hyperplasia,
 atrophy
 metaplasia

Hypertrophy
Definition:
Hypertrophy is defined as an increase in the size
of the tissue or organ due to increase in the
size of cells.
 It develops in organs composed of non
dividing cells such as muscles, e.g. cardiac
and skeletal muscles.

Causes
 Hypertrophy can be physiological or
pathological.

Physiological
It occurs when there is increased functional
demand/workload.
 Hypertrophy of skeletal muscle: For
examples, the bulging muscles of body-
builders, manual laborer and athletes and
those engaged in "pumping iron".
 Hypertrophy of smooth muscle: For
example, growth of the uterus during
pregnancy from estrogenic (hormone)
stimulation.

Pathological
It is caused by increased functional
demand/workload.
 Hypertrophy of cardiac muscle: For
examples, left ventricular hypertrophy due to
hypertension or damaged heart valves (aortic
stenosis, mitral incompetence).

 Hypertrophy of smooth muscle: For
examples, hypertrophy of urinary bladder
muscle in response to urethral obstruction
(e.g. prostate hyperplasia).

Hyperplasia
 Definition: Hyperplasia is defined as an
increase in the number of cells in an organ or
tissue, usually resulting in increased size/
mass of the organ or tissue

Causes
Physiological: It can be caused by hormonal
stimulation, or as compensatory process.
 Hyperplasia due to hormones: For
examples, hyperplasia of glandular epithelium
of the female breast at puberty, pregnancy and
lactation, hyperplasia of the uterus during
pregnancy.
 Compensatory hyperplasia: For example, in
liver following partial hepatectomy (removal of
part of liver) the remaining normal liver cells
proliferate and may grow back to its original
size.

Pathological: It may be due to excessive endocrine
stimulation or chronic injury/ irritation.
 Excessive hormonal stimulation: For example,
endometrial hyperplasia (due to estrogen) and
benign prostatic hyperplasia due to androgens
 Chronic injury/irritation: Long-standing
inflammation or chronic injury may lead to
hyperplasia especially in skin or oral mucosa.
 Pathological hyperplasia can progress to cancer.
For example, endometrial hyperplasia can
develop into endometrial cancer.

Morphology
 Gross: The size of the affected organ is
increased
 Microscopy: Shows increased number of
cells

Atrophy
 Definition: Atrophy is defined as reduced size
of an organ or tissue resulting from decrease
in cell size and number. In atrophy, function of
an organ is also reduced.

Causes
Atrophy may be physiological or pathological

Physiological
It is common during normal fetal development,
and in adult life.
 During fetal development: Atrophy of
embryonic structures, e.g. thyroglossal duct.
 During adult life: For examples, involution of
thymus, atrophy of brain and heart due to
aging (senile atrophy).

Pathological:
It can be local or generalized.
 Local : Disuse atrophy (decreased workload): Atrophy of
limb muscles immobilized in a plaster cast (as treatment for
fracture) or after prolonged bed rest.
 Denervation (loss of innervations) atrophy: For example,
atrophy of muscle due to damage to the nerves as in
poliomyelitis.
 Ischemic (diminished blood supply) atrophy: Brain atrophy
produced by ischemia due to atherosclerosis of the carotid
artery.
 Pressure atrophy: For example, atrophy of renal
parenchyma in hydronephrosis (distention of the pelvis and
calices of the kidney with urine, as a result of obstruction of
the ureter).

Generalized
 Starvation (inadequate nutrition) atrophy: For
example, protein-calorie malnutrition

Morphology
 Gross: The organ is small and often shrunken.
 Microscopy: The cells are smaller in size.

METAPLASIA
Definition: Metaplasia is defined as a reversible
change in which one adult cell type (epithelial
or mesenchymal) is replaced by another adult
cell type

Types of Metaplasia
 There are two types namely
 epithelial
 mesenchymal.

1. Epithelial metaplasia: It is the most common type of
metaplasia.
 Squamous metaplasia: In this the original epithelium is
replaced by squamous epithelium.
 Respiratory tract: Chronic irritation due to tobacco smoke,
the normal ciliated columnar epithelial cells of the trachea
and bronchi are replaced by squamous epithelium
 Cervix: Squamous metaplasia in cervix is associated with
chronic infection.
 Columnar metaplasia: The subtypes are:
 Squamous to columnar: In Barrett esophagus the
squamous epithelium of the esophagus replaced by columnar
cells.
 Intestinal metaplasia: The gastric glands are replaced by
cells resembling those of the small intestine.

2. Connective tissue
metaplasia
 Osseous metaplasia: Formation of new bone
at sites of tissue injury is known as osseous
metaplasia. Bone formation in muscle, known
as myositis ossificans, occasionally occurs
after intramuscular hemorrhage.

Causes of Cell Injury
Reduced Oxygen Supply
 Hypoxia refers to inadequate oxygenation of
tissues. Hypoxia is an important and common
cause of cell injury and cell death. Hypoxia
may be due to decreased blood flow (called
ischemia) or inadequate oxygenation of the
blood.

Physical Agents
 These include: mechanical trauma, radiation,
electric shock, sudden atmospheric pressure
changes and thermal injury

Chemical Agents
 This includes a wide variety of agents such as:
 Heavy metals and poisons (e.g. arsenic, mercuric
salts or cyanide)
 Chemicals, strong acids and alkalies
 Environmental and air pollutants (e.g.insecticides and
herbicides)
 Industrial and occupational hazards (carbon monoxide
and asbestos)
 Other chemicals like alcohol and cigarette smoking
 Iatrogenic, i.e. the consequence of taking a drug
prescribed by the physician can produce undesirable
effects.

Infectious Agents
 These include viruses, bacteria, fungi,
rickettsiae and parasites.

Abnormal Immunologic Reactions
 The immune system is required for defense
against infectious pathogens. However,
abnormal immune reactions itself may cause
cell injury
 Autoimmunity: Immune reactions to self-
antigens can result in autoimmune diseases.
 Hypersensitivity reactions: Exaggerated
immune reactions may cause cell injury

Nutritional Imbalances
 It may result from either nutritional deficiencies
(deficiencies of specific vitamins) or nutritional
excesses (excess of cholesterol predisposes
to atherosclerosis). Obesity is associated with
several diseases,such as diabetes.

Genetic Factors
 Diseases may result from abnormal mutated
genes or chromosomal abnormalities (e.g.
Down syndrome). Genetic defects may cause
cell injury

Idiopathic
 Idiopathic diseases are those in which the
cause is not known

Types of Cell Injury
 The cell injury may be mainly divided into
reversible and irreversible. Reversible injury
may progress to an reversible stage and result
in cell death.

Reversible Cell Injury
 If the stimulus is acute and brief or mild, the
cell injury produces changes in the cells which
are reversible up to a certain point.
 Light microscopic features of reversible cell
injury: There are two patterns of reversible cell
injury namely cellular swelling and fatty
change.

Irreversible Cell Injury
 If the cell is exposed to continuous injurious
stimulus or if the injury is severe, the cells
undergo cell death. There are two main types
cell death namely necrosis and apoptosis.
Necrosis: Necrosis is always a pathologic
process

NECROSIS
 Definition: Necrosis is the morphological
changes indicative of cell death in a living
tissue following extremely harmful injury.

Causes of Necrosis
 All the causes of cell injury if severe, persistent
can cause necrosis

Morphology
 The general changes occurring in necrotic cell, irrespective of type
of necrosis are as follows:
 Cytoplasmic changes: Increased eosinophilia.
 Nuclear changes : These may take up one of the three following
patterns.
 Pyknosis: It is characterized by shrinkage of nucleus which
appears solid, shrunken and (blue) stains deeply basophilic (similar
to ink drop).
 Karyolysis: This manifests as progressive fading of basophilic
staining of the nuclei and leads to ghost nuclei.
 Karyorrhexis: The pyknotic nucleus breaks up into many smaller
fragments.
 Inflammatory reaction: The necrotic cells bring out acute
inflammatory reaction in the surrounding tissue.

Patterns/Types of Tissue
Necrosis
 1. Coagulative Necrosis
 It is a common type of necrosis in which the
outline of dead tissues in preserved for few
days. A localized area of coagulative necrosis
is known as infarct.
Causes:Ischemia caused by obstruction in a
vessel, potent bacterial toxins, phenol,
mercury and other corrosive chemicals.

Gross:
 Organs affected: All organs except the brain.
More frequently involved are heart, kidney and
spleen
 Appearance: The involved tissue has an
opaque appearance similar to that of boiled
meat. The necrotic tissues appear dry, pale,
yellow and soft in consistency.
Microscopy: The outline of dead tissue is
preserved for some days. Nuclear and
cytoplasmic changes take place as described
under necrosis above.

2. Liquefactive Necrosis (Colliquative
Necrosis)
 The term is applied in which the dead tissue
rapidly undergoes softening and transformed
into a liquid viscous mass.

Causes:
 Ischemic injury to central nervous system
(CNS)
 Suppurative infections: Focal infectionsnby
bacteria which stimulate the accumulation of
leukocytes

Organs affected: Brain, abscess (any organ or
tissue). The necrotic area in the brain is soft and
center is liquefied.
Microscopy: Abscess is localized collection of pus.
It consists of a cavity containing pus formed by
liquefactive necrosis and inflammatory cells in a
solid tissue. Pus consists of liquefied necrotic cell
debris, dead leukocytes and macrophages
(scavenger cells). Abscess shows a cavity
containing pus and surrounding wall with
granulation tissue and inflammatory cells.

3. Caseous Necrosis
 It is a distinctive type of necrosis. This shows
combined features of both coagulative and
liquefactive necrosis.
 Cause: It is characteristic of tuberculosis and
is due to hypersensitivity reaction.

Gross:
 Organs affected: Tuberculosis may involve
any organ. Most common are lung and lymph
nodes.
 Appearance: The necrotic area appears
yellowish-white, soft, granular, friable and
sharply circumscribed.The necrotic tissue
resembles dry, clumpy cheese, hence the
name caseous (cheese- like) necrosis.

Microscopy:
 It is characterized by a focal lesion known as a
granuloma. The granuloma in tuberculosis is
tuberculous granuloma or tubercle. The
granulomas may be caseating (soft
granuloma) or noncaseating (hard granuloma).

4. Fat Necrosis
 It refers to a focal areas of fat destruction,
which affect adipose tissue.
Types: The two types are enzymatic and
traumatic. The most common is enzymatic
necrosis resulting from pancreatitis.
 Enzymatic fat necrosis: It is peculiar to
adipose tissue around acutely inflamed
pancreas (in acute pancreatitis).

Mechanism: In pancreatitis, the enzymes leak
from the injured pancreatic acinar cells and
cause tissue damage. The activated lipase
enzyme destroys fat cells and liberates free
fatty acids. These fatty acids combine with
calcium and are precipitated as calcium soaps
(fat saponification).
Gross: Fat necrosis appears as chalky-white
areas.
Microscopy: The necrotic foci appear as fat
cells with pale, shadowy outlines, surrounded
by an inflammatory reaction.

 Traumatic fat necrosis: It occurs in tissues
with high fat content (like in breast and thigh)
following severe trauma.

5. Fibrinoid Necrosis
 It is a special form of necrosis characterized by
deposition of pink-staining (fibrin-
like)proteinaceous material. It usually involves
arteries and walls of arterioles and glomeruli of
the kidney. It is usually seen in immune
mediated vascular injury

6. Gangrene (Gangrenous Necrosis)
Definition: Gangrene is defined as massive
necrosis with superadded putrefaction.
Putrefaction is decomposition by
microorganisms, resulting in production of foul
smelling substances and gas.
 Types: It is mainly of two types namely dry
and wet gangrene. A variant of wet gangrene
known as gas gangrene is caused by clostridia
(Gram positive anaerobic bacteria).

Dry gangrene
Causes: Arterial occlusion (e.g. atherosclerosis).
 Sites: It usually involves a limb, generally the
distal part of lower limb (leg, foot and toe).
 Gross: The affected part is dry, shrunken,
shriveled, (mummified) and dark brown or black in
color resembling the foot of a mummy. The black
color is due to the iron sulfide. A line of
demarcation is usually seen between gangrenous
and adjacent normal area.
 Microscopy: The necrosis shows smudging of
soft tissue and overlying skin. The line of
demarcation consists of granulation tissue with
inflammatory cells.

Wet gangrene
 Sites: Usually occurs in moist tissues or organs
(e.g. bowel, lung, mouth, etc.).
 Causes: Usually due to the venous blockage (e.g.
strangulated hernia, intussusception or volvulus).
In diabetics, the gangrene foot is of wet type
because of the high sugar content in the necrotic
tissue which favors growth of bacteria.
 Gross: The affected part is soft, swollen,putrid,
rotten and dark. There is no clear line of
demarcation between the gangrenous part and
viable part.
 Microscopy: It is usually liquefactive type of
necrosis.

Gas gangrene:
 It is a special type of wet gangrene caused by
infection with gas forming anaerobic clostridia.

7. Gummatous Necrosis
 The necrotic tissue is firm and rubbery and the
original architecture can be seen on
histological examination. It is usually found in
syphilis.

APOPTOSIS
 Definition: Apoptosis is a type cell death in
which cells activate enzymes that degrade the
cell's own nuclear DNA and nuclear and
cytoplasmic proteins.

Causes of Apoptosis
 Apoptosis may be physiological or
pathological.

Physiological Situations
 Apoptosis is a physical process during embryogenesis,
development and throughout adulthood. Important
physiologic situations associated with apoptosis are:
 Removal of excess cells during embryogenesis and
developmental processes: For example, disappearance of
web tissues between fingers and toes.
 Elimination of cells after withdrawal of hormonal stimuli: For
example, Endometrial cell breakdown during the menstrual
cycle.
 Elimination of cells after withdrawal of tropic stimuli: For
example, neutrophils in an acute inflammatory response,
lymphocytes after immune response
 Elimination of potentially harmful cells: In immunology, the
clones of self-reactive lymphocytes that recognize normal self
antigens are deleted by apoptosis.

Pathological Conditions
 Apoptosis is responsible for cell loss in many
pathologic states. For example, elimination of
cells with damaged DNA, killing of viral
infected cells, elimination of neoplastic cells
and elimination of parenchymal cells in
pathologic atrophy

INTRACELLULAR
ACCUMULATIONS
 Metabolic derangements may result in
retention or excess accumulation of various
substances inside the cells. Intracellular
accumulation of substance may occur by two
mechanisms.

 Accumulation of excess amount of normal
cellular constituent: This occurs when normal
substance is produced at a normal or
increased rate, but the rate of metabolism is
inadequate to remove it. For examples, water,
lipids, proteins, carbohydrates (glycogen), etc.

Accumulation of an abnormal substance:
The abnormal substance may be:
 Exogenous: Abnormal substances accumulate
because the cell can neither degrade the
substance nor has the ability to transport it to
other sites. For examples, accumulations of
carbon articles, inhaled silica, injected tattoo
pigments.
 Endogenous: Substances that cannot be
metabolized because of deficiency or defect of the
enzyme and thus accumulate in cells. These are
usually due to the genetic defect, e.g. hereditary
storage diseases.

Steatosis (Fatty Change)
 Definition: Steatosis or fatty change is defined
as abnormal accumulations of triglycerides
within parenchymal cells.

Fatty Liver
 Definition: Steatosis (fatty change) of liver is
defined as abnormal accumulations of
triglycerides within parenchymal cells of
liver.es
 Mild fatty change may not have any effect on
cellular function. But more severe fatty change
may impair cell function and lead to cell death.

Morphology of fatty liver
 Gross: Liver is enlarged and becomes yellow,
soft and greasy to touch.
 Microscopy: Accumulation of fat is first seen as
small vacuoles in the cytoplasm around the
nucleus. As the process progresses the
vacuoles coalesce, creating cleared spaces
that displace the nucleus to the periphery of
the cell . Occasionally contiguous cells rupture
and the enclosed fat globules coalesce,
producing so-called fatty cysts.

Demonstration of Fat
 In fatty change, the fat appears as clear
vacuoles within parenchymal cells of the
involved organ when stained with Hematoxylin
and Eosin. The clear vacuole can be
demonstrated as fat by frozen sections stained
with Sudan IV or Oil Red-o, both stains give an
orange-red color to the contained fat. Osmic
acid can also used which gives a black color.

Heart
 Lipid in the cardiac muscle can have two patterns.
 Alternate involvement: Prolonged moderate
hypoxia (e.g. severe anemia), causes intracellular
deposits of fat, which create grossly apparent
bands of involved yellow myocardium alternating
with bands of darker, red-brown, uninvolved
myocardium (tigered effect, tabby cat
appearance).
 Uniform involvement: More severe hypoxia or
some types of myocarditis (e.g. diphtheria
infection) shows more uniform involvement of
myocardial fibers.

PATHOLOGIC CALCIFICATION
Definition: Pathologic calcification is the
abnormal deposition of calcium salts (together
with minute quantities of other mineral salts) in
tissues other than osteoid or enamel.

Types
There are two categories
 pathologic calcification namely dystrophic
calcification
 metastatic calcification.

Dystrophic Calcification
 Definition: Deposition of calcium salts in dying or
dead tissues is known as dystrophic calcification.
Causes:
 Necrotic tissue: Dystrophic calcification is
encountered in areas of necrosis, e.g. caseous,
enzymatic fat necrosis. Calcification can occur in
dead eggs of Schistosoma, cysticercosis, hydatid
cysts.Degenerating tissue: Examples include:
 Heart valves: Dystrophic calcification may occur in
aging or damaged heart valves.

 Metastatic Calcification
 Definition: Deposition of calcium salts in
apparently normal tissues is known as
metastatic calcification. Metastatic calcification
is almost always associated with an increased
serum calcium concentration(hypercalcemia)
secondary to deranged calcium metabolism.

 Causes: Calcification is seen in various disorders,
including chronic renal failure, vitamin D
intoxication, and hyperparathyroidism. There are
four principal causes of hypercalcemia:
 1. Increased secretion of parathyroid hormone
(PTH) with subsequent bone resorption
 2. Destruction of bone tissue: Secondaryto
primary tumors of bone marrow (e.g. multiple
myeloma, leukemia).
 3. Vitamin D-related disorders: Vitamin D
intoxication.
 4. Renal failure: It causes retention of phosphate,
leading to secondary hyperparathyroidism.

Sites: Any disorder with hypercalcemia can lead
to metastatic calcification in any normal tissue
throughout the body, but principally affects the
following locations:
 Lungs
 Kidney
 Blood vessels
 Stomach.

Morphology of Calcification
Gross
 Calcium salts appear as fine, white granules or
clumps. On palpation they feel gritty and sand
like deposits.
Microscopy
 Calcium salts have a basophilic, amorphous
granular, sometimes clumped appearance.

HYALINE CHANGE
 Definition: The term hyaline usually refers to
an alteration within cells or in the extracellular
space which gives a homogeneous, glassy,
pink appearance in routine histological
sections.

Causes
Intracellular hyaline
 Mallory body in the liver is alcoholic hepatitis
 Russell bodies are excessive accumulation of
immunoglobulins in the plasma cells.
Extracellular hyaline
 Collagenous fibrous tissue in old scars
 Hyaline change in uterine leiomyoma
 - In chronic glomerulonephritis, the glomeruli show
hyalinization.

INFLAMMATION
Definition: Inflammation is a complex local
response of the living vascularized tissues to
injury. It mainly consists of responses of blood
vessels and leukocytes.

Type of Inflammation
 Inflammation may be divided into acute or chronic.
The differences between acute and chronic
inflammation
 Inflammation is usually a protective beneficial
response. It localizes the cause of cell injury such
as microorganism, foreign particles, or any other
injurious agents.
 Sometimes inflammation may be harmful. For
example, destruction of joint in septic arthritis,
hypersensitivity reactions and autoimmune
diseases

Cardinal Sign of Inflammation
 Cornelius Celsus first described the four
cardinal signs of inflammation: rubor
(redness), tumor (swelling), calor (heat), and
dolor (pain). A fifth clinical sign, loss of function
(functio laesa) was later added by Rudolf
Virchow.

ACUTE INFLAMMATION
 Causes of (Stimuli for) Acute Inflammation
 Infections (bacterial, viral, fungal, parasitic) and
microbial toxins
 Tissue necrosis: This may develop due to ischemia
 Physical agents: include mechanical trauma,
radiation, electric shock and sudden changes in
atmospheric pressure.
 Chemical injury: include strong acids and alkalis,
insecticides, etc.
 Foreign bodies.
 Immune reactions

SEQUENCE OF EVENTS IN
ACUTE INFLAMMATION
Two major components of acute inflammation
are:
 Reactions of blood vessels (vascular changes)
 Reactions of leukocytes (cellular events).

Reactions of Blood Vessels (Vascular Events)
 Purpose: Reactive changes in the blood
vessels deliver the circulating cells, fluid and
plasma proteins from the blood circulation to
sites of tissue injury (e.g. infection).
Changes in blood vessel: It consists of
 (1) changes in the vascular flow and caliber
(hemodynamic changes) and
 (2) increased vascular permeability

1. Changes in vascular flow and
caliber
The changes are as follows:
 Vasodilatation and increased blood flow: The
earliest change of acute inflammation is dilatation
of the arterioles in the injured site. Vasodilatation
results in increased blood flow and is responsible
for the local heat (calor) and redness (rubor).
 Increased vascular permeability: Vasodilatation is
followed by increased permeability of the
microvasculature (which consists of arteriole,
capillaries and venules). Increased vascular
permeability leads to escape of protein-rich fluid
from the blood circulation into the extravascular
tissues (causing edema).

 Slowing of blood flow: The loss of fluid along
with vasodilatation results in slowing of blood
flow, and concentration of RBCs in small
vessels.
 Stasis: In the dilated small vessels with slowed
blood flow, the slow moving RBCs get packed,
a condition named stasis. It is responsible for
localized redness (rubor).
 Reaction of leukocytes (leukocyte events)

 2.Increased vascular permeability (vascular
leakage): It results in escape of protein-rich
fluid from the blood circulation into the
extravascular tissues

Definitions
 Exudation: It is the process of escape of fluid,
proteins and circulating blood cells from the
blood vessels into the interstitial tissue or body
cavities. Increased vascular permeability
causes escape of a protein-rich fluid (exudate)
resulting in edema (tumor).
 Edema: It is defined as accumulation of
excess of fluid in the interstitial tissue or
serous cavities. It can be either an exudate or
a transudate

MORPHOLOGIC PATTERNS OF ACUTE
INFLAMMATION
 Serous Inflammation
 Serous inflammation is characterized by marked
outpouring of a thin serous fluid. Accumulation of
serous fluid in serous cavities (peritoneal, pleural,
and pericardial) is called an effusion. A serous
effusion has a yellow, straw-like color and
microscopically shows either few or no cells.
 Example: Pleural effusion as a complication of
lobar pneumonia.

CHRONIC INFLAMMATION
 Definition: Chronic inflammation is defined as
inflammation of prolonged duration(weeks or
months) in which inflammation, tissue
damage, and healing occurs at same time.

 Chronic inflammation may develop when acute
inflammation does not resolve or chronic
inflammation may begin as chronic from the
beginning as insidious/ gradual low-grade
inflammatory reaction.
 Chronic inflammation can cause disabling
tissue damage, e.g. rheumatoid arthritis,
tuberculosis and atherosclerosis

Causes of Chronic
Inflammation
 Persistent infections by microbes which are
difficult to eradicate, e.g. mycobacteria. Immune-
mediated inflammatory diseases: Chronic
inflammation may be caused by abnormal
activation of the immune system. These include
immune mediated diseases such as autoimmune
diseases and allergic reactions.
 Prolonged exposure to potentially toxic agents:
When a toxic agent (either exogenous or
endogenous) cannot be degraded, it may result in
chronic inflammation. For example, silicosis
caused by inhalation of silica particles which
cannot be degraded.

Morphologic Features
Chronic inflammation is characterized by:
 Mononuclear cell infiltrate: These include cells
with single nucleus namely macrophages,
lymphocytes, and plasma cells.
 Tissue destruction: This is due to persistence of
injurious agent or by the inflammatory cells
themselves.
 Healing by fibrosis:Tissue destruction is
accompanied by an attempt to heal. The damaged
tissue is replaced by granulation tissue which later
leads to fibrosis

GRANULOMATOUS
INFLAMMATION
 Granulomatous inflammation is a distinctive
pattern of chronic inflammation. It is produced
by limited number of Infectious as well as
noninfectious conditions and involves immune
reactions. The microscopic feature is the
presence of granuloma.

Granuloma
Definition: A granuloma is defined as a
distinctive type of chronic inflammation
characterized by microscopic aggregation of
macrophages that are transformed into
epithelium-like (epithelioid) cells, surrounded
by lymphocytes and occasional plasma cells.
 Older granulomas in addition shows rim of
fibroblasts and connective tissue as the
outermost layer.

Types of Granuloma
 Granulomas are divided into two types
according to pathogenesis.
 Foreign body granulomas: It is caused by inert
foreign bodies. For examples, foreign body
granulomas form around material such as sutures
and talc.
 Immune granulomas: They are caused by poorly
degradable or particulate agents which can
induce cell-mediated immune response. For
example, the most common immune granuloma is
seen in infection with Mycobacterium
tuberculosis.

Important questions
I. Essay
 1. Define inflammation. Mention the types. Explain the sequential vascular
changes in acute inflammation.
 2. Mention the cardinal signs of inflammation. Describe the cellular changes
in acute inflammation.
II. Short Notes
 1. Chemotaxis
 2. Phagocytosis
 3. Outcomes of acute inflammation
 4. Morphological types of acute in-flammatory reaction
 5. Ulcer
 6. Chronic inflammation
 7. Differences between acute and chronic inflammation
 8. Differences between transudate and exudate
 9. Define granuloma and mention its types.

Puviyarasi MSC Nursing,PATHOLOGY UNIT-1.pptx

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