Book Matter

Introduction to Pathology
Chapter No. 01
PAT H O LO GY
Pathos means disease while logos means
discourse or study. The science which deals with
the cause and nature of disease is called
Pathology. Pathology is divided into two branches;
1. General Pathology
It deals with general principles and mechanisms of
disease production.
2. Special Pathology
It deals with diseases of specific organs or systems
of body.
Centre / Core of Pathology

There are four main aspects of a disease.
(I) Etiology or Cause
To study the cause of disease is called etiology.
This may be;
a)
Genetically
Abnormalities in chromosomes.
b)
Acquired
a:
Infections / Micro biological.
Physical Agents.
c: Immunological causes.
d: Chemical / Nutritional factors.
b:
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(II) Pathogenesis
To study the origin and development of disease is
called pathogenesis.
(III)
Morphologic Changes
This refers to the structural and associated functional
changes in the cells or tissue of the body.
Morphology may be:
a. Microscopic morphology.
morphology.
b.
Macro
(IV) Clinical Findings

The manifestations of a disease are the sum of the
damage done by a harmful agent and the bodys
response. They may be observed clinically. It includes;
a. Disease onset.
b. Signs and symptoms.
c. Course and prognosis of the disease.
=========================
======
Disease
Disease refers to any deviation from or
interruption of the normal structure or function of
any part, tissue, organ or system that is
manifested by a characteristic set of symptom and
signs.
Types of Disease
There are following types of disease.
1. Genetic Disease
These are the Marfans syndrome, sickle

cell anemia, Downs syndrome etc.
2. Inflammatory Disease
Tonsillitis,
otitis
appendicitis etc.
media,
T.B
and
3. Neoplastic Disease
Carcinoma, malignant melanoma etc.
4. Environmental Disease
Pneumoconiosis and asbestoses etc.
5. Nutritional Disease
PEM ( Protein Energy Malnutrition ) etc.
6. Infectious Disease
T.B and diphtheria etc.
Causes of Disease
The various factors involved in the disease are
classified
into
two broad groups.
1.
2.
Environmental Factors
Physical agents
Chemical poisons
Nutritional deficiencies and excesses
Infection and infestations
Abnormal immunological reaction
Psychological factors
Genetic Factors
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The genetic polymorphisms strongly

susceptibility and resistance to disease.
influence
Pathogen
It refers to disease producing agent e.g. micro
organism or other any causative agent.
Biopsy
The removal of tissue or cell or any part from body
during life for diagnostic purpose is called biopsy.
Cytology
The branch of science which deals with the study
of individual cell is called cytology.
=======================
========
Cell
1. Cell is the smallest and basic unit of life.
OR
2. Cell is an atom of living things.
OR
3. Cell is the structural and functional unit of
organism.
Cell Structure
1.
Cell Membrane
It is an outer membrane, which gives the shape
and protection to the inner parts of the cell.
2.
Cytoplasm
Cytoplasm is living material of the cell. External to

the nucleus in cytoplasm there are some
organelles serving various functions. They are as
following.
Mitochondria
It is power house of the cell. It extracts
energy from nutrient in the form of ATP (Adenosine
tri-phosphate).
For Example;
O2 + glucose .. Co2 + H2O + ATP (energy)
ATP used for all cellular activities.
a.
Ribosome
Ribosomes are present in cytoplasm and
they synthesize protein.
b.
c.Lysosomes
These membrane bound organelles
contain hydrolytic enzymes and are responsible for
digestion and disposition of complex substances.
d.
Endoplasmic Reticulum
It detoxifies the damaging substances in
the cell.
2. Nucleus
The nucleus is present in the centre of cell. It
controls all cellular activities through the action of
at least 50,000 genes, each of which encodes a
protein with structural, enzymatic or control
function.
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=========================
======
Chapter No. 02
CELL INJURY AND ADAPTATION
Normal Cell
The cell that has tendency to stable its normal or
homeostatic state/condition and is able to handle
physiological demands is called normal cell.
Cell Injury
When the cell fails to preserve its healthy state in
the face of continued physiological stress and
pathological stimuli, its structure and function
undergo abnormal changes, which is called cell
injury."
Types
The cell injury may be reversible or irreversible.
a.Reversible Cell Injury
When former steady state of cells structure and

function can be re-gained after the removal of
pathogen (physiologic stress or pathologic stimuli),
it is called reversible cell injury. It results in
recovery and re-establishment of cells health.
b.Irreversible Cell Injury:
When former steady state of cells structure and

function cannot be regained after the removal of
physiologic stress or pathologic stimuli, it is called
irreversible cell injury. It results in cell death.
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Causes of Cell Injury

Causes of cell injury are given below;
1. Genetic Abnormalities
Genetic abnormality leads to cell injury e.g. sickle
cell anemia, Marfans Syndrome, congenital
malformation etc.
2. Physical Agents
The physical agents which cause cell injury are the
following.
i. Trauma
ii.
High and low
temperature
iii. Atmospheric pressure sudden alteration
iv. Radiation and electrical shock/accident
3.
Hypoxia
Hypoxia means diminished or inadequate supply /
amount of oxygen to the tissues- Hypoxia may be
due to;
a. Cardio respiratory failure.
b. Loss of O2 carrying capacity of blood as in CO
(carbon mono oxide) poisoning and sickle cell
anemia.
c. Loss of blood supply (Ischemia) due to arterial
occlusion.
d. Inadequate oxygenation of blood in case of
pulmonary disease.
4. Micro Organism
Following micro organisms cause the cell injury i.e.
viruses, bacteria, fungi, protozoa and helminthes

etc.
5. Chemical and Drugs
1. Glucose in high concentration can cause cell
injury.
2. Toxins and drugs also can lead to cell injury, e.g.
cyanide, alcohols, CO and mercuric chloride etc.
6. Immune Reactions
Immunologic reactions can cause cell injury which
may be due to, Auto immune diseases:
e.g. SLE (systemic lupus erythematosus).
Hypersensitivity reactions.
7. Nutritional Imbalance:Nutritional imbalance also cause cell injury, lead to
the specific disease. e.g. Beri-beri, Scurvy,
Kwashiorkor, atherosclerosis etc. Both (excess and
low) quantities of nutrient lead to cell injury and
produce disease.
8. Aging ( growing old )
Cell injury caused by aging is explained by two
groups of theories.
Wear and tear group of theories.
Genome based theories.
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Necrosis
Definitions
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1. Necrosis means a sequence of morphologic

changes that follow cell death.
2. Morphologic changes caused by progressive
on lethally injured cell.
3. Necrosis is the sum of structural changes that
come in the cell after its death. It can be
summarized as;
Cell death + morphological change =
Necrosis
Death of the cell is associated with rapid depletion
of intra cellular energy system. Initially there are
no morphological changes but within a few hours
the cell membrane and intra cellular organelles are
disrupted.
Causes of Necrosis
Necrosis is due to denaturation and coagulation of
protein and or digestion of the cell by released
enzymes.
Types
Following are the basic types of necrosis.
i. Coagulative Necrosis
In this type of necrosis, the necrotic cell retains its
cellular outline for several days.
Coagulative necrosis is frequently caused by lack
of blood supply and is exemplified well in infarcts
of solid organs e.g. heart, spleen and kidney.
ii. Liquifactive Necrosis:-
11
In this types of necrosis the autolytic and

heterolytic action of enzymes convert the cells
protein into liquid and characterized by pigmented
or turbid fluid, with complete loss of cells
structure.
Liquifactive necrosis caused by the enzymatic
action of poly morphonuclear leukocytes and
example is an ischemic necrosis of brain.
iii. Caseous Necrosis
In this type of necrosis the necrotic tissue assumes
a cream-cheesy appearance, slightly greasy to the
touch.
It is commonly seen in tuberculosis.
iv. Fat Necrosis
Fat necrosis is the special site necrosis. In this type
of necrosis the adipose tissue is damaged as in
pancreatitis and occasionally due to trauma. The
special appearances are due to the action of
lipases on triglycerides. e.g. Appearances in
omentum and mesenteries.
v. Fibrinoid Necrosis
Fibrinoid necrosis is also the special site necrosis.
In this type of necrosis the connective tissues and
especially arterial walls are infiltrated by strongly
eosinophilic hyaline material, which shows some of
the characteristics of fibrin.
This type of necrosis is in two conditions:1. Malignant hypertension. 2.
Auto
immune
disease e.g.
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S.L.E (systemic lupus erythematosus)

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Gangrene
Definitions;
1. This is a complication of necrosis.
2. Gangrene is the necrosis of tissue with more
putrefaction.
3. Cell death + morphological changes = necrosis
+ bacterial putrefaction = gangrene
In certain circumstances necrotic tissue is liable to
be invaded by putrefactive organisms which are
both saccharolytic and prototypic foul smelling
gases are produced, and the tissue becomes green
or black due to breakdown of heamoglobin.
Obstructions of the blood supply to the bowed are
almost to be expected followed by gangrene.
Causes
a. Trauma.
Chemicals.
d. Frost bite. e.
Arterial obstruction.
b. Burns.
c.
Infection.
f.
Types
There are three clinical types of gangrene, which
are given below;
1. Dry Gangrene
This type of gangrene occurs due to arterial
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obstruction and drainage of blood from affected

part is adequate. The tissue becomes shrunken,
black, and dry and discoloured. The most common
sites of dry gangrene are limbs.
2. Wet Gangrene
This type of gangrene occurs when venous
drainage of the necrotic tissue is inadequate so
that the tissue is swollen and moist due to fluid
accumulation. Wet gangrene is common in
intestine and appendix.
3. Gas Gangrene
This type of gangrene occurs when there are
bacterial infections (mostly in the intestine of
human being) caused necrosis and then later on
gangrene with abundant gas formation.
Gas gangrene is the sum of wet gangrene and gas
formation.
Most common site of gas gangrene is intestine,
liver and muscle.
=======================
========
Autolysis
Greek word auto means self, lysis means a
loosening. The process of self digestion is called
autolysis. This process begins after the death of
the cell and proceeds at a rate dependent on the
local enzyme content. It is expected result of
necrosis. However, the term is more commonly
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applied to the changes which take place in tissue

removed from the body and in the whole body
after death.
Apoptosis
Greek word apoptosis means falling off like
leaves from a tree. Apoptosis is an important
process in health and disease by which affected,
abnormal or unwanted cells are eliminated. It
differs from necrosis and is an active process.
Apoptosis in Health
In embryo genesis and development.
I. Metamorphosis of tadpole to frog.
II. Loss of auto reactive response of T cells in the
thymus preventing auto immune attack.
Apoptosis in Diseases
I. Virus infection.
II. Acting of cytotoxic T cell e.g. in rejection of
transplanted organs.
III. In tumours, apoptosis and proliferation rates
together control the rate of tumour growth.
Apoptosis is a rapid process usually affecting single
cells scattered in a population of healthy cells.
=========================
======
Intracellular Accumulation
In some conditions or circumstances cells may
accumulate
abnormal
amount
of
various
substances. The substances may be synthesized or
15
produced by affected cells or may be produced

else where.
Regarding intracellular accumulation, we shall
discuss two such conditions. i.e.
a. Fatty change.
b.
Pigmentation.
(a) Fatty Change or Steatosis:
Fatty change refers to any abnormal accumulation
of fat within
parenchymal cell. This term
embraces both the terms of fatty degeneration and
fatty infiltration.
Etiology or Causes
i.
Metabolic disturbances (more common in
obese people)
ii.
Toxins (organic, inorganic and micro
organisms)
iii. Absence of lip tropic
iv. Factors in food can cause fatty change
v.
Infective diseases
vi.
Diabetes mellitus
vii.
Pregnancy
viii.
Alcohol and other drugs
Organs Involved
Fatty change is commonly seen in the following
organs.
1. Liver; (most common due the involvement in
the fat metabolism).
2. Kidney
3. Muscles ( mostly skeleton muscles )
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4. Heart
Pathogenesis of fatty liver
Accumulation of triglycerides in the cytoplasm of
liver cells occurs due to:
1. High mobilization of adipose tissue i.e.
D.M
2. Rate of conversion of fatty acid i.e.
alcohol
3. Decreased oxidation of in glycosides i.e.
hypoxia
4. Decreased synthesis of lipid accepter
protein
Morphology
Macroscopically
In mild case liver may not affect the gross
appearance - with progressive accumulation, the
liver enlarge and may weight 3-6 kg, yellow, soft
and greasy organ.
Microscopically
It is first manifested by the appearance of small fat
vacuoles in the cytoplasm around the nucleus.
As the process progresses, the vacuoles fuse to
create cleared spaces that displace the nucleus to
the periphery of the cell.
(b) Pigmentation
Deposition of coloring material in different parts
of body is called pigmentation.
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Classification: Pigmentation is of two types;

( i ) Exogenous Pigmentation
In this type, the external pigment is introduced into
body by following way.
a. Inhalation
The commonest substances inhaled are;
Coal dust (produces anthrocosis)
Asbestos (produces asbestosis)
Silica
(produces silicosis)
Iron dust (produces haemosiderosis)

b. Injection
Tattooing is the most common and suitable
example of pigmentation following injection.
(ii) Endogenous Pigmentation
The pigments are produced metabolically by
tissues of the body itself, which get accumulated in
the body. The endogenous pigments are the
following;
a. Heamoglobin derived pigments
There are two main pigments derived from the
breakdown of R.B.Cs.
1. Haemosiderin. 2.
Bilirubin.
1. Haemosiderin
The iron derived from R.B.C breakdown is held in
the spleen, liver and bone marrow, and thus the
total amount of iron increased in the body, known
as haemosiderosis. The colour of haemosiderin is
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a golden yellow to brown granular.

2. Bilirubin
Bilirubin is also formed due to the breakdown of
R.B.C. The colour of bilirubin is yellow.
b. Non Heamoglobin Derived Pigments:
The non-heamoglobin derived pigments are the
following;
1. Melanin.
2.
Lipochromes
and
lipofuscines.
=========================
======
Melanin
Melanin is a normal endogenous pigment found in
the form of fine brown granules in the skin, hair,
choroids of eyes, adrenal medulla and some time
in the meninges.
Melanin Synthesis
Melanin is formed from tyrosine by an enzyme
called tyrosinase by producing a series of
oxidations. Administration of MSH (melanocyte
stimulating hormone) increase serum level of
copper causing pigmentation.
Pigment carrying cells are present in the sub
epithelial
tissue,
and
are
known
as
melanocytes .The amount of melanin in the skin
is increased by exposure to sun light and it varies
from man to man and from race to race.
Melanin production is under the control of MSH of
19
pituitary gland. Hydro-cortisone from adrenal

cortex inhibits the release of hormone from
pituitary gland.
Albinism
Albinism is the condition in which melanin is
congenitally absent. It is due to an autosomal
recessive
genetically
transmitted
lack
of
tyrosinase. In albinism the skin becomes milky
white, the hair white and the iris blue gray.
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Chapter No. 03
CELLULAR ADPTATION
CELLULAR ADPTATION
Cellular adaptation
pathological.
may
be
physiological
or
a.
Physiological Adaptations
These occur in response to with in normal
threshold stimulation by hormones or endogenous
chemical substances. e.g., enlargement of breast
and induction of lactation during pregnancy.
b.
Pathological Adaptations:These occur in response to environmental stress
(above normal limits) that tends to cause cellular
injury e.g. Metaplasia of normal columnar ciliated
epithelium of trachea and bronchi into stratified
squamous epithelium as a result of smoking.
Types
Different types of cellular adaptations are;
1.
Atrophy. 2.
Hypertrophy.
3.
Hyperplasia. 4.
Metaplasia.
1.
Atrophy
21
This is a simple decrease in cell size resulting in

shrinkage of affected tissues and organ. Atrophy
is a type of cellular response under stress by which
cell shrinks to a smaller size at which level survival
is still possible.
Causes
(i)
(ii)
(iii)
(iv)
(v)
(vi)
(vii)
Decreased workload.
Inadequate nutrition.
Aging.
Loss of innervations.
Loss of endocrine simulation.
Diminished blood supply.
Pressure.
Types of Atrophy
Following are the types of atrophy.
1. Vascular atrophy.
2. Endocrine atrophy.
3. Neurogenic atrophy.
4. Disuse atrophy.
5. Pressure atrophy.
6. Brown atrophy.
Mechanism of Atrophy
Increased degradation or decreased synthesis of
proteins can lead to atrophy. Hormones, e.g.
insulin, thyroid hormones, glucocorticoids and
prostaglandins play some role in genesis of
atrophy. Increase in number of autophagic
vacuoles also leads to atrophy.
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2. Hypertrophy
Hypertrophy means increase in the size of the
organ due to increase in the size of cell. In
hypertrophied organ has no new cell. The cellular
enlargement is due to the synthesis of more ultra
structural components and is not due to an
increased uptake of H2o (water).
Types
There are the following three types of hypertrophy,
which are given below;
1. Physiological Hypertrophy
Physiological hypertrophy occurs apart from
disease.
The best example is the enlargement of uterus of
pregnant female.
2. Adaptive Hypertrophy
Hypertrophy as an adaptive response is
exemplified by muscular enlargement. The
environmental changes that produced hypertrophy
of striated muscle, appears mainly to be increased
workload. In the heart a stimulus is high blood
pressure, in skeletal muscles, heavy work and body
building etc.
3. Compensatory Hypertrophy
Compensatory hypertrophy is an increase in size
to compensate for loss of tissue. It is best seen in
paired organs. e.g. when one kidney is removed or
atrophies because of disease the remaining kidney
23
does the work of two and becomes correspondingly

enlarged.
3. Hyperplasia
Hyperplasia means an increase in number of
cells in an organ or tissue. Hyperplasia can
only occur in the cells, which has capable or ability
of mitotic division in post embryonic life.
Types
There are two types of hyperplasia, which are
given below.
a. Physiological Hyperplasia
It is further divided into two;
(i) Hormonal Hyperplasia
Proliferation of uterine smooth muscles during
pregnancy is an example of hormonal (estrogen)
hyperplasia. Enlargement of prostate in old age is
another example.
(ii) Compensatory Hyperplasia
This type of hyperplasia that occur when a portion
of a tissue is removed or disease. For example,
when a portion of the liver is removed, mitotic
activity in the remaining cell begins as early as 12
hours after hepatectomy, eventually restoring the
liver to its normal weight.
(iii) Pathological Hyperplasia:Pathological hyperplasia represents instances of
excessive hormonal stimulation or effects of
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growth factors on target cell. e.g. if the normal

balance between estrogen and progesterone is
disturbed, hyperplasia results.
4.
Metaplasia
Metaplasia is a reversible change in which one

adult cell type (epithelial or mesenchymal) is
replaced by another adult cell types.
Causes
Common causes of metaplasia are the following.
(i)
Chronic inflammation.
(ii)
Chronic irritation.
(iii)
Vitamin A deficiency.
It represents an adaptive substitution of cells more
sensitive to stress by other cell types better able to
with stand the unfavorable environment.
1. Epithelial Metaplasia
Replacement of columnar epithelium by stratified
squamous epithelium in
gallbladder, trachea in
response to irritation or inflammation is an
example of epithelial metaplasia.
2. Mesenchymal Metaplasia
Metaplasia may also occur in mesenchymal cells.
For example, metaplasia of fibroblast to osteoblast
may follow the scarring. Thus bone is formed in the
area of injury.
=========================
======
25
Pathological
Calcification
Pathological calcification is defined as an
abnormal deposition of calcium salts within
different bodys parts/tissues. This abnormal
deposition of calcium salt occurs with smaller
amounts of iron, magnesium and other mineral
salts.
Types
Following are the types of calcification.
1.
Dystrophic Calcification
The deposition of calcium salt in dead, dying or

degeneration tissue is known as D.C . Plasma
calcium level is normal, and local conditions are
most probably of over riding importance.
Common Sites
(1) In Dead Tissues
(a)
(b)
(c)
(d)
(e)
(2)
Thrombi
Area of infraction
Hematomas
Old caseous lesion of T.B.
Dead parasites
In degenerating tissues
(i) Cysts
(ii) Atheromas
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(iii) Scars
(iv) Senile degenerate tissue
(v)
Chronic inflammatory granulation
tissue
(vi) Degenerative tumors
Morphology
Calcification appears as intra-cellular or extra
cellular basophilic deposits or both-sometimes,
hetero tropic bone is formed in the focus of
calcification.
2. Metastatic Calcification
Deposition or precipitation of calcium salt in
normal or healthy tissue is called metastatic
calcification.
Generalized met static calcification is usually due
to hypercalciemia, but occasionally, as in renal
osteodystrophy,
a high plasma phosphate
appears to be the precipitating factor.
Causes
(a)
/ bowel
(b)
(c)
(d)
(e)
(f)
Excessive absorption of calcium from GIT

Excessive milk intake
Hyper vitaminosis D
Neoplasia
Renal tubular acidosis
Hyper thyrodism etc
Common Sites
a. Kidney
27
b. Lungs
c.
Stomach
d. Blood vessels
e. Cornea
Morphology
Calcium salts morphology in all cases, resemble
those described in dystrophic calcification.
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Chapter No. 04
IN F L A M M AT I O N
Inflammation
Inflammation is the dynamic / energetic process
by which living tissues react to injury. They
concern
vascular
and
connective
tissues
particularly.
Merit of Inflammation
Inflammation is essentially a protective response
for the destroying of invading pathogens.
Demerit of Inflammation
Although the inflammation is an immediate
protective response, but in some condition it may
be lethal.
Types:
Inflammation may be acute or chronic,
depending upon the duration of the process.
1.
Acute Inflammation
An immediate and early response to injurious

agents
(pathogens)
is
known
as
acute
inflammation. The critical function of an acute
inflammation is that to deliver leukocyte to the
injury site, and clear it from invading infectious
agent, as well as to degrade the necrotic tissue.
Causes
(i)
Chemical injury.
(ii)
Mechanical
29
trauma.
(iii) Radiation injury.
(iv) Injury by the
living organism.
(v) Injury due to cold and heat.
(vi)
Injury due to immunological mechanisms.
Features of Acute Inflammation
The classical signs are;
(i) Redness (rubor) (ii)
Pain (color)
(iii) Heat (dolor)
(iv)
Swelling (tumor)
(v)
Loss of function (functionless).
These gross sign are explained by changes
occurring at microscopic level. There essential
features are;
(i)
Hyperaemia
(i)
Exudation of fluid
(i)
Emigration of leucocytes
(1) Hyperaemia
The hyperaemia in inflammation is associated with
the well known micro vascular changes, which
occur in "Lewis triple" response, a Flush, a Fleare
and a Weal.
The stroke is marked momentarily by a white
line due to vasoconstriction.
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The flush, a dull red line, immediately follows

and is due to capillary dilation.
The flare, a bright red irregular surrounding
zone, is due to arteriolar dilation.
Hyperaemia explains the classical signs of
redness and heat.
(2) Exudation
In the earliest phase of inflammation, the
vasodilatation and increased blood flow raise
intravascular hydrostatic pressure. This results in
increased filtration of fluid from the capillaries.
As vascular permeability increase, protein rich fluid
and even cells start to appear in the interstitial
spaces. This protein rich fluid is then called
exudates.
(3) Emigration of Leucocytes:Neutrophils and mononuclear leucocytes pass
between the endothelial cell junctions by
amoeboid movement through the venule wall into
the tissue spaces.
In this process both neutrophils and endothelial
cells are activated and both express cell adhesion
molecules initially selection and then integrins.
(2) Chronic Inflammation
Chronic inflammation is defined as a prolonged
process in which destruction and inflammation are
proceeding at the same time as attempts at
healing. Chronic inflammation may follow acute
31
inflammation if the causative agent is not removed

or be primary i.e. there is no existing acute stage.
Causes
(i) Persistent infection by some intracellular microorganism
e.g. mycobacterium
tuberculosis.
(ii)
Prolong exposure to non-degradable
inanimate material e.g. Silica particles.
These cause persistent chemical and mechanical
irritation that lead to chronic inflammation.
(iii) Autoimmune Disease: e.g. Rheumatoid
arthritis etc.
Features of Chronic Inflammation:
Chronic inflammation is characterized by;
(i)
Infiltration with mononuclear cells including
lymphocytes, macrophages and plasma cells.
(ii)
Tissue destruction largely induced by
inflammatory cells proliferation and fibrosis.
Difference b/w exudates and

transudate
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S
#
1
Exudate
Its cause may be

bacteria, virus
or trauma
It is formed as a
result of
endothelial
damage and
increase
permeability.
Exudate
resembles blood
plasma in its
constituent.
It is slightly
turbid.
It is not sterile.
Specific gravity
is more than
1.016.
RBCs may be
present.
Coagulability
present due to
fibrinogen.
The part affected
by exudation is
red in colour
(redness).
5
6
7
8
9
1
0
It is an
accumulates due
to acute
inflammatory.
S
#
1
Transudate
Transudation is a passive
phenomenon by which
fluid leaves the vascular
channels and collects
outside.
Its cause may be local or
general.
It is formed as a result of
increased vascular
hydrostatic pressure.
Transudate resembles
interstitial fluid.
It is clear and watery.
It is sterile.
Specific gravity is less

than 1.016.
RBCs never present.
Coagulability absent due

to lack of fibrinogen.
10
Part affected is pale and

puffy.
33
Difference b/w acute and chronic

inflammation.
Features
Duration
Onset
Inflammatory
Cells
Specificity
Fluid exudation
and edema.
Sign
&
symptoms
Fibrosis
Systemic
Manifestation
Acute
Short (days)
Acute
Neutrophils,
Macrophage
Non specified
--------------Present
Present
Absent
Fever, Often
HighLeukocytosis
Chronic
Long (week to
months)
InsidiousLymphocytes,
plasma cell
Fibroblasts
Specific
--------------Absent
Absent
Present
Low grade fever
Weight
loss,
anemia
=========================
======
Giant Cells
The large cell with more than one nucleus is called
giant cell.
Types
I.
Miscellaneous Group.
(ii) Foreign body type of giant cell.
(iii) Tumor giant cell.
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i.
Miscellaneous Group
In malignant disease of lymph node known as
Hodgkins disease, cells are seen and are named after
two workers as Read and Dorothy cells. The cell is
small (12-14 micron) with many nuclei. Sometimes only
two nuclei lie opposite to each other, which are almost
mirror image and hence called as mirror image giant
cells.
(ii) Foreign Body Type of Giant Cell
It is formed by the fusion of macrophages, but the
nucleus are scattered throughout the cytoplasm e.g.
due to inert foreign bodies such as suture, splinter and
breast implant.
(iii) Tumor Giant Cell:It is commonly seen in malignant disease i.e.,
Carcinomas and sarcomas. It contains more than one
nucleus due to atypical mitosis. So each individual
nucleus is hyper chromatic.
=========================
======
35
36
For Paramedics
Chapter No. 05
HE A LING
Repair
Repair means the replacement of dead or
damaged cells by healthy or viable cells. The
new cells may be derived either from parenchyma
cells or from connective tissue of injured organ.
Factors Effecting Repair
The factors that influence repair are given below.
A.
B.
Local Factors:i
Poor bloody supply.
ii
Adhesion to bony surfaces.
iii
Movement.
iv
The effect of drying.
v
Ultraviolet light.
General Factors
i. Age.
ii.
Protein deficiency.
iii. Vitamin-C deficiency.
iv. Gluco corticoids frequent use.
v.
Immunity.
vi. Temperature.
37
There are two processes of repair;

1. Regeneration
The
replacement
of
destroyed
cells
by
proliferation of surrounding undamaged cells of
the same type is called regeneration.
Regenerative Capacity and Cells Types:The bodys cells are divided into three groups on
the basis of their regenerative capacity as
following;
1. Labile Cells
Labile or continuously dividing cells are those
types of cells which proliferate through out the life
and replacing those cells that are continuously
dying e.g.
a. Stratified squamous epithelium of skin, oral
cavity and vagina etc.
b. Cubical epithelium of the duct i.e. billiary duct.
c. Columnar epithelium of GIT etc.
2. Quiescent Cells
Quiescent or stable cells are those type of cells,

which have capacity to regenerate but in normal
condition do not actively replicate. In stable cells
the chances of regeneration are good e.g.
a. Parenchymal cells of liver, kidney and
pancreas.
b. Mesenchymal cells i.e. smooth muscle,
cartilage & connective tissue etc.
3.
Permanent Cells
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For Paramedics
Permanent or non-dividing cells are those types of

cells, which are incapable of division and
regeneration. If they are destroyed, the loss is
permanent. e.g.
a. Nerves cells (neurons).
b. Cardiac muscles etc.
2.
Repair by Connective Tissue
( Scar
Formation)
Following are the condition in which tissue repair is

achieved by scar formation.
(i) When resolution (recovery) fails to occur in an
acute inflammation.
(ii)
When parenchymal cell necrosis cannot be
repaired by regeneration because,
a. Necrotic cells are permanent cells.
b. Stable cells are destroyed.
c. Necrosis is so extensive that no cells
are available for regeneration.
=========================
======
Healing
The filling up of wound is called healing. Healing
is the final stage of the response of tissue to injury.
Types of wound
The types of wound are the following;
1.
Abrasion
39
This is the mildest form of the main injury

characterized by removal of the superficial part of
the epidermis. The underlying germinative layer of
cells is intact, the epithelium regenerates from
below, and the integrity of the epithelium is
resorted with no scarring.
2.
Incisicion (Cut) and Laceration
(Tear):Incision and lacerations involve the full thickness

of the skin (both epidermis and dermis) but with
minimal loss of germinative cells. If the skin edges
are carefully opposed, as in sutured surgical
incision, only a small gap remains to be repaired.
This process, in which necrosis and inflammation
are minimal, is known as healing by first intention.
3.
Wounds with Epidermal
Defects:Severe injuries (e.g. crush injuries extensive

laceration, burn) are characterized by loss of large
areas of the complete epidermis, including the
germinative cells.
The extensive necrosis that is present in such
wounds is accompanied by a phase of
inflammation prior to the repair process. This
process of healing is known as healing by second
intention.
Healing Mechanisms OR Types of Healing:Following are the two healing mechanisms.
Healing by first or primary intention.
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Healing by second intention.
1.
Healing by First Intention
This occurs in clean, incised wounds with good

apposition of the edges, either produced by
surgery or produced by sharp edged weapons and
then sutured by the surgeon.
There is minimal loss of tissue.

There is no septic contamination.
Steps
1. Immediately
Blood clot and debris fill the small cleft.
Dehydration of surface clot forms a scale that
covers the wound.
2. With in 24 hours
Neutrophils appear at margins of incision,
moving toward fibrin clot.
Epithelium regenerates at its cut edges
thickness due to mitotic activity of basal cells.
3. Within 48 Hours
Projection of adjacent epithelial cells from edges
migrates and grows along cut margins of
dermis,
depositing
basement
membrane
components.
4. 3rd Day
Neutrophils are replaced by macrophages.
41
Granulation tissue forms in incision space.

5th Day
Incision space is filled with granulation tissue.
New vascularization is formed.
Collagen fibers form bridge at the incision.
Weeks
Continued accumulation of collagen and
proliferation of fibroblasts become prominent.
First Month
Scar consists of cellular connective tissue
devoid of inflammatory infiltrate, covered by
intact epidermis.
2. Healing By Secondary Intention

This occurs when there is more extensive loss of
cell and tissue (e.g. infarction, inflammatory
ulceration, abscess and large surface wounds).
Healing in this type is slow and results in a large
scar formation.
Steps
1. In Early Stages
The wound is filled up with blood and fibrin clot
(Coagulum), which later dries on its surface to
form a scale.
2. In few Days
Wound contraction, reducing its size.
Mitotic activity in the epithelium is seen.
New capillary loops bring macrophages,
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For Paramedics
neutrophils and fibroblasts.

3. In One Week
Epithelium continues to grow across.
Capillary loops form small granulations in the
base of the wound.
Granulations
tissue
forms
a
temporary
protective layer until the surface is covered.
4.
2 Weeks Onwards
Epithelial covering complete.

Collagen arranged transversely and capillaries
become less prominent.
5. In Months
The regenerated epidermis becomes thicker
and sends short processes into the underlying
tissue.
The regenerated epidermis is less firmly
adherent to the dermis than is the normal.
The scar is at first pink, but subsequent
devascularization leaves it white.
Complications of wound
1. Infection
A wound may provide the portal of entry for a
variety of organisms.
2. Wound Dehiscence
Dehiscence, bursting upon of a wound, is
particularly important after laparotommy.
In appropriate suture material, poor technique,
43
poor wound healing and increased mechanical

stress can cause this condition.
3.
Implantation Cysts
Epithelial cells which slide into the healing wound

may some times persist, and later proliferate to
form an epidermoid cyst.
4. Keloid Formation
Accumulation of excessive amount of collagen that
produces protruding tumorous scar is called
keloid.
5. Pigmentary Changes:Coloured particles introduced into the wound may
persist and lead to tattooing.
Healed chronic ulcers sometimes have a rust
colour due to staining with haemosiderin.
6. Painful Scars: (Scars)
Pain either local or referred, may be experienced if
a neuroma is included In the scar tissue.
7. Weak Scars
If scar tissue is continuously subjected to strain,
stretching may result. An incissional hernia
redevelops in this way.
8. Cicatrisation
This is late reduction in the size of a scar. It is a
frequent complication in cases of burning and in
hollow viscera e.g. urethra.
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9. Neoplasia
Rarely trauma acts as promoting agent and
squamous cell carcinoma develops in scars.
Difference
Between
Second Healing
Primary
And
The basic difference in the two types of wound

healing is quantitative not qualitative.
Primary
Little amount of tissue is lost.
Less
necrotic
tissue
is
produced
and
inflammatory reaction is also minimal.
Formation of small amount of granulation
tissue.
Fewer scars are formed.
Wound contraction is minimal.

Rapid healing.
Secondary
There is loss of greater amount of tissue.
Excessive necrotic tissue production
inflammatory exudates.
Large amount of granulation tissue.
Large scar is formed.
Slow healing.
and
=========================
======
45
46
For Paramedics
Chapter No. 06
CIRCULATORY DISTURBANCE
OEDEMA
Oedema is an accumulation of abnormal/excess
fluid in the extra vascular tissues or body cavities.
Depending on the site collection of fluid in the
different parts of the body cavities is designed as.
(i) Anasarca
Anasarca is the term used for severe generalized
oedema.
(ii) Hydro Pericardium
Excessive fluid accumulation in pericardial sac.
(iii) Hydro peritoneum or Ascites
Excessive fluid collection in the peritoneal cavity.
(iv) Hydro thorax
Collection of fluid in pleural cavity.
Classification
Oedema may be local or general.
1.
3.
5.
6.
A: General Oedema
Hepatic oedema.
2. Myxo oedema.
Renal oedema.
4. Cardial oedema.
Pregnancy oedema.
Oedema due to unknown causes (idiopathic
47
oedema).
B: Local Oedema:
1. Pulmonary oedema
2.
Hypersensitivity
oedema
3. Acute inflammatory oedema
4. Angioneuretic oedema
5. Oedema due to local venous obstruction
Pathology
Oedema is the result of an increase in the forces
that tend to move fluids from the intravascular
compartment into the interstitial spaces.
The opposing effects of intravascular hydrostatic
pressure and plasma colloid osmotic pressure (also
called oncotic pressure) are the major factors to be
considered in the pathogenesis of oedema.
Thus fluid leaves at the arteriolar and of the
capillary bed and returns at the venular end, some
fluid is drained off through lymphatic to be
returned to the lymphatic circulation indirectly.
Whenever the balance between the forces, that
keep the fluid in the vascular spaces against those,
which tend to remove it, is impaired then oedema
occur.
Causes of Oedema : Following are the causes

of oedema.
A: Renal Oedema:
Following are the causes of R.O.
(i) Acute glomeruler nephritis.
syndrome.
(ii)
Nephrotic
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For Paramedics
(iii) Chronic glomeruler nephritis.

B: Cardiac Oedema
Cardiac oedema occurs due to the following
causes.
(i) Congestive cardiac failure.
(ii)
Acute
heart failure.
Other Factors
There are some other factors, which may
aggregate the oedema.
(i) The constriction of both afferent and efferent
arterioles.
The renal blood flow is reduced
and there is reduction in glomeruler filtrate.
(ii) The adrenal cortex is also affected producing
excessive
amount
of
aldosterone
and
reabsorption of sodium from renal is increased.
This result in increased plasma volume and
leading to oedema.
(iii)
An element of hypo albuminemia is also
present in patient with cardiac failure.
(iv) There is also lymphatic obstruction due to
lack of muscular activity in cardiac patient.
Difference between Renal and Cardiac
Oedema
Characteristic
s
Causes
Distribution
Cardiac
Oedema
Congestive
cardiac failure
with
high
pressure
Usually affected
parts are lower
Renal Oedema
Nephritis and
nephrosis
Effected parts are
face
particularly
Effect of gravity
Composition
Blood
Examination
extremities
The
fluid
change
its
position under
the action of
gravity
Protein contain
and
high
specific gravity
Blood
cholesterol level
is normal
49
of the eyelids
The fluid is less
influenced
by
gravity
Protein
contain
and low specific
gravity
Blood cholesterol
level is raised
Thrombosis
Thrombosis is the formation of a solid mass
(blood constituents) with in a blood vessel or
the heart during life.
The mass itself is called a thrombus and it
consists of aggregated platelets and fibrin in which
the red and white cells are trapped.
Blood clotting is a physiological protective
mechanism, but thrombosis is a pathological
process with serious consequences.
Etiopathogensis
There are three main factors leading to thrombosis
are known as Virchows triad.
a. Alterations of blood flow.
b. Damage to endothelium of vessel.
c. Changes in constituents of the blood.
a. Alteration of Blood Flow
The main effect is to bring platelets into contact
50
For Paramedics
with the vessel wall. This result from slowing of

blood flow, e.g. in cardiac failure or during bed
rest.
With slowing, the normal axial stream of blood
cells is lost and white cells and platelets fall out of
the main stream and accumulate in the peripheral
plasma zone. e.g. ulcerated atherosclerotic plaque
causes local turbulence.
b. Damage to Endothelium of Vessel
It has been suggested the lining surface of the
blood vessel (endothelial) carries electrical charge
(-ve), and it is change into (+ve) due to any injury
or factor.
This leads to attract and adhere the platelets.
There are some factors that cause change or injury
in the vessel wall.
a. Arthroma
b. Trauma
c. Surgical operation d. Hypertension
e. Bacteria toxin
f.
Cigarette
smoking
g. X-ray exposure
c. Change in Constituent in Blood:Conditions associated with an increased platelet
count are complicated by thrombosis. Such as;
Increase
in
platelets,
fibrinogen
and
prothrombin after operation and childbirth,
usually after 5-10 days.
Miscellaneous factors e.g., contraceptives,
smoking and some cancers etc.
51
Types of Thrombi
Following are the type of thrombi.
1. Morphological type.
2.
Clinical type.
1. Morphological types
These are the following two types.
(i) Pale Thrombi
They are dry, easily breakable, granular masses
mainly composed of platelets and fibrin with few
entrapped RBCs.
These are developed in arterial circulation.
(ii) Red Thrombi
These thrombi are composed of platelets, fibrin
and large number of RBCs entrapped in fibrin
mesh. These are typically developed in venous
circulation.
2.
Clinical or depending upon Site

(i) Arterial thrombi.
(ii)
thrombi.
(iii) Venous thrombi.
Cardiac
(i) Arterial thrombi

Thrombi are common in arteries as a complication
of artheroma. Forming in a rapid circulation, the
thrombus consists mainly of platelets.
Common sites include aorta, carotid arteries and
coronary arteries.
(ii)
Cardiac thrombi:
This type of thrombi may be seen in the heart
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For Paramedics
valves in the following conditions.

(i) Inflammation of the cardiac valve
(ii) Damage to endocardium
(iii)
Turbulence and stasis in arterial
chambers
Venous thrombi
Systemic venous thrombosis is common because
of the slow blood flow and lower pressure. It
consists of red cells, platelets and fibrin.
Common sites include femoral vein, popliteal
veins, iliac vein and deep calf veins etc.
=======================
========
Fate of Thrombus
1. Propagation
The thrombus may continue to progress
accumulation of more platelets and fibrin.
by
2. Embolization
Thrombi may dislodge and may be transported to
other sites in the vessels called embolization.
3. Dissolution
Many small thrombi are completely removed by
the fibrinolytic system, which exists to limit
thrombosis.
4. Organization
Thrombi may induce inflammation and fibrosis
called organization. They may eventually
53
become recanalized, i.e. may re-establish vascular

flow.
Embolism
Embolism refers to occlusion of some parts of
cardiovascular system by implication of some
mass transported to the site through blood
stream. The transported mass that occludes blood
vessel is called embolus.
Types
Emboli are classified as;
1.
According to consistency:
a. Solid Emboli
1 Tumour fragments.
2.
Dislodged
thrombus.
3 Atherosclerotic debris.
4. Foreign body.
5 Parasites.
6. Bits of bone marrow.
b. Liquid Emboli
1 Fat droplets
2 Amniotic fluid
c. Gas Emboli
1
Aseptic gas emboli
bubbles
2. According to Site of Origin
1 Venous emboli
emboli
3 Lymphatic emboli
Nitrogen
Arterial
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3. According to Sepsis
1 Septic emboli
emboli
Aseptic
Clinical Effects
If emboli are small, or if the collateral circulation in
involved area is sufficient, no effect is produced. If
emboli are medium in size, it blocks the artery but
not completely and slightly blood flow is continued
and it does not lead to infarctions.
If emboli are large in size then it completely
blocked the blood flow and sudden death occurs.
Such as the stock age of pulmonary and coronary
arteries.
Pulmonary Embolism
The occlusion of some part of pulmonary
circulation by embolus, which is brought to the site
through the circulation is called pulmonary
embolism.
The consequences depend on the size of the
embolus and the patients previous health.
Pathogenesis
In pulmonary embolism a clot 20-45 cm long is
detached from the femoral or popliteal vein and is
carried to the heart, where it reaches the right
ventricle and then becomes lodged in pulmonary
circulation.
Systemic Embolism
The occlusion of systemic arteries due to detached
55
thrombus is called systemic embolism.

Pathogenesis
Emboli of the arterial system are derived from the
heart or the larger arteries which have become
athermatous. The results of arterial obstruction are
very important matter entering the vascular
system may be:
1 Solid e.g. fats, parasites etc
2
Gaseous e.g. air
3 Liquid e.g. amniotic fluid
Fat embolism
Fat globules may appear in the circulation and
obstruct the arterioles and capillaries in various
organs.
Aetiology
1. Bones fracture
This may occur when a long bone particularly
femur and tibia are fractured usually 2472 hours
later. Fatty marrow present in these bones may
pass in disrupted vessels and is ultimately
transported as an embolus in the venous system.
2.
Trauma of adipose tissue
Fat embolism can also be caused by laceration of
adipose tissue (e.g. in subcutaneous tissue). It
occasionally occurs during child birth as a result of
injury to the pelvic fatty tissue associated with
trauma of the child birth.
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3.
Miscellaneous causes
Extensive cutaneous burns, inflammation in bones
and adipose tissue, poisoning, nutritional or
alcoholic fatty liver, diabetes mellitus and
decompression sickness are the conditions which
can also lead to fat embolism.
Extrinsic fat or oil introduced into the body for
therapeutic purposes may also cause fat
embolism.
Amniotic fluid embolism
During parturition (labour), amniotic fluid may
enter in a uterine vein, especially after
manipulations or with certain obstetric treatment.
It is a major cause of maternal mortality during
labor and is characterized by sudden dyspnoea,
cyanosis, collapse, hemorrhage convulsion and
coma.
Gas or air embolism

Gas bubbles in vessels can obstruct the flow
readily as thrombotic masses. The amount of air is
100 ml required to produce a clinical effect.
Causes
Atmospheric air may enter the blood when a
neck or intra cranial vein is incised.
An air may be forced into ruptured uterine by
the powerful uterus contraction during delivery.
During deep sea diving all body nitrogen get
dissolved in blood a body tissue. While coming
57
back to surface abruptly. The nitrogen bubbles

out from blood and tissues and causes air
embolism.
Injury to the lung or chest wall may open large
vein and permit air to enter during breathing.
=========================
======
Infarction
An infarct is an area of necrosis due to ischemia
with in a tissue or an organ. It is caused due to
occlusion of either arterial supply or its venous
drainage.
The process whereby the lesion is developed is
known as infarction at the periphery of an organ.
Etiology
1. 99% of all infarcts are caused by thrombi and
emboli.
2. Twisting of vessels of ovary or a loop of bowel.
3. Compression of vessel by expansible tumors.
4. Traumatic rupture of the artery.
Types
Infarcts are classified according to different
criteria.
1.
Depending upon Colour
These are further divided as follow.

a.
Pale (anemic) Infarct
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This type of infarction is due to the occlusion of

arterial blood supply. This type usually occurs in
solid compact organ such as; heart, spleen etc.
Reason for white appearance is that solid state of
tissues limit the amount of hemorrhage into the
area of is chemic necrosis.
b. Red (hemorrhagic) Infarct:
This type of infarction is due to the occlusion of
venous drainage. It is occurs in soft loose tissues
such as lungs and intestines. Loose or spongy
organs permit blood to collect in the infarct from
anastigmatic capillaries in margins of necrosis
area.
2.
Depending upon Age

(i) Recent
3.
(ii) Old
Depending upon Infectivity

(i) Septic
(ii) Bland (sterile)
Pathogenesis
1 Immediately after the obstruction of blood
supply, there occurs anoxia which causes
hyperemia.
2 In the meantime, due to lack of blood supply, the
area involved shows initially necrosis of
parenchymatous cells followed by necrosis of
the stroll cells.
3 Necrosis develops fully in 48 hours.
4 After some time (days to week) the red cell are
lyses and the pigment is taken away by
59
macrophages leaving behind a pale coloured

area.
5 There is a zone of hyperemia surrounding the
infarct and there also occurs inflammatory
reaction in response to the breakdown products.
=========================
======
Morphology
On Gross Examination
1 Infarcts are commonly wedge shaped.
2 Apex of wedge is towards focus of vascular
occlusion.
3 Base is towards periphery.
4 Involved surface of organ is covered with fibrous
exudates.
Microscopically
1 Ischemic Coagulative necrosis of affected cells
occurs
2 In brain liquifective necrosis
Factors Aggravating Infarction
Following are the factors which aggravate the
infarction.
1. Nature of the vascular supply
2. Rate of development of occlusion
3. Vulnerability to hypoxia
4. Oxygen content of blood
Congestion
General venous congestion is a condition where
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all the veins of the body are distended with blood

due impaired to venous drainage.
It is accompanied with the infection of the heart or
lungs since all the circulating blood must pass
through them.
Causes
(i) Vessels obstruction
(ii) Mitral stenosis
(iii)
Aortic valvular disease
(iv) Emphysema
(v) Lungs fibrosis
Types
1. Acute Passive Venous Congestion:
(i) Local
(ii) General
2. Chronic Passive Venous Congestion:
(i) Local
(ii) General
=======================
========
Shock
(1) Shock is a condition in which the vital
functions of the body are depressed due to a
severe and acute reduction in cardiac output and
effective circulating blood volume.
OR
(2) Shock or vascular collapse is a widespread
hypo perfusion of cells and tissues due to any
serious assault on the bodys homeostasis
resulting in reduction of blood volume or cardiac
61
output or redistribution of blood leading to a

decreased effective circulatory volume.
Summarized as:
Hypotensionimpaired
tissue
cellular hypoxia death.
Shock can
1.
2.
3.
4.
1.
perfusion
Classification
be classified into four categories.
Cardiogenic shock.
Hypovolemic shock.
Septic shock.
Neurogenic shock.
Cardiogenic Shock
Cardiogenic shock
myocardial pump.
results
from
failure
of
Causes
(a)
(b)
(c)
(d)
(e)
Myocardial infarction.
Rupture of heart.
Arrhythmias.
Cardiac temponade.
Pulmonary embolism.
Principal Mechanism Is:

Failure of myocardial pump (due to intrinsic
myocardial damage or extrinsic pressure or
obstruction to flow) .. decreased cardiac outflow
hypotension .. impaired tissue perfusion ..
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cellular hypoxia shock.
2.
Hypovolemic Shock
Hypovolemic shock results from decreased blood

volume.
Causes
1. Hemorrhage
2. Fluid loss (e.g. vomiting, diarrhea and bums)
3. Severe burning
4. Severe injury
Principal Mechanism Is
Hemorrhage or fluid loss .. inadequate blood or
plasma volume .. decreased cardiac output .
Hypotension ..
impaired tissue perfusion
cellular hypoxia shock.
3. Septic Shock
Septic shock is caused by systemic micro bacterial
infection, most commonly due to bacteria (gram
negative bacilli).
Causes
Overall bacterial infections.
(i) Gram -ve septicemia (endotoxic shock).
(ii) Gram +ve septicemia.
Endotoxins. . . . complement activation . . . .
release of C3a and C5a. . . mast cell deregulation
and histamine release . . . . peripheral
63
vasodilatation. . . . peripheral pooling of blood. . . .

relative hypovolemia. . . . impaired tissue
perfusion. . . . cellular hypoxia. . . . shock
4. Neurogenic Shock
Neurogenic shock occurs due to loss of vascular
tone resulting in peripheral pooling of blood.
Causes
1 Anesthesia
2 Brain stem injury
3 Spinal card injury
Injury to vasomotor center (due to any cause) . . . .
decreased sympathetic discharge . . . . peripheral
vasodilatation. . . . peripheral pooling of blood. . . .
relative hypovolemia. . . .
impaired tissue
perfusion. . . . cellular hypoxia. . . .
shock.
Morphology of Shock
Late stages of shock are characterized by failure of
multiple organ systems and hence the cellular
changes may appear in any tissue.
Changes are particularly evident in the following
organs;
Brain
Ischemic encephalopathy is prominent in this type
of shock.
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Heart
The heart may undergo a variety of changes such
as:
1 Myocardial infarction
2 Sub endocardial hemorrhages and necrosis
Kidney
Acute tubular necrosis (ATN) is a characteristic
feature of shock.
Lungs
Lungs are resistant to hypoxia and therefore no
effect is seen in hypovolemic shock.
=======================
========
65
Chapter No. 07
NE OP L ASIA
Dysplasia
Dysplasia means loss of uniformity in structure of
individual cell, as well as loss of their architectural
orientation as a whole (in a tissue).
Causes
(i) Chronic irritation
(ii)
Chronic
inflammation
(iii)
Chronic
infections
Features of a Dysplastic Cell:
The dysplastic cell show:
(i) Polymorphism; variation in size and shape.
(ii)
Hyper chromasia; deeply staining and
large nuclei.
(ii) Increased mitotic figure along normal
pattern.
(iv)
Mitosis in abnormal locations within
epithelium.
Examples
(1) Cervix
Dysplasia is commonly seen in the uterine cervix
due to long span cervicitis.
(2) Respiratory Passage
Dysplasia is seen in the
(respiratory tract).
epithelium
of
RT
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Neoplasia
Neoplasia
means
new
growth
and
is
characterized by unceasing, abnormal and
excessive proliferation of cells.
Neoplasm
A neoplasm as defined by Willis is an abnormal
mass of tissue, which is uncoordinated and
excessive in quantity with that of normal tissues
and persists in the same exclusive manner after
cessation of the stimuli/cause, which evoked the
change.
Features of Neoplasm
Fundamental to the origin of all neoplasm is loss of
responsiveness to normal growth controls.
1. Neoplastic cell are said to be transformable and
they continue to replicate.
2. The growth rate of neoplastic cell is different
from their parent cells growth rate.
3. The neoplastic cells are uncoordinated to the
parent cells.
4. The mass of neoplasm disturb the symmetry of
the body.
Oncology
The study of neoplasm is called oncology.
Differentiation
The extent to which the neoplastic parenchymal
cells resemble their normal parent cells both
morphologically
and
functionally
is
called
67
differentiation.
Anaplasia
Irreversible loss
anaplasia.
of
differentiation
is
called
Composition of Neoplasm
Parenchyma
It constitutes the
neoplasm.
1
proliferating
part
of
the
2. Stroma
It consists of connective tissue, blood vessels and
lymphatic it provides support for the growth of
parenchymal cells.
Desmoplasia
The excess of stroma component in a tumor
(neoplasm) is called desmoplasia and such a tumor
is called scirrhous tumour.
Types of Neoplasm
Tumour (neoplasm) is classified into following two
types;
1. Benign tumours
2.
Malignant
tumours
1. Benign Tumour:
Benign tumour is the simple form of tumor having
the characteristics, which are given below.
1. It will remain localized
2. Usually well differentiated
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3.
4.
5.
6.
7.
Closely resemble the organic tissue

Grow slowly
Metastatize (do not spread)
It can be surgically removed
Patient survives.
2. Malignant Tumour
Malignant tumour is the complicated form of
tumour and characterized as following;
1. Do not remain localized
2. Usually less differentiated
3. Very less
resemblances
4. Speedy growth
5.
Spread to
adjacent tissues
6. Reoccurring on surgical removing
7.
Patient dies
Nomenclature of Tumors
The tumour is named on the basis of the following
methods.
1. Origin production site
2. Benign
or malignant
A: Benign Tumors
They are donated by the suffix Oma as in lipoma
and fibroma etc.
Example
Tumour
of
Benign
Epithelial
Cell
Some benign epithelial cell tumours are described

bellow;
1.
Papilloma
69
Papilloma is a benign neoplasm most often arising

from surface epithelium, such as squamous
epithelium of the skin, larynx, or tongue. It consists
of delicate finger like epithelium process overlying
core of connective tissue stroma that contains
bloods vessels.
2. Adenoma
It is the benign tumour of epithelial origin that is
derived from glandular tissue or exhibit clearly
defined glandular structure.
Adenomas may undergo malignant change. Some
show recognizable tissue elements, such as fibrous
tissue while other, such as some bronchial
adenomas, may produce active compounds giving
rise to clinical syndrome.
3. Cystadenoma
The case in which retention of secretion is marked,
a cyst forms
and tumour is called a
cystadenoma .which may reach an enormous size,
e.g some cystadenomas of the ovary may be 30-40
cm in diameter, particularly those which secrete
mucus.
Example of Benign Mesenchymal

Cell Tumours
Following are the some
mesenchymal cell tumours.
example
of
benign
1. Lipoma
A common benign tumour composed of well
differentiated fat cells. This benign tumour arises
from fat of cells in subcutaneous tissue of arms,
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shoulder and buttock.

2. Myxoma
This benign tumour is a variant of fibroma and
represents a degenerative change characterized
by accumulation of group substances in mature
tissues.
3. Fibroma
Fibroma is a nonmalignant tumour of connective
tissue.
Fibroma arises in subcutaneous tissues, fascia,
periosteum, kidney and ovary.
4. Myoma
Myoma is a benign tumour of muscle. It may
originate in smooth muscle (leiomyoma) or in
striated muscle (rhabdomyoma).
5. Chondroma
A chondroma usually arises with in the medullary
cavity of the tubular bones of the hands and feet,
it grows slowly, causing gradual expansion of the
bone.
B.
Example of Malignant Tumour
(Cancer)
Following are the example of malignant tumour.
1. Carcinoma
Cancer that arises in epithelium tissue that line the
skin and internal organ of the body. It may occur in
any tissue containing epithelia cells .e.g. renal cell
carcinoma.
71
2. Sarcoma
It is a malignant tumour of mesenchymal origin. It
is often with a prefix that denotes the tissue of
origin of the tumour, as in osteosarcoma (bone),
rhabdomyosarcoma (skeletal muscle), liposarcoma
(fatty tissue) and lieomyosarcoma (smooth
muscles).
3. Teratoma
It is usually arises in the ovaries or testes. Its
neoplasm is derived from all three germ cell layers,
which may contain structures such as skin, bone,
cartilage, tooth and intestinal epithelium.
Classification of Tumours
Tumours can be classified on the basis of more
than one character;
1. Embryogenesis Classification
In these tumours, the suffix blastoma is used, e.g
nephroblastoma,
aneuroblastoma
and
medulloblastonia.
These tumours are of embryonic origin.
2. Naked Eye Appearance:On gross examination, tumours may be;
Fungating, like cauliflower.
Annula.
Scirrhous, tumour is hard, feature due to large
amount of fibrous tissue present in the stroma.
Mucoid.
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3. Histogenic Classification
The cell type of origin forms an important feature
of this classification. The body by convention has
been divided into epithelium and connective
tissue. Two groups of tumors are therefore
recognized.
(i) Tumours of epithelial origin
(ii) Tumours of connective tissue origin
4. Histological Classification
It is that classification in which the tumours are
classified on the bases of cell type under the
microscope, e.g. small cell carcinoma, large cell
carcinoma, giant carcinoma, basal cell carcinoma
etc.
5.
Classification
Behavior
According
to
Tumour
Benign or innocent tumours.
Malignant tumours.
Intermediate tumours. (Locally invasive but

not spreading e.g basal cell carcinoma).
Latent Cancer
A proliferation of cell which has all the
characteristics of carcinoma, but yet remains
clinically silent and does not metastasize e.g
carcinoma of prostate.
73
Carcinoma in Situ
This is a pre-invasive proliferation of the epithelium
that has the cytological features of malignancy.
Spontaneous Regression
These are most attractive tumours. These cancers
suddenly regress, spontaneously and permanently
e.g. Burketts tumours.
Dormant Cancer
This is the late appearance of metastasis after the
primary tumour has been successfully removed.
6. Archeological Classification
This classification is based upon etiology e.g.
tumours due to radiation, chemical and viruses
etc.
7. Functional Classification
Some tumours produce hormones in sufficient
quantity to produce characteristic clinical and
pathological signs e.g. glaucoma & insulinoma etc.
Difference between
Malignant Tumour
S
#
1.
Benign
Tumour
and
Characteri
stics
Benign
Malignant
Differentiati
on
Well
differentiated
Range from well

differentiated
to
highly
undifferentiated
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2.
Anaplasia
3.
Spread
4.
Size
5.
Not
show
anaplasia
Remains
localized
Usually
of
small size
Show anaplasia
Spread to
surrounding tissue
Usually of large
size
Growth
Slowly
Rapid
6.
Metastasis
Never
metastasize
Metastasis
unequivocally
7.
Encap
solution
Capsulated
Non-Capsulated
Gross
appearance
Degeneration
necrosis
ulcerat-ion,
hemorrhage
less frequent
Degeneration
necrosis
ulceration,
hemorrhage more
frequent
Effects
They do not
endanger the
life unless a
vital organ is
involved
Acts as parasite
and tend to kill the
patient. Whenever,
its grow
Recurrence
Do
not Usually
reoccur
reoccur after after removal or
their removal radiotherapy
Death
Usually
fatal
patient
survives
8.
9.
10.
11.
not
and Very
fatal
patient die
and
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Spread of Malignant Tumours

Metastasis is a very prominent and the most
destructive character of malignant tumours. The
spread of malignant tumours occur through the
following channels.
Pathways of Spread
There are two main pathways of spread.
1. Direct Spread
Tumour may spread directly to the surrounding
tissue by,
a. Local Spread
The direct infiltration of surrounding tissues
(common to all malignant tumours) means that the
microscopic extent of a tumour exceeds its
macroscopic boundaries. The invading cells tend to
follow natural clefts or tissue planes and move in
the line of least resistance.
b. Invasion of Lymphatic
Carcinoma shows a particular tendency to invade
the local lymphatic at an early stage. In breast
cancer, the tumour cells grow progressively within
the lumen of the lymphatic as a solid cord which
extends in all direction. This process is called
permeation.
The central area of the malignant cord may
undergo necrosis and even disappear while the
advancing and proliferates.
c. Venous Invasion
The invasion of large veins is seen most frequently
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in lung cancer because of large number of vessels

available. Clear cell carcinoma of kidney is another
tumour in which venous invasion is very common.
d. Arterial Invasion
Local arterial invasion may obstruct the arteries
which may be responsible for tumour necrosis.
3. Embolic Spread
Embolic spread may be through following routes.
a. Lymphatic Spread
The detachment of group of tumour cells in an
invaded lymphatic lead to the production of
emboli, which become lodged in the subcopsular
sinus of regional lymph node.
If a lymphatic is blocked, the flow of lymph may be
reversed, and subsequently embolism produces
metastasis at un-usual sites.
b. Blood Spread
This pathway is typical of all sarcomas but also the
favoured route for certain carcinomas. For
example, those which originating in the kidneys
invade the branch of renal vein and then the renal
vein itself to grow in a snake like fashion up to the
inferior vena cava reaching the right side of the
heart.
c.
Spread Through infiltration of
Tissue Space
Spread of cancer cells through tissue space is one
of the chief characteristics of a malignant tumour.
77
The cancer cells are amoeboid and motile. The

cells of benign tumours and of normal tissue are in
capable of movement because they are firmly
anchored to one another by the cell adhesiveness.
Cancer cells are free because of a greatly reduced
adhesiveness. So they detach and metastasize.
d. Spread through CSF
The spread of tumour may also occur in cranial
cavity, where no lymphatic vessels are. Thus the
spread of tumour cells from brain to spinal cord or
spinal cord to brain is a passive phenomenon and
the malignant cells are carried through CSF.
=======================
========
Carcinogens
Any substances that, when exposed to living

tissue, may causes the production of cancer,
known as carcinogens.
OR
Carcinogens are substances that are known to
cause cancer or aggravate an incidence of
cancer.
The carcinogens damage the DNA of cells that may
persist if the cell divides
before damage is
repaired. Damaged cells may subsequently
develop into a cancer.
Types of Carcinogens
1. Chemical carcinogens
2.
Physical
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carcinogens
3. Viruses
preposition
5. Hormonal imbalance
factors
4.
Hereditary
6.
Nutritional
1. Chemical Carcinogens
Historically, chemical agents were the first to be
associated with cancers. Now-a-days, many
chemical carcinogens are known and their number
is constantly increasing.
Some are direct acting and require no chemical
transformation to induce carcinogenicity, but
others are indirect acting and become active only
after metabolic conversion. Such agents are
referred to as pro-carcinogens and their active end
products are called ultimate carcinogens.
2. Physical Carcinogens
The important physical agents associated with
neoplasia are in ionizing radiation and ultraviolet
radiations.
a. Ultraviolet Radiation (Sunlight)
Ultraviolet radiation in sunlight is associated with
skin cancers especially on exposed areas.e.g.
S.N
o
Chemical
79
Types of Cancer
1.
2.
3.
4.
5.
6.
7.
Cigarette smoking
Lung, bladder cancer
Tobacco chewing
Oral cavity cancer
Aflatoxins
Liver cancer
Asbestos
Lungs cancer
Benzene
Leukemia
Vinyl chloride
Liver (angoras coma)
Poly cycle hydro Skin cancer
carbons
8.
Nickel
Lung cancer
a. Squamous cell carcinoma.
b. Basal
cell carcinoma.
c. Malignant melanoma.
b. X-Ray Radiation
Excessive exposure to x-ray radiation is associated
with,
Leukemia
Papillary thyroid carcinoma
Sarcoma
c. Radioisotopes
The carcinogenic effect of radioactive materials
was first recognized when many cases of
osteosarcoma occurred among factory workers,
who used radium containing paints to produce
luminous watch faces. e.g.
1 Lung cancer
2. Liver cancer
3 Thyroid cancer
d. Nuclear Fall-Out
Leukemia and carcinoma of the breast is common in
the people of Hiroshima and Nagasaki (Japan), who
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survived the bomb blast.
3. Virus
Tumor producing (oncogenic) viruses have been
demonstrated in most species including man.
Some are DNA viruses and other contains only
RNA.
Oncogenic viruses are classified as below;
A. RNA Viruses
RNA containing viruses are the following,
i.
Human
immunodeficiency
(HIV).
ii.
Human T cell leukemia virus.
B. DNA Viruses
(i) Herpes viruses
a.
Ebstein Barr virus.
b.
simple virus.
virus
Herpes
(ii) Papova Viruses

a. Papilloma virus
b.
Polyoma
virus
c. Simian virus 40
d. Hepatitis B
virus
e. Adeno viruses
All these viruses have in common the ability to
integrate their genetic material (RNA or DNA) into
the DNA of the host cell. The effect of this is to
transform the cell such that it is capable of forming
a tumor by continuous growth.
4. Hereditary Predisposition
81
There is little significant hereditary predisposition

to most of the common cancers.
Illustrative
examples are:
a.
Retinoblastoma
b.
Neurofibromatosis
c.
Nephroblastoma
d.
Familial adenomatous polyposis coli (APC)
e.
Xeroderma pigmentosum
5. Hormonal Imbalance
Following hormones quantity also leads to tumour
production condition;
a.
High estrogen
b. Endometrial carcinoma.
c.
Anabolic steroids
d. Liver cell carcinoma.
6. Nutritional Factors
Nutritional imbalance also leads to tumour
formation which is given below.
(a) Low fiber diet (Colon cancer).
(b)
High fat diet
(Colon and breast
cancer).
(c) Vitamin C and E have protective effect.
Difference
Sarcoma:-
between
Carcinoma
and
Carcinoma
Epithelial origin.
More common.
Metastasis preferly via lymphatics in early
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stages.
Necrosis common.
Hemorrhages less frequent.
Sarcoma
Mesenchymal origin.
Less common.
Metastasis preferly via blood vessels (veins).
Necrosis less common.
Hemorrhages more frequent.
=========================
======
83
Chapter No. 08
Immunity
Immunity
The ability of human body to resist almost all

kinds of organisms and toxin that tend to
damage or produce toxic effects in the tissue
and organ is called immunity.
OR
Non-Susceptibility to a given organism. The
bodys ability to resist infection, afforded by the
presence of circulating antibody and white
blood cells is called immunity.
Types
There are two types of immunity.
1.
Innate Immunity
It is present in all living being irrespective of their

stage in evolution. It can be initiated immediately
against any invader with out any previous contact.
The main components are.
Phagocytes
(neutrophills,
monocytes
and
macrophage by WBCs)
Resistance of skin to invasion of micro
organism.
Acid in stomach also destroys organisms which
are ingested.
Presence in blood of certain chemicals, such as
lymphocytes, basic polypeptide & natural killer
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lymphocytes.
2. Acquired Immunity
Much of immunity is caused by special immune
system that forms antibodies and activated
lymphocytes that attack and destroy the specific
organism or toxin. Such immunity is called
acquired immunity. It is of two sub type.
a. Active Immunity
It is the immunity which an individual develops as
a result of infection or by specific immunization
and is usually associated with presence of
antibodies or cell having specific action on micro
organism of particular disease. e.g. chicken pox
and rubella etc.
b. Passive Immunity
When preformed antibodies in one body (human or
animal) are transferred to another it produces
passive immunity.
Passive immunity may be induced,
By administration of an antibody containing
preparation.
By transfer of maternal antibodies across the
placenta.
By inoculation of immune blood or serum from
convalescents.
Antigens
An antigen is any substance which provokes a
specific immune response.
85
Common antigens are infectious agents and other

foreign substances can also stimulate immune
response.
Chemistry of Antigens
The chemistry of antigen is mostly protein. But it
may
be
carbohydrates,
lipid
and
lipopolysaccharide.
Types
(i) Hepaten
The small molecule is called a hapten, which are
unable to act as antigen, if they get attached to a
protein, antibody to the chemical may be induced.
(ii) Carrier
The large molecule which is directly stimulates
immune system and act as antigen.
Antibody (Immunoglobulin)
A special kind of blood protein that is synthesized
in lymphoid tissue in response to the presence of a
particular antigen, and circulates in the plasma to
attack the antigen and make it harmless.
The production of specific antibodies against
antigen as diverse invading bacteria, inhaled
pollen, virus, fungi and other foreign material.
Blood contain three types, of globulin, alpha, beta
and gamma. Antibodies are gamma globulin.
Types of Immunoglobulin
Ig G
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It is the abundant type of immunoglobulin

present in serum.
It is the smallest but most common antibody
about 75% to 80%.
Ig G antibodies are very important in fighting
bacterial and viral infections.
Ig G antibody is the only antibodies which cross
the placenta in a pregnant female to help
protect her baby (fetus).
It is the most abundant antibodies in newborn.
It acts as opsonin and therefore enhances
phagocytosis.
Ig M
Ig M antibodies are the largest antibody.

Ig M antibodies are about 5% to 10% of all the
antibodies in the body.
It provides defense against bacteria and
viruses.
It does not cross placenta.
It can activate other immune cells to react
against pathogens.
It is found in blood and lymph fluid.
Ig A
IgA antibodies are found in parts of the body

such as nose breathing passage, GIT, eyes and
vagina.
This type of antibody is also found in saliva.
IgA antibodies prevent attachment of micro
87
organism to mucus membrane.

IgA amount in serum is about 10% to 15%.
IgA cant cross placenta & not activate other
immune cells.
Ig E
Ig E antibodies are found in the lungs, skin and

mucus membranes.
Its concentration in serum is very low, but rises
in allergic conditions and helminthes infections.
It reacts against pollen, fungus, spores and
animal dander.
It mediates types I hypersensitivity reaction by
causing release of mediators from mast cells
and basophiles upon exposure to antigen.
Ig D
Ig D antibodies are found in small amounts in

the tissues that line the belly or chest. How they
work is not clear till.
=========================
======
Cells of Immune System

Immune system consists of the following cells.
Lymphocytes
Lymphocytes are spherical cells, approximately 10
micron meter in diameter with a prominent
nucleus of densely packed nuclear chromatin.
There are two main types, the T and B
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lymphocytes.
(a) T-Lymphocytes / cells
T cells are developing in the thymus of the fetus.
They have principal functions, and are divided into;
HELPER / INDUCER CELLS
Induce cells enhances certain immune response.
They receive antigen form specialized presenting
cells and initiate or reinforce antibody production,
natural killer cells (NKCs) and cytotoxic responses.
T-helper cells can be distinguished by the presence
of the CD4 protein on their surface.
CYTOTOXIC / SUPPRESSOR CELLS
Suppressor cells which can kill another cells. This
kind of response is used in dealing with virus
infection and cancer cells.
The suppressor cells can down-regulate immune
responses at an appropriate time. The cytotoxic
/suppressor lymphocytes can be recognized by the
presence of the CD8 cells surface molecule.
(b) B- Lymphocytes / cells
B-cells are developing in the fetal liver or bone
marrow. These cells produce antibody and
comprise approximately 25% of the lymphocytes
population.
B lymphocytes capable of producing a specific
antibody to a given antigen are rapidly encouraged
to multiply by a mechanism called clonal
expansion. In this process, once a B cells has
been exposed to a specific antigen, and in the
presence of cytokines, it is activated and divided.
89
Following this expansion step, B lymphocytes

differentiate to become plasma cells which
produce large amounts of antibody. B lymphocytes
can be distinguished by the presence of the CD19
and CD20 molecules.
NKCs (natural killer cells)
The natural killer cells (NKCs) are large granular
lymphocytes which are capable of lysing a variety
of tumor cells, virus-infected cells and fungi. They
differ from T&B lymphocyte in respect that they do
not require prior sensation for expression of their
function.
The granules, which contain acid, are thought to
be involved in the cytotoxic events. NKCs are nonphagocytic, and most are CD4-, CD8-and surface
immunoglobulin negative but carry the CD56+,
CD2+ marker on their surface.
Macrophages
A large scavenger cell (a phagocyte) present in
connective tissue and many major organs and
tissues, including the bone marrow, spleen, lymph
node, liver(Kupffer cells), and the central nervous
system (microglia). They are closely related to
monocyte. Fixed macrophages (histolytes) are
stationary within connective tissues.
Free macrophages wander between cells and
aggregate at focal sites of infection, where they
remove bacteria or other foreign bodies from blood
or tissues.
Hypersensitivity Reactions
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Hypersensitivity is the term used when an immune

response results in exaggerated or inappropriate
reactions harmful to the host.
Types : Hypersensitivity reactions are the flowing
types.
Type
Immediate
( Anaphylactic )
Hypersensitivity Reaction
An immediate hypersensitivity reaction occurs
when an antigen (allergen) binds to IgE on the
surface of the mast cell with the consequent
release of several mediators.
Mechanism
1 On first exposure to antigen there is production
of IgE antibodies by B cell.
2 The IgE antibody in them bound to Fc receptors
on basophiles and mast cells.
3 On subsequent exposure to antigen, the antigen
reacts with bound IgE antibody causing cross
linking (bridging) of adjacent IgE molecules.
4 This binding results in degranulation of
basophiles and mast cells.
5 Degranulation results in release of histamine
and other mediators.
Chemical mediators involved in type 1
reaction
Following chemical mediators are involved in type
1 reaction.
1 Histamine.
2. Leukotrienes.
3 Eosinophilic chemotactic factor.
91
Prostaglandins and thromboxanes.
Cell involved in type 1 reaction

The mast cells and basophiles are involved in type
1 reaction.
Antibodies involved in type 1 reaction:IgE are mainly involved.
Phase of type 1 reaction
a) Initial phase
1 It occurs within minutes after exposure to the
offending antigen.
2 It is mediated by histamine which causes
vasodilatation, increased capillary permeability
and smooth muscle contraction.
b)
Late phase
1 It occurs after several hours within additional
exposure to the offending antigen.
2 It is mediated by chemical mediators other than
histamine, which not only cause effects similar
to histamine, but also tissue infiltration by
basophiles and mast cells and other cell types.
Clinical example
The
clinical
manifestations
of
type
1
hypersensitivity can appear in various forms e.g.
urtricaria (hives), eczema, rhinitis, conjunctivitis
and asthma.
The clinical appearance occurs depends in large
part on the route of entry of the allergen and on
the location of the mast cells bearing the IgE
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specific for the allergens.
Type II cytotoxic hypersensitivity

Cytotoxic hypersensitivity occurs when antibody
directed at antigen of the cell membrane activities
complement. This generates a membrane attack
complex, which damages the cell membrane.
Mechanism
According to the mechanism there are three
varieties of type II
reactions;
Complement mediated cytotoxicity.
Antibody dependent cytotoxicity.
Antibody mediated cellular dysfunction.
The mechanism of hypersensitivity is different in
each of these three part types.
1. Complement mediated cytotoxicity
1. Complement fixing antibodies react with cell
surface antigen.
1. Complement fixes to antigen antibody complex.
1. There is resulting cell lyses and destruction.
1. Serum complement level is found to be
decreased.
Clinical examples.
Warm antibody auto immune hemolytic.
Hemolytic transfusion reaction.
Erthoblastosis fetalis.
Good pasture syndrome.
2.
Antibody dependent cytotoxicity (ADCC)
1
2
93
In this type antibody reacts directly with target

cell without involvement of complement.
Firstly Fc portion of the antibody molecule
reacts with Fc portion of a variety of cytotoxic
leukocytes, most important seeing natural killer
(NK) cells.
Then there is interaction of antibody bound Fc
portion of NK cells and Fc portion of target cells
which results in their destruction.
3.
Antibody mediated cellular hyper
function:
1 In this type antibodies directed against cell
surface receptors either impair cellular function
(antibody mediated cellular hypo function) or
cause hyper functioning of cellular function
(antibody mediated cellular hyper function)
Clinical examples are;
a.
Myasthenia gravis
There is an example of antibody mediated cellular
hypo function.
b. Graves disease.
There is an example of antibody mediated cellular
hyper function.
Antibodies involved in type II reaction
Ig G is chiefly involved in type II reaction.
Type III immune complex hypersensitivity
Immune complex hypersensitivity occurs when
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antigen
antibody
complex
induced
an
inflammatory response in tissues. Normally
immune complex are rapidly removed by reticulo
endothelial system. But occasionally they persist
and are deposited in tissue, resulting in several
disorders.
Mechanism
1
2
3
4
After exposure to an antigen antibodies are

produced and antigen antibody complexes are
thus formed.
These immune complexes are deposited in
tissues.
Immune complexes cause several reactions.
A platelet aggregation causes formation of
micro thrombi and thus ischemia.
Antibodies involved in type III reaction

Mostly Ig G is involved.
Clinical examples
Two typical type III hypersensitivity reactions are
the arthus reaction and serum sickness.
a) Arthus reaction
Arthus reaction is the inflammation caused by the
deposition of immune complex at a localized site.
Mechanism
If animals are given an antigen repeatedly until
they have high level of Ig G and that antigen is
then injected subcutaneously or interdermally,
95
severe hypersensitivity reaction occurs as a result

of formation of immune complex.
Clinical example
A clinical manifestation of Arthus reaction is
hypersensitivity
pnuemonitis
which
follows
inhalation of actinomyecetes (farmers lung).
c)
Serum sickness
Serum sickness is a systemic inflammatory
response to the presence of immune complex
deposited in many areas of the body.
Mechanism
After the injection of foreign serum or drug, the
antigen is released slowly and during this period
antibody production starts.
This lead to the formation of immune complexes.
The symptoms of serum sickness improve as the
immune system gradually removes the antigen.
Clinical example
Following are the S / S of serum sickness.
1. Fever
2. Urtricaria
3. Lymphadenopathy
3. Spleenomegaly
5. Eosinophilia
Immune complex diseases
Many diseases are associated with immune
complex deposition although the exact nature of
aggravating antigen is not known.
Examples include.
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1
2
3
Rheumatoid arthritis
Posts streptococcal glomeralonephritis
Systemic lupus erythematosus (SLE)
Type of hypersensitivity reaction

It is also called cell mediated hypersensitivity.
This hypersensitivity reaction is mediated by T
lymphocytes and is delayed i.e. it starts hours or
days after exposure to antigen.
Mechanism
According to the mechanism involved there are
two types of type IV reaction.
Delayed hypersensitivity
1 Antigens are presented by macrophages with
HLA class II MHC.
2 There is interaction of CD 4 + lymphocytes with
this antigen.
3 There is formation of CD 4 + memory T cells.
4 On subsequent exposure to antigen CD 4 +
memory T. cells proliferate and secrete
cytokines (1L 2 and others).
5 These cytokines stimulate the recruitment of
macrophages and their transformation into
epithelia cells and thus granuloma formation.
6 Two
clinical
examples
are
contact
hypersensitivity
and
tuberculin
type
hypersensitivity.
Contact hypersensitivity
1 This occurs after sensitization with sample
97
examples (e.g. nickel) topically appeared drug

(e.g. sulfonamides) soaps and cosmetics.
These small molecules act as hapten and enter
the skin, attach to proteins and become
complete antigen and then induce delayed
hypersensitivity reaction. Upon later contact
with same antigen hypersensitivity reaction
occurs.
c.
Tuberculin type hypersensitivity:When a person is exposed to mycobacterium
tuberculosis the antigens induced delayed type of
hypersensitivity reaction.
Upon re-exposure to the antigen clinically
manifested hypersensitivity reaction occurs. This is
basis of Mantoux test.
=========================
======
Mantoux Test
Procedure
0.2 Ml of inactivated antigen of mycobacterium
is injected interdermally.
The test is evaluated by measuring the
diameter of indurations around the injection
site.
The positive response develops in 24-48 hours
and remains positive for some days.
T-Cell mediated cytotoxicity
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In this CD 8 + T lymphocytes directly will target

cells without involvement of cytokines.
This kind of reaction is seen against virus
infected cells and humor cells whose antigens
present on cell surface with class 1 MHC and
direct killing by CD + T lymphocytes occurs.
Cell involved in type IV reaction

T lymphocytes are involved.
Auto Immune Disease
These are conditions in which immune reactions
are directed towards tissues of the host with
apparent inability to distinguish self from non self.
Characteristics of auto immune diseases:These are characterized by one or more of the
following features.
The presence of auto antibodies.
More common in female
Association with other auto immune diseases.
Genetic predisposition
Fibrinoid change in connective tissues so also
called sometimes as connective tissue diseases.
Association with HLA types.
These diseases can involve one organ or one
type of cell or may involve multiple organs.
Mechanism
Several mechanisms have been
explain auto immune disease.
proposed
to
99
a. Molecular mimicry
The environmental trigger (e.g. some virus or
bacteria) can resemble a component of the body
so that the immune attack is directed against the
cross reacting body components e.g. rheumatic
fever.
b.
Alteration of normal protein
Drugs can bind to normal protein and can make
them immunogenic. For example procainamide
included systemic lupus erythematosus (SLE).
c.Release of requested antigen
Certain tissues e.g. CNS, lens and uveal tract of
the eyes are requested, so that their antigens are
not exposed to immune system. When such
antigens enter in the circulation accidently e.g.
after trauma they elicit an immune response. For
example encephalitis and endophthalmitis etc.
Important auto immune diseases
a. One organ or one type of cell involved:1 Diabetes.
2 Auto immune thrombocytopenia.
3 Auto immune hemolytic anemia.
4 Gravess diseases.
5 Multiple sclerosis.
6.
Hashimotos
thyroiditis.
7 Myasthenia gravis.
8.
Acute
glomerulonephritis.
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b.
1
2
3
4
5
6
Multiple organs involved

System lupus Erythematosus (SLE).
Rheumatoid arthritis.
Rheumatic fever.
Good Pasteur syndrome.
Vasculitic syndromes.
Dermis.
Transplant Immunology
For a successful graft, donor and recipient must be
matched for ABO blood group and for as many HLA
antigens as possible.
Types
Grafts can be of following types.
a Autograft
Transfer of tissue b/w genetically identical
individual e.g. identical twins.
b Xenograft
Transfer of tissue between individuals of different
species. It is always takes permanently.
c
Allograft
Transfer of time b/w generally different member of
same species. It is always rejected unless the
patient recipient immune system is suppressed by
immune suppressant drugs radiation or recipient T
cell depletion, but each of these can result in
clinically significant immunodeficiency.
d Transplant Rejection
The success of organ transplantation is affected by
101
the compatibility of MHC games of the donor and

the recipient.
Unless immune suppressive measures are takes,
allograft are rejected by a process called allograft
rejection.
The severity rejection will vary depending upon the
degree of the differences between the donor and
the recipient at the MHC (major histocompatibility
complex) locus.
Graft Rejection
Graft rejection is of following types.
1 Hyper acute Rejection
It occurs within minutes of transplantation. It is
primarily antibody mediated and occurs when
there is presence of pre existing antibody to donor
antigens.
It is a localized arthus reaction marked by acute
inflammation, fibrinoid necrosis of small vessels
and extensive thrombus.
i
Acute Rejection
It occurs within months of transplantation.
It is primarily T cell mediated and is characterized
by infiltration of lymphocytes and macro phages.
ii Chronic Rejection
It occurs months to years after transplantation.
It is primarily due to antibody mediated vascular
damage.
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Graft Versus Host Disease (GVHD)

If immune suppressed individual (e.g. leukemia
patients) undergo bone marrow transplantation T
cells from the graft proliferate in the host and
develop and immune response against the host
tissues.
The principal target organs are skin, liver and
alimentary tract.
=========================
======
103
Chapter No. 09
M I C R O B I O LO G Y
Parasite
Parasite means eating from the table of
another. A living organism that lives in
(endoparasite) or on (ectoparasite) another living
organism (host) is called parasite.
Parasitology
The study and science of parasite is called
Parasitology.
True parasite:
The organisms which nourish
themselves on living material are true parasite.
Saprophyte:
Any free-living organism that
lives and feeds on the dead and putrefying tissue
of animal or plant.
Host
Animal or plant in or upon which a parasite lives /
harbor is called host.
(a) Intermitted Host
The host in which a parasite passes its larval or
asexual stage.
(b)
Definitive Host
The host in which a parasite develops to it sexual
stage.
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Symbiosis
An intimate and obligatory association between
two different species of organisms (symbionts) in
which there is mutual aid and benefit they are so
dependent upon each other that one cannot live
without help other.
Infection
When the parasite establishes it self with the
host, it is termed infection.
OR
Invasion of the body by harmful organism
(pathogen) such as bacteria, fungi, virus and
protozoa etc.
Infestation
The presence of animal parasite either on skin
(e.g. tick) or inside the body (e.g. tapeworm).
CLASSIFICATION OF PARASITES
Parasites occur in two distinct forms, single called
protozoa and multi-cellular metazoan called
helminthes or worms. Furtherly the protozoa can
be subdivided into four groups i.e. sarcodina
(amebas), sporoza (sporozoans), mastigophora
(flagellates) and ciliate (ciliates).
Metazoans are subdivided into two phyla; the platy
helminthes (flatworms) and the nemathelminthes
(roundworms and nematodes). The phylum platy
helminthes contains two important classes i.e.
cestoda (tape worm) and trematoda (flukes). This
classification is diagrammed in figure.
105
Parasites
Protozoa
(Helminthes)
Sarcodina
Metazoan
sporoza Mastigophora
Platy helminthes (Plat worm)

(Round worm)
Ciliata
Nemathelminthes
Trematoda (Flukes)
Cestoda (Tape worms)
=========================
======
INTESTINAL
PROTOZOA
Entamoeba
Entamoeba
histolytica
causes
dysentery and liver abscess.
amoebic
Life Cycle
The life cycle of E. Histolytica has two stages the
motile amoeba (trophozoites) and the non motile
cyst.
Definite host:
Man
Intermediate host:
No intermediate host
The organism is acquired by ingestion of cyst
that is transmitted primarily by the fecal oral
route in contaminated food and water.
The ingested cysts differentiate into trophozoite
in the ileum, but tend to colonize in the cecum
and colon.
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The trophozoites invade the colonic epithelium

and secrete enzymes that produced flask
shaped ulcer, that can damage and destroy
large areas of the intestinal epithelium.
Progression into the sub mucosa leads to
invasion of the portal circulation by the
trophozoites causing the liver abscesses which
consists trophozoites.
Some of the amoeba from large intestine
develop into cyst and are extracted in the
faeces which contaminate water and food
materials and cycle repeated.
Clinical findings
Acute intestinal amebiasis present as dysentery
i.e. bloody mucus containing diarrhoea along with
lower abdominal discomfort and flatulence.
Amebic abscess of the liver is associated with pain,
weight loss, fever and a tender enlarged liver right
lobe abscesses can penetrate into the diaphragm
and cause lung disease.
Lab Diagnosis
1. Stool D / R
Diarrhoeal stools should be examined within 1 hour
of collection to see the amoeboid motility of the
trophozoites. Trophozoite contains ingested red
blood cells.
2. Serological Test
Serologic testing is useful for the diagnosis of
107
invasive amebiasis. In this type of test detect the

antibodies.
Diagnosis of hepatic amebiasis
Ultra sound.
Aspiration of pus for detection of E. histolytica.
Examination of stool (cyst may be present).
Treatment
The treatment of choice for symptomatic intestinal
amebiasis or hepatic abscesses is metrionidazole
or tinidazole.
Prevention
Prevention is avoiding fecal contamination of food
and such as hand washing.
Giardia lamblia
Giardia lamblia causes giardiasis and is present
in two forms, i.e. trophozoites and cysts.
Life Cycle
The life cycle consists of two stages, the
trophozoite and the cyst. The trophozoite is pear
shaped with two nuclei, four pairs of flagella and a
suction disk.
The oral cyst is thick walled with four nuclei and
several internal fibers. Each cyst gives rise to two
trophozoites during excystation in the GIT.
Transmission occurs by ingestion of the cyst in
faceally contaminated food and water. Excystation
take place in the duodenum, where the
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trophozoites attach to the gut wall, but does not

invade.
The trophozoite causes inflammation of the
duodenal mucosa, leading to malabsorption of
protein and fat. The cysts excrete with stool and
contaminate water and food particles.
Clinical finding
Non-bloody foul smelling diarrhea, flatulence and
abdominal cramps persisting for weeks or month.
There is no fever.
Laboratory diagnosis
Diagnosis is made by finding trophozoites or cyst
or both in diarrhoeal stools.
Treatment
The treatment of choice is metrionidazole (flagyl)
or quinacrine hydrochloride.
Prevention
Prevention involves boiled filtered or iodine treated
water in endemic areas and while hiking no
prophylactic drug or vaccine is available.
=========================
======
Blood and Tissue

Protozoa
Plasmodium
Malaria is caused by four plasmodia.
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1. Plasmodium Vivax
Producing benign tertian fever and its incubation
period is 12-15 days.
2. Plasmodium Ovale
Producing benign tertian fever and its incubation
period is 18 days.
3. Plasmodium Malariae
Producing benign quartan fever and its incubation
period is 24 days.
4. Plasmodium Falciparum
Producing malignant tertian fever and its
incubation period is 8-20 days. P-Vivax and P.
Falciparum are more common than the P. Ovale
and P. Malariae worldwide. Malaria is one of the
most common infectious diseases, and a leading
cause of death.
Life Cycle
Definitive Host
Female anopheles mosquito (only female takes a
blood meal).
Intermediate host:
Man
There are two phases in the life cycle. The sexual
cycle, which occurs primarily in mosquito and the
A sexual cycle, which occur in humans the
intermediate hosts.
The sexual cycle is called sporogny because
sporozoites are called schizogony because
schizonts are formed.
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Cycle in Man
1. The life cycle in human begins with the
introduction of sporozoites into the blood from
the saliva of the biting mosquito.
2. The sporozoites are taken up by hepatocytes
within 30 minutes. This exoerythrocytic phase
consists of cell multiplication and differentiation
into merozoites.
3. Merozoites are released from the liver cell and
infect RBCs. During the erythrocytic phase, the
organism differentiates into a ring shaped
trophzoite.
The trophozoites differentiate into schizont filled
with merozoites. RBCs rupture and merozoites
released. Merozoites infect other red blood cell.
This cycle in the red blood cell repeats at regular
intervals typical for each species. The periodic
release of merozoites causes the typical recurrent
symptoms of chills fever and sweats seen in
malaria patients.
Cycle in Mosquito
Gametocytes zygote Ookinatte oocyst
sporozoites sporozoites in saliva injection in
man and then cycle are repeated.
Clinical Findings
Malaria presents with sudden onset of fever and
chills, along with headache, myalgia and arthralgia
about 2 weeks after the mosquito bite.
Fever may be continuous early in the disease the
typical periodic cycle does develop for several
111
days of onset. Untreated malaria caused by P.

falciparum is more life threatening as a result of
extensive brain and kidney damage.
Lab Diagnosis
MP:
Malaria parasite is detected in patient
blood.
PCR: PCR (polymerase chain reaction) based test
for
plasmodium nucleic acid.
ELISA: Test for a proteins specific for P. falciparum
can be useful.
Treatment
Chloroquine is the drug of choice for acute malaria.
For Chloroquine or a combination of quinine and
doxycycline used.
=========================
======
Leishmania
The genus leishamania includes four major
pathogens, leishamania donovani, leishamania
tropica, and leishamania mxicana and leishamania
braziliensis.
a.
Leishmania donovani
L. donovani is the cause of kala-azar (visceral
leishminasis).
Definite host:
Intermediate host:
Life cycle
Female sand fly

Dog and rodents
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In sand fly
When the sand fly sucks blood from an infected
host ingests macrophages containing amastigotes.
After dissolution of the macrophages the freed
amastigotes differentiate into promastigotes in the
gut.
They multiply and then migrate to the pharynx,
where they can be transmitted during the next
bite. The cycle in the sand fly takes approximately
10 days.
In human
When sand fly bites human being, their
promastigotes are engulfed by macrophages
where they transfer into amastigotes.
The infected cells die and release progeny
amastigotes, which infect other macrophages and
reticulo endothelial cells. The cycle is completed
when the sand fly ingests macrophages containing
the amastigotes.
Pathogenesis
In visceral leishminasis, the organ of the reticulo
endothelial system i.e. liver spleen and bone
marrow are the most severely affected. Reduced
bone marrow activity coupled with cellular
destruction in the spleen result in anemia,
leucopenia and thrombocytopenia.
They lead to secondary infections and a tendency
to bleed.
Clinical findings
113
Symptoms
begin
with
intermittent
fever,
weakness, weight loss and massive enlargement of
the spleen. The course of disease runs for months
to years.
Initially patients feel reasonably well despite
persistent fever. As anemia, leucopenia and
thrombocytopenia become more severe weakness,
infection and GIT bleeding occur.
Lab Diagnosis
1 Serologic test.
2 Biopsy of spleen, bone marrow or lymph node
for the detection of organism.
3 Very high level of serum IgG is indication of
infection.
Treatment
The treatment is sodium stibogluconate, a
pendtrardent antimony compound, with proper
therapy. The mortality rate is reduced to near 50%
recovery results in permanent immunity.
=========================
======
Trichomonas Vaginalis
Trichomonas vaginalis causes trichomoniasis. T.
vaginalis is a pear shaped organism with a central
nucleus and four anterior flagella. It exists only as
a trophozoite, there is no cyst form.
Transmission
The organism is transmitted by sexual contact and
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hence there is no need for a durable cyst form.

Clinical findings
In women
A watery foul smelling, greenish vaginal discharge
accompanied by itching and burning occurs.
In men
In men is usually asymptomatic, but about 10% of
infected men have urethritis.
Lab diagnosis
In a wet mount of vaginal or prostatic secretions,
the pear shaped trophozoites have a typical jorkey
motion.
Treatment
The drug of choice is metrionidazole (flagyl) for
both partners to prevent re-infection. The usage of
condoms limits its transmission.
=========================
======
Toxoplamsa
Toxoplamsa
gondii
causes
toxoplasmosis
including congenital toxoplasmosis.
Definitive host:
Domestic cats.
Intermediate host:
Humans and other
mammals.
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Life cycle
The cyst ingested with the undercooked meat or
from contact with cats faeces. In the small
intestine the cysts rupture and release from that
invade the gut wall. Where they are ingested by
macrophages and differentiate into rapidly
multiplying trophozoites, which kill the cells and
infect other cells.
Congenital infection of the fetus occurs only when
the mother is infected during pregnancy. If she is
infected before the pregnancy, the organism will
be in the cyst form and there will be no
trophozoites to pass through the placenta.
Clinical findings
Most primary infections in immuno competent
adults are a symptomatic but some reasonable
infections
mononucleosis,
except
that
the
heterophil antibody test is negative.
Congenital infection can result in abortion, still
birth or neonatal disease with encephalitis,
chorioretinitis and hepatospleenomegally. Fever
jaundice and intracranial calcification are also
seen.
Lab diagnosis
Acute disease is diagnosed by the presence of
trypomastigotes in thick or thin films of the
palinodes blood.
Serological test also performed.
Treatment
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The drug of choice for the acute phase is

nifutimox, when kills trypomastigotes in the blood.
Benzindazole is an alternative drug.
Prevention
Prevention involves protection from the red uriid
bite, improved housing hygienic condition and
insect control.
=========================
======
Cestodes
Platy helminthes (platy means flat while
helminthes means worm) are divided into two
classes, which included cestoda (tape worm) and
trematoda (flukes).
Cestoda (tape worm) consists of two main parts a
rounded head called a scolex and a flat body of
multiple segment called proglottids.
Taenia
There are two important human pathogens in the
genus taenia.
Taenia solium
T. Saginata
1. Taenia Solium
The adult form of T. Solium causes taeniasis. T.
Solium larvae cause cysticercosis.
Definite host:
Man
Intermediate host:
117
Pig
Life Cycle
In cysticercosis, a more dangerous sequence
occurs when a person ingested the worm eggs in
food or water that has been contaminated with
human faces. Note that in cysticerosis, human are
infected by eggs excreted in human faeces, not
ingested undercooked pork (animal protein).
The egg hatch in the small intestine and the
oncospheres borrow through the wall into a blood
vessel. The adult tapeworm attached to the
intestinal wall causes little damage.
The cystcerci on the other hand, can become very
large especially in the brain where they manifest
as a space occupying lesson.
Clinical findings
Most
patients
with
adult
tapeworm
are
asymptomatic but anorexia and diarrhea can occur.
Cysticercosis in the brain causes headache,
vomiting and seizures.
Cysticercosis in the eye can appear as uveitis or
retinitis.
Lab diagnosis
Eggs are found in the stools. Serologic test e.g.
ELISA (Enzyme Linked Immunosorbent Assay) that
detect antibodies to T. Solium antigens are
available but they may be negative in
neurocysticercosis.
Treatment
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The treatment of choice for the intestinal worm is

praziquantel. Albendazole is an alternative to
praziquantel.
Prevention
Prevention of taeniasis involves cooking pork
adequately and disposing of waste properly.
Taenia Saginata
T.Saginata causes taeniasis. T. Saginata larvae
do not cause cysticercosis.
Intermediate Host:
Definite host:
Cattle and cow.

Man.
Life Cycle
Egg are passed in faeces of infected man or
though portal circulation. They reach to liver, lung,
heart systemic circulatory carried to muscle,
where they settle in muscle each oospores from
oval sac containing larvae called cysticerus.
Infected meat containing the larvae is eaten by
man development of adult worm in human GIT
adult worm eggs of worm released in faeces and
ingested by cattle, thus continuing the cycle.
Clinical features
Most
patients
with
adult
tapeworm
are
asymptomatic, but malaise and mild cramps can
occur. In some patients proglottids appear in the
stools and may even protrude from the anus.
Lab Diagnosis
119
Eggs are found in the stools less often than are the
proglottids.
Treatment
The treatment of choice is praziquantel.
=========================
======
Nematodes
Nematodes (nemathelminthes) are round worm
with a cylindrical body and a complete digestive
tract, including a mouth and an anus.
The body is covered with a non cellular, highly
resistant coating called a cuticle. Nematodes have
separates sexes; the female is usually larger than
the male. The male typically has a called tail.
Intestinal Nematodes
Enterobius
Enterobius vermicularis
infection enterobiasis.
causes
porn
worm
Life cycle
The life cycle is limited to human.
The infection is acquired by ingesting the worm
eggs.
The egg hatch in the small intestine, where the
larvae differentiate into adults and migrate to
colon.
The adult male and female worms live in the
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colon. Where mating occurs.

At night, the female migrates from the anus and
release thousands of fertilized eggs on the
perianal skin and into the environment.
Within 6 hours, the eggs develop into larvae
become infectious.
Re-infection can occur if they are carried to the
mouth by finger after scratching - the itching
skin.
Clinical findings
Perianal pruritus is the most prominent symptom;
pruritus is though to be an allergic reaction to the
presence of either the female or the eggs.
Scratching predisposes to secondary bacterial
infection.
Scotch tape technique
The eggs are recovered from perianal skin by using
the scotch tape technique and can be observed
microscopically.
These eggs are not found in the stool.
Treatment
Mebendazole or pyrantel pemoate is effective.
They treat adult worms in the colon, but not the
eggs, so that treatment for 2 weeks is suggested.
Re-infection is very common.
=========================
======
121
Ascaris
Ascaris lumbricoides causes ascariasis.
Intermediated host:
Definite host:
No intermediated host.
Man.
Life cycle
1. Humans are infected by ingesting worm eggs in
food or water contaminated with human faeces.
2. The egg hatch in the small intestine and the
larvae migrate through the gut wall into the
blood stream and then to the lungs.
3. They enter the alveoli and pass up the bronchi
and trachea and are swallowed.
4. With in the small intestine, they become adult
and live in the lumen, do not attach to the wall,
and derive their nourishment from ingested
food.
5. Thousands of eggs are laid daily. Which are
passed in the faeces and form embryos in warm
& moist soil. Ingestion of the embryonated eggs
completes the cycle.
Clinical findings
The major damage occurs during larval migration
rather than from the presence of the adult worm in
the intestine. Most infection is asymptomatic.
Ascaris pneumonia with fever, cough and
eosinophila can occur with a heavy larval burden.
Abdominal pain and even obstruction can result
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from the presence of adult worms in the intestine.

Diagnosis is usually made microscopically by
detecting egg in the stools. The egg is oval with an
irregular surface. Occasionally the patient sees
adult worm in the stools.
Treatment
Both mebendazole and pyrantel pemoate are
effective.
=========================
======
Wuchereria
Wuchereria
bancrofti
causes
filariasis.
Elephantiasis is a striking feature of this disease.
Definite host:
Human.
Intermediate host: No intermediated host.
Life cycle
Human are infected when the female mosquito
(anopheles and culex) deposit infective larvae
on the skin while biting.
The larvae penetrate the skin, enter a lymph
node and after one year they became mature to
adult that produce microfilariae.
These circulate in the blood, chiefly at night and
are ingested by biting mosquitoes.
Within the mosquito, the micro filariae produce
123
infective larvae that are transferred with the

next bite.
Clinical findings
Early infection is asymptomatic. Later fever,
lymphangitis and cellulites develop. Gradually the
obstruction leads to edema and fibrosis of the legs
and
genitalia,
especially
the
secrotum.
Elephantiasis occurs mainly in patient who have
been repeatedly infected occur a long period.
Thick blood smears taken from the patient at night
reveal the microfilariae. Serological tests are not
useful.
Treatment
Diethylearbamazine is affective only against
microfilariae. No drug therapy for adult worm is
available.
=========================
======
Bacteriology
Bacteriology is the science concerned with the
study of bacteria. It is a branch of microbiology.
Bacteria
Shape and size
Bacteria are mostly unicellular organism. Bacteria
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are variable in shape and are said to be

pleomorphic (many shaped).
The shape of a
bacterium is determined by its rigid cell wall.
Bacteria range in size from about 0.2 to 5 um. The
smallest bacteria (mycoplasma) are about the
same size as the largest viruses (pox viruses) and
are the smallest organisms capable of existing
outside a host. The longest bacteria rods approach
the size of some yeasts and human red blood cells.
Bacteria structure
The structure of a typical bacterium is illustrated in
following.
Cell wall
Cytoplasmic membrane
Cytoplasm
1. Cell Wall
The cell wall is the outermost common to all
bacteria (except mycoplasma species).
The cell wall is a multi layered structure located
external to the cytoplasmic membrane. It is
composed of an inner layer of peptidoglycan
(compound of protein and carbohydrates) and an
outer membrane that varies in thickness and
chemical composition depending upon the
bacterial type.
The cell wall provides structural support and
maintains the characteristics shape of the cell.
2. Cytoplasmic membrane
Just inside the peptidoglycan layer of the cell wall
125
lays the cytoplasmic membrane, which is

composed of a phospholipids bilayer, similar in
microscopic appearance to that in eukaryotic
membrane.
They are chemically similarly, but eukaryotic
membrane contain setrals, where as prokaryotes
generally do not.
The membrane has four important functions.
Active transport of molecules into the cell.
Energy
generation
by
oxidative
phosphorylation.
Synthesis of precursors of the cell wall.
And secretion of enzymes and toxins.
3. Cytoplasm
The cytoplasm has two distinct areas, when seen
in the EM (electron microscope).
An amorphous matrix that contains ribosomes,
nutrients granules, metabolites and plasmids.
An inner, nucleoid region is composed of DNA.
Cytoplasmic components
Ribosomes
Bacterial ribosomes are the site of protein
synthesis as in eukaryotic cells. Bacterial
ribosomes are 70s in size with 50s and 30s sub
units.
B. Granules
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The cytoplasm contains several different types of

granules that serve as storage areas for nutrients
and stain characteristically with certain dyes.
For examples volutin is a reserve of high energy
stored in the form of polymerized metaphosphate
and appears in red staining.
A.
Nucleoid
These are the areas where the genetic materials
(DNA) are present.
The DNA of prokaryotes as a single, circular
molecule that has a molecule weight (MW) of
approx: 2x109 and contains about 2000 genes. The
nucleoid contains no nuclear membrane, no
nucleolus, no mitotic spindle and no histones.
B.
Plasmids
Plasmids are extra chromosomal, double stranded,
circular DNA molecules that are capable of
replicating
independently
of
the
bacterial
chromosome.
There are several different types of plasmids can
exist in one cell.
Transmissible plasmid can be transferred from

cell to cell by conjugation.
Non-transmissible plasmids are small; they do
not contain the transfer genes.
Plasmids carry the genes for the following

functions and structure of medical importance.
Antibiotic resistance, which is mediated by a
127
variety of enzymes.
Resistance to heavy metals such as mercury
and silver which is mediated by a reductive
enzymes.
Resistance to ultraviolet light, which is
medicated by DNA repair enzyme.
Pili (fimbriae) which mediate the adherence of
bacteria to epithelial cells.
E. Transposons
Transposons are pieces of DNA that transport more
readily from one site to another, either within or
between the DNAs of bacteria, plasmids and
bacteriophages.
Classification
The classification of bacteria is based on their
gram staining.
Gram staining
This staining procedure developed in 1884 by the
Danish physician Christian grams is the most
important procedure in microbiology.
It separates most bacteria into two groups.
1. The gram positive bacteria which stain blue
and,
2. The gram negative bacteria which stain red.
Classification of Bacteria
Bacteria
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Aerobes
Anaerobes
Gram staining
Cocci
Bacilli
Aerobic gram (+ve) cocci
Staphylococcus aureus
St: epidermis
Strepto: pneumoniae
Streptococcus agalactiae (group B)
Streptococcus pyogenes (group A)
Gram (-ve) Cocci
Neisseria gonorrhoeae.
Neisseria meningitidis.
Moraxella catarrhalis.
Gram (+ve) rod (Bacilli)
Bacillus anthrax
Nocardia SP
Bacillus cereus
Listeria monocytogenes
Corynebacterium diptheriae
Propronibacterium acnes
Gram ( ve) rod (Bacilli)
Salmonella typhi
Proteus SP
Klebsiella pneumoniae
Propronibacterium anus
Escherichia coli or E-Coli
Brucella SP
Shigella
Vibro chloreae
Bordetella pertusis
Anaerobic
Gram +ve Cocci
Peptostreptococcus SP
Gram ve cocci
Veillonella SP
Gram +ve rod (Bacilli)
Actinomyces SP
Clostridium botulinum
Clostridium tetani
Clostridium perfringes
Gram ve rod (Bacilli)
Bacteriodes fragilis
Bacteriodes SP
Prevotalla
Fusobacterium
129
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Bacteria
Streptococcus
Staphylococcus
Bacillus
Clostridium
Corynebacterium
Listeria
Actinomyces
Nocardia
Neisseria
Bordetella
Lagroxella
Brucello
Posteurella
Yersinia
Serratra
Klebsiella
Salmonella
Shigella
Proteus
Helicobacter
Vibro cholera
Pseudomonas
Bacteriodes
Mycobacterium
Rickettsia
Chlamydia
Treponema
Mycoplasma
Representative
Diseases
Pneumonia,cellutitis,
pharyngitis
Abscess of skin and other
organ
Anthrax
Tetanus & gas gangrene
Diphtheria
Meningitis
Actionmycosis
Nocardiosis
Gonorrhea and meningtitis
Whooping cough
Pneumonia
Brucellosis
Cellutitis
Plague
Pneumonia
Pneumonia and UTI
Typhoid fever, entrocolitis
Entrocolitis
UTI
Gastritis and peptic ulcer
Cholera
Pneumonia and UTI
Peritonitis
TB and leprosy
Q fever
U
rethritis and trachoma
Syphilis
Pneumonia
=========================
======
131
Virology
It is the branch of microbiology which deals with
the study of viruses.
Virus
Virus is unicellular organism, but the viral cell is
not a complete cell. Because they are not capable
of independent replication, cant synthesized their
own energy or protein and are too small to be seen
in the light microscope.
Fig: Bacteriophages virus.

Structure
A complete virus particle is known as verion.
Virus particles composed of an internal core
containing either DNA or RNA (but not both at
time) covered by a protective protein coat.
Some viruses have outer lipoprotein membrane,
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called an envelope, external to the coat. Viruses do

not
have
a
proper
nucleus,
cytoplasm,
mitochondria or ribosomes.
Size and shape
Viruses range from 20 to 300 nm in diameter, this
corresponding rough to a range of single from that
of the largest protein to that of the smallest cell.
Their shapes are frequently referred to in
geometrical terms e.g. sphere, rods, bullets or
brick etc. The shape of virus particles is
determined by the arrangement of the repeating
sub unit that from the protein coat (capsid) of the
virus.
Viral nucleic acid
The viral nucleic acid (genome) is located
internally and can be either single or double
stranded DNA or single or double stranded RNA.
The nucleic acid can be either linear or circular.
The DNA is always a single molecule while the RNA
can exist either as a single molecule or in several
pieces.
Viral capsid
The nucleic acid is surrounded by a protein coat
called a capsid, made up of sub units called
capsomers. Each composer consists of one or
several protein.
The structure composed of the nucleic acid
genome and the capsid protein is called the
nucleocapsid. The arrangement of capsomers
133
gives the virus structure in geometric symmetry.

Viral protein
Viral protein serves important function. The outer
capsid protein protects the genetic material and
mediated the attachment of the virus to specific
receptors on the host cell surface.
Outer viral proteins are also important antigens
that induce neutralizing antibody are activating
cytotoxic T cells to virus infected cells.
Viral envelope
The envelope is a lipoprotein membrane composed
of lipid derived from the host cell membrane and
protein that is virus specific. Furthermore there are
frequently glycoprotein in the form of spike like
projection on the surface which attach to host cell.
Classification of viruses
The classification of viruses is based on chemical
and morphologic criteria. The two major
components of the virus used in classification are;
The nucleic acid.
The capsid (its size and symmetry and
whether it is enveloped).
Viruses are classified into two sub classes.
i. DNA virus
ii.
RNA virus
1. DNA Viruses
Following are the DNA virus.
Virus
Naked/Envelop
Capsid
Nucle
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ed
ic
Adenovirus
Naked
Icoschedral
Papilloma
Virus
Naked
Icoschedral
circular
Naked
Icoschedral
SS
II
Herpes
simplex virus
Enveloped
Icoschedral
DS
Small pox
virus
Complex coat
completed
DS
Hepatitis B
virus
Enveloped
Icoschedral
DS circular
VII
Polyoma
virus
Naked
Icoschedral
DS circular
Tarqueteno
virus
Naked
Icoschedral
SS circular
II
Parvovirus
RNA Viruses
Following are the RNA viruses.
Virus
Rotavirus
Naked/Envelo
ped
Naked/
enveloped
Capsid
Capsid
Nuclei
c Acid
III
Rhinovirus
Naked
135
Icoschedral
SS
Rubella virus
Enveloped
Complex
SS
Dengue virus
Enveloped
Icoschedral
SS
Influenza
Enveloped
virus
Mumps virus
Helical
SS
(-)
Enveloped
Helical
SS
(-)
Rabies
Enveloped
Helical
SS
(-)
Encephalitis
Virus
Enveloped
Helical
SS
(-)
Viruses and its producing infections or

diseases
Virus
Influenza virus
Rhinovirus
IV
Disease
Influenza
Common cold
IV
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Syncytial virus
Bronchiolitis
Vericella zoster virus
Chicken pox
Measles virus
Measles
Mumps virus
Mumps
Rubella virus
Rubella
Hantavirus
Pneumonia
Adenovirus
Pneumonia
Hepatitis A virus
Hepatitis A
Poliovirus
Poliomyelitis
Rotavirus
Diarrhea
Rabies virus
Rabies
Yellow fever virus
Yellow fever
Dengue virus
Dengue fever
Hepatitis B virus
Hepatitis B
Hepatitis C virus
Hepatitis C
Hepatitis D virus
Hepatitis D
Human T-Cell lymphotropic virus
Leukemia
Human immuno deficiency virus
AIDS
Herpes simplex virus type 2
Papillomas (Warts)
Congenital
Cytomegalovirus
abnormalities
=========================
======
Chapter No. 10
Laboratory Diagnosis
The laboratory diagnosis of infectious diseases
involves two main approaches.
One is the bacteriological approach in which the
organism is identified by staining and culturing the
organism and the other is the immunologic
(serologic) approach in which the organism is
identified by detection of antibodies against the
137
organism in patients serum.

Bacteriologic methods
Following are the bacteriologic methods.
1. Blood cultures
Blood cultures are performed most often when
sepsis, endocarditic, osteomylitis, meningitis or
pneumonia is suspected.
The micro organism most frequently isolated from
blood cultures are two gram positive cocci
(staphylococcus
aureus
and
streptococcus
pneumoniae) and the gram negative rods
(Escherichia coli, Klebsiella, pneumoniae and
pseudomonas aeruginosa).
It is important to obtain at least three 10 ml blood
sample in a 24 hours period because the number
of organism can be small.
The blood obtained is added to 100 ml of a rich
growth medium such as brain heart infusion broth.
Blood cultures are checked for turbidity or for Co 2
production daily for 7 days or longer. If growth
occurs, gram stain subculture and antibodies
sensitivity test are performed. If no growth is
observed after 1 or 2 days, when injective
endocarditic, fungemia or infection by slow
growing bacteria e.g. brucella is suspected.
2. Throat cultures
When the specimen is being obtained, the swab
should touch not only the posterior pharynx but
both tonsillar fossae as well.
The material on the swab is inoculated into a blood
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agar plate and streaked to obtain single colonies. If

colonies of beta hemolytic streptococci are found
after 24 hours of incubation at 35 Co, a bacitracin
disk is used to determine whether the organism is
likely to be a group A streptococcus. If growth is
inhibited around the disk, it is a group A
streptococcus, if not it is a non group A beta
hemolytic streptococcus.
Throat cultures are used primarily to detect the
presence of group A beta hemolytic streptococci
(streptococcus pyogenes) an important and
treatable cause of pharyngitis. They are also used
when diphtheria gonococcal pharyngitis or thrush
(candida) is suspected.
3. Sputum Cultures
Sputum cultures are performed primarily when
pneumonia or tuberculosis is suspected. The most
frequent cause of community acquired pneumonia
is S. Pneumoniae, whereas S. aurous and gram
negative rods, such as K. Pneumoniae and P.
aeruginosa, are common causes of hospital
acquired pneumonias.
It is important that the specimen for culture really
be sputum, not saliva. A reliable specimen has
more than 25 leukocytes and fewer than 10
epithelial cells per 100 x filled.
Culture of the sputum on blood agar frequently
reveals characteristic colonies and identification is
made by various serologic or biochemical test.
Cultures of mycoplasma are infrequently done;
diagnosis is usually confirmed by a rise in antibody
139
titer.
If legionella pneumonia is suspected, the organism
can be cultured on charcoal yeast agar, which
contains the high concentration of iron and sulfur
required for growth. If tuberculosis is suspected, an
acid fast stain should be done immediately and the
sputum culture on special medium, where are
incubated for at least 6 weeks. In diagnosis
aspiration pneumonia and lung abscess, anaerobic
cultures are important.
4. Spinal Fluid Cultures
Spinal fluid culture are performed primarily when
meningitis from cases of encephalitis, brain
abscess and emphysema usually show negative
cultures. The most detectable microorganism in
meningitis
is
naisseria
meningitides,
S.
pneumoniae and homophiles influenza.
If organisms resembling N. meningitides H.
influenza or S. pneumoniae are seen the quelling
test or immunoflurescene with specific antisera
can identify the organism rapidly. Cultures are
done on blood and on chocolate agar, and
incubated at 35 Co in a 5% Co2 atmosphere.
Hematin and nicotinamide adenine dinucleotide
(NAD) are added to enhance the growth of H.
influenza.
Immunologic tests to detect the presence of
capsular antigen in the spinal fluid can be used to
identify N. meningitides, S. pneumonia and Cneoformans. The two tests most frequently used
are later particle agglutination and counter
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For Paramedics
immunoelectrophoresis.
5. Stool cultures
Stool cultures are performed primarily for cases of
entro-colitis pathogen which are detected in this
type of test are shigella, salmonella and
campylobacter.
A direct microscopic examination of the stool can
be informative from two points of view.
A methylene blue stain that reveals many

leukocytes indicates that an invasive organism
rather than a toxigenic one is involved.
A gram stain may reveal large numbers of
certain
organism, such as staphylococcus
clostridia, or campylobacter.
Gram stain of the stool is not usually done because

the large numbers of bacteria in the normal flora of
the colon make the interpretation difficult.
6. Urine cultures
Urine in the bladder of a healthy person is sterile,
but it acquires organism of the normal flora as it
passes through the distal portion of the urethra.
To avoid after washing the external orifice is used
for urine cultures. In special situations, suprapubic
aspiration or catheterization may be required to
obtain a specimen. Because urine is a good culture
medium, it is essential that the cultures be done
with 1 hour after collection or stored in a
refrigerator at 4 Co for no more than 18 hours.
141
It is commonly accepted that a bacterial count of

at least 100,000/ml must be found to conclude that
significant bacteriuria is present.
There is evidence that as few as 100/ml are
significant in symptomatic patient. For this
determination to be made, quantitative or semiquantitative cultures must be performed. Urine
cultures
are
performed
primarily
when
pyelonephritis or cystitis is suspected. By far the
most frequent cause of urinary tract infections is
E.coli, other common agent are enterobacter,
proteus and enterococcus facealis.
7. Wound and abscess cultures
Abscess of the brain, lungs and abdomen are
frequently caused by anaerobes such as
Bacteriodes fragilis and gram (+ve) cocci such as
S. aureus and S. pyogenes.
Traumatic open wound infections are caused
primarily by membranes of the soil flora such as
clostridium tetani, clostridium perfringes, surgical
wound infections are usually due to S. aurous.
Infections of dog or cat bites are commonly due to
posteurella multocida. Where as human bites
primarily involve the mouth anaerobes.
It is important to place the specimen in aerobic
collection tubes and transport it quickly to the lab.
It is important to culture the specimen on several
different media under different atmospheric
conditions. The gram stain can provide valuable
information regarding the range of organisms
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For Paramedics
under consideration.
=========================
======
Immunologic
Methods
There are two basic approaches;

Using known antibody to identify the pathogen.
Using known antigen to detect antibodies in the
patients serum.
Identification of an organism with known
antiserum:A. Capsular swelling reaction
Several bacteria can be identified directly in
clinical specimen by this reaction, which is a base
on the microscopic observation that the capsule
swells in the presence of homologues antiserum.
Antisera against the following organism are
available, all serotypes of S. pneumoniae (omni
serum) H. influenza type B and N. meningitidis
group A and C.
B. Slide agglutination test
Antisera can be used to identify salmonella and
shigella by causing agglutination (clumping) of the
unknown organism. Antisera directed against the
143
cell wall O antigens of salmonella and shigella is

commonly used in hospital labs.
Antisera against the flagella H antigens and the
capsular Vi antigen of salmonella are also used in
public health labs for epidemiologic purpose.
C.
Enzyme Linked Immunosorbent Assay
(ELISA)
In this test, a specific antibody to which an easily
assayed enzyme has been linked is used to detect
the presence of the homologous antigen. Because
several techniques have been devised to
implement this principle, the specific steps used
cannot be detailed here. This test is useful in
detecting a wide variety of bacterial, viral and
fungi.
C.
Florescent Antibody Tests
A variety of bacteria can be identified by exposure
to known antibody labeled with fluorescent dye,
which is detected visually in the ultraviolet
microscope.
Various methods can be used such as the direct
and indirect techniques.
Identification of
known antigens
serum
antibodies
with
A. Slide or tube agglutination test

In this test, serial 2-gold dilutions of a sample of
the patients serum are mixed with standard
bacterial suspensions.
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For Paramedics
The highest dilution of serum capable of

agglutinating the bacteria is the titer of the
antibody. As with most test of a patients antibody
at least a 4-fold rise in titer between the early and
late sample must be demonstrated for a diagnosis
to be made. This test is used primarily to aid in the
diagnosis of typhoid fever, brucellosis, tularemia,
plaguae, leptospirosis and rickettsial diseases.
B. Serological Test for syphilis
The detection of antibody in the patients serum is
frequently used to diagnosis syphilis, because T.
pallidum does not grow on laboratory media. There
are two kinds of test.
The non-treponamal test uses a cardiolipin

lecithin cholesterol mixture as the antigen, not
an antigen of the organism. Cardiolipin is a lipid
extracted from normal beef heart. Flocculation
(clumping) of the cardiolipin occurs in the
presence of antibody to T. pallidum. The VDRL
and RPR tests are non treponamal test
commonly used as screening procedures. They
are not specific for syphilis but are inexpensive
and easy to perform.
The treponamal test use T. pallidum as the
antigen. The two most widely used treponamal
test are the FTA-ABS and the MHA-TP (micro
hemagglutination treponema pallidum) test, in
the FTA-ABS test, the patients serum sample,
which has been absorbed with treponemes
other than T. pallidum to remove non specific
145
antibodies is reacted with non viable T. pallidum

on a slide. Fluorescent labeled antibody against
human immunoglobulin G (IgG) is then used to
determine. Whether IgG antibody against T.
pallidum is bound to the organism.
In the MHA-TP test, the patients serum sample is
reacted with sheep erythrocytes (RBCs) coated
with antigens of T. pallidum. If antibodies are
present hemagglutination occurs.
C. Cold Agglutinin Test
Patients with mycoplasma pneumonia infections
develop autoimmune Antibodies that agglutinate
human red blood cells in the cold at (4 C o) but not
at 37 Co. These antibodies occur in certain
diseases other than mycoplasma infections thus,
false positive results can occur.
=========================
======
146
For Paramedics
Objectives
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16
17
18
19
20
21
22
23
24
The scientific study of disease is called pathology.

To study the cause of disease is called etiology.
The removal of tissue/cell from body for the
diagnostic purpose is called biopsy.
The study of individual cell is called cytology.
Ribosome of cell is responsible for protein
synthesis.
Basic function of lysosomes is digestion.
DNA transmits hereditary character.
Homeostasis is tendency to remain stable.
Hypertrophy means an increase in the size of cell.
Hypoxia means lack of oxygen.
Hypoxia is the most common cause of cell injury.
Atrophy is a decrease in the size of cells.
Atrophy is caused by loss of blood supply.
Apoptosis means falling of.
Denaturation of protein is the basic mechanism of
coagulative necrosis.
Fat necrosis associated with trauma to breast.
Alcohol causes fatty change in liver.
Gangrene is necrosis of tissue with superadded
putrefaction (bacterial infection).
Wet gangrene is that type of gangrene in which
tissue appears moist.
Wet gangrene is found in internal organs.
Gas gangrene is caused by clostridia.
In dry gangrene the effected part become dry,
wrinkled and discolored.
Wet gangrene of foot is common in diabetic
patients.
Deposition of coloring material in different parts of
25
26
27
28
29
30
31
32
33
34
35
36
37
38
39
40
41
42
43
147
body is called pigmentation.

Bilirubin is an endogenous pigmentation.
Bilirubin is formed by breakdown of haemoglobin
by RE system.
Increase total amount of iron in the body is called
haemosiderosis.
Skin colour is due to the presence of a melanin
pigment.
Melanin is an endogenous, brown black pigment
produced by melanocytes.
Absence of melanin in skin is termed as albinism.
Deposition of calcium salt in dead tissue is called
dystrophic calcification.
Metastatic calcification is the deposition of calcium
salt in normal tissue.
Hypercalcimia with deposition of calcium salt in
normal tissue is metastatic calcification
Hypercalcimia is the cause of metastatic
calcification.
Fatty change is also called Steatosis.
Karyorrhexis means break up of nucleus into
numerous small particles.
Pyknosis means nucleus shrinking.
Karyolysis means the lysis of pyknotic nucleus due
to enzyme DNAase.
Inflammation is the process by which WBCs
&macrophages clear injurious agent.
Inflammation is not a degenerative process.
Neutrophils are the most prominent cell in acute
inflammation
Inflammation of a tissue is indicated by placing the
suffix itis at the end of the tissue.
Inflammation is the response of living tissue to an
injury.
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For Paramedics
a characteristic feature
44 Exudate is
of acute
inflammation.
45 Exudate has high protein contents.
46 Transudate is an ultra filtrate of plasma.
47 Transudate has low protein contents.
48 The large cell with more than one nucleus is called
giant cells.
49 Repair is the process by which destroyed cells are
replaced by viable cells.
50 During the regeneration the dead tissue is replaced
by same type of living tissue.
51 Labile cells proliferate through out the life.
52 Nerve cells not divide.
53 Abrasion is the mildest form of skin injury.
54 Clean surgically incised would heals by 1st intention.
55 Keloid is an excessive scar formation.
56 Infection is most commonly due to bacteria.
57 Abnormal accumulation of fluid in the body cavities
is called edema.
58 Hydrothorax means collection of fluid in pleural
cavity.
59 Anasarca means generalized edema.
60 Ascites means abnormal accumulation of fluid in
peritoneum cavity.
61 Local increase blood volume caused by dilation of
arteriole is called hypereamia.
62 Haematoma localized collection of blood with the
tissue.
63 Cardiogenic shock is usually secondary to
myocardial Infarction.
64 Increased volume of blood in effected part is
congestion.
65 Cardiogenic shock is due to failure of myocardial
pump.
149
66 Healing by first intention occurs in clean surgical

wound.
67 Rupture of blood vessel with the leakage of blood is
called hemorrhage.
68 Haematuria means blood in urine.
69 Haemoptysis means vomiting of blood.
70 Melaena means blood in faeces.
71 The formation of clotted mass of within vessels or
heart during life is known as thrombosis.
72 Embolus is a detached intra vascular mass.
73 Infarction means ischemic necrosis.
74 Infarction is an area of localized ischemic necrosis.
75 Pleomorphism means variation in size and shape.
76 Neoplasia means new growth.
77 Metaplasia is an adaptive response.
78 Irreversible loss of differentiation is called
anaplasia.
79 The study of neoplasm is called oncology.
80 Fibroma is the simple form of tumor.
81 Carcinoma spread by infiltration in the early stage.
82 Sarcoma is a malignant tumor.
83 Granuloma is formed in T.B.
84 Lipoma is benign tumor.
85 Carcinogen is a substance capable of causing
cancer.
86 Smoking act as a carcinogen in lungs carcinoma.
87 Immunity provides resistance against micro
organism.
88 Humoral immunity is mainly dependent on the
presence of immunoglobulins.
89 Lymphocytes are the key cells of cell mediated
immunity.
90 The natural resistance of a body against pathogen is
known as innate immunity.
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For Paramedics
91 The engulfment of foreign particles by neutrophills is
called phagocytosis.
92 Any agent that can produce an immune response is
known as antigen.
93 Antibody is the specific goblin protein.
94 Against antigen antibody reacts.
95 Ig G is the most abundant type of antibody present
in serum.
96 Ig G is the only antibody that can cross placenta.
97 Ig M antibodies are the largest antibodies.
98 Ig E mediates types 1 hypersensitivity.
99 T.Lymphocyte develops in thymus of the fetus.
100 B.Lymphocytes develops in fetal liver and bone
marrow.
101 The natural killer cells are large granular
lymphocytes.
102 The immunologically mediated tissue damaging
reaction is called hypersensitivity.
103 Rh incompatibility indicates type 2 hyper
sensitivity.
104 Arteriosclerosis means hardening of the arteries.
105 Candida albican is an opportunistic fungus.
106 An organism which harbors a parasite is called a
host.
107 A host which harbors the larval stage of the
parasite is called intermediate host.
108 Protozoa can be divided into four groups
109 Entamoeba histolytica causes abscess in the liver.
110 Entamoeba histolytica causes ulcers in small
intestine.
111 Trophozoite is the infective form of Entamoeba
histolytica.
112 Malaria is protozoal disease.
113 Quatrain fever comes every fourth day.
151
Tertian fever comes every third day.

The definitive host of plasmodium is mosquito.
Man is an intermediate host of plasmodium.
MP test is done for the diagnosis of malaria.
The best time for the collection of blood for the
detection of malarial parasite is 6 hours.
119
The most dangerous malarial parasite is
plasmodium falciparum.
120 Giardia lamblia causes giardiasis.
121 Leishmania donovani is the cause of kala-azar.
122 Bacteria are uni cellular organism.
123 Bacteria range in size from about 0.2-5 micron
meter.
124 Gram -ve bacteria appear red/pink under the
microscope.
125 Viruses are uni cellular organism.
126 Virus range from 20-300 nm in diameter.
127 Viruses are classified into two groups.
128 Taenia Saginata is called tape worm.
129 Iron deficiency anemia is seen with hook worm.
130 Medical name of pin worm is enterobius
vermicularis.
131 Enterobius vermicularis causes enterobiasis.
132 Ascaris lumbricoides causes ascariasis.
133 Wuchereria bancrofti causes filariasis.
134 Tuberculosis is a chronic inflammation.
135 Serological test for syphilis includes mountex.
136 ASO titer test is for diagnosis of rheumatic fever.
137 Spiral like micro organism is called spirochaetes.
138 Treponema pallidum is a spirocheate.
139 Labor pneumonia in healthy adult is generally
caused by St: pneumoniae.
140 Pyogenic osteomylitis is commonly caused by
staphylococcus aureus.
114
115
116
117
118
152
For Paramedics
141 Anthrocosis is caused due to inhalation of coal
dust.
142 Culture is a term that indicates growth of micro
organism.
143 Filaments of fungi are called hyphe.
144 Candidiasis is the example of opportunistic
mycosis.
145 ARDS stands for
adult respiratory distress
syndrome.
146 ADC stands for
antibodies dependent
cytotoxicity.
147 ASD stands for arterial septal defect.
148 APC stands for adenomatous polyposis coli.
149 ATP stands for adeno tri phosphate.
150 ATN stands for acute tubular necrosis.
151 CML stands for chronic mylocytic leukemia.
152 CHF stand for congestive heart failure.
153 CBC stands for complete blood count.
154 CSF stands for cerebro spinal fluid.
155 CVA stands for cerebro vascular accident.
156 DVT stands for deep venous thrombosis.
157 DIC stands for
disseminated intravascular
coagulation.
158 ELISA stands for
enzyme linked immuno
sorbent assay.
159 FBC stand for full blood count.
160 GFR stands for glomerular filtration rate.
161 GVHD stands for graft versus host disease.
162 HDL stands for high density lipoprotein.
163 ITP stands for idiopathic thrombocytopenia
purpura.
164 LDH stands for lactic dehydrogenase.
165 MSH stands for
melanocytes stimulating
hormone.
153
NAD stands for

nicotinamide adenine
dinucleotide.
167 SLE stands for systemic lupus erythromatosis.
168 TIA stands for transient ischemic attacks.
169 VLDL stands for very low density lipoprotein.
170 VSD stands for ventricular septal defect.
166
=========================
======

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Introduction to Pathology

Centre / Core of Pathology

(IV) Clinical Findings

These are the Marfans syndrome, sickle

Nutritional deficiencies and excesses

Infection and infestations

Abnormal immunological reaction

The genetic polymorphisms strongly

Cytoplasm is living material of the cell. External to

When former steady state of cells structure and

When former steady state of cells structure and

Causes of Cell Injury

viruses, bacteria, fungi, protozoa and helminthes

1. Necrosis means a sequence of morphologic

In this types of necrosis the autolytic and

S.L.E (systemic lupus erythematosus)

obstruction and drainage of blood from affected

applied to the changes which take place in tissue

produced by affected cells or may be produced

Classification: Pigmentation is of two types;

Coal dust (produces anthrocosis)

Asbestos (produces asbestosis)

Iron dust (produces haemosiderosis)

a golden yellow to brown granular.

pituitary gland. Hydro-cortisone from adrenal

This is a simple decrease in cell size resulting in

does the work of two and becomes correspondingly

growth factors on target cell. e.g. if the normal

Metaplasia is a reversible change in which one

The deposition of calcium salt in dead, dying or

Excessive absorption of calcium from GIT

An immediate and early response to injurious

The flush, a dull red line, immediately follows

inflammation if the causative agent is not removed

Difference b/w exudates and

Its cause may be

It is clear and watery.

Specific gravity is less

RBCs never present.

Coagulability absent due

Part affected is pale and

Difference b/w acute and chronic

There are two processes of repair;

Quiescent or stable cells are those type of cells,

Permanent or non-dividing cells are those types of

Repair by Connective Tissue

Following are the condition in which tissue repair is

This is the mildest form of the main injury

Incisicion (Cut) and Laceration

(Tear):Incision and lacerations involve the full thickness

Wounds with Epidermal

Defects:Severe injuries (e.g. crush injuries extensive

Healing by first or primary intention.

Healing by second intention.

Healing by First Intention

This occurs in clean, incised wounds with good

There is minimal loss of tissue.

Granulation tissue forms in incision space.

2. Healing By Secondary Intention