Faculty of Dentistry

Volume 1

By

Professor Dr Hala Kheidr

Head of Pathology Department

2021-2022
INTENDED LEARNING OUTCOMES (ILOs):

l-: KNOWLEDGE and UNDERSTANDING:

By the end of the course, student should be able to:

1- Define and discuss the main disease categories that may
affect the body (general pathology) as well as the basic
mechanisms underlying these disorders (etiology,
pathogenesis & natural history)
2- Describe the morphologic (gross & microscopic) changes
occurring as a result of such disease processes in various
organ systems
3- Determine the fate & complication of each particular
disease and outline the general management procedures
ll- CLINICAL & LABORATORY SKILLS:

By the end of the course, students should be able to be

prepared for their upcoming clinical training by:
1- Diagnosing and fully Describing the pathologic picture
of a disorder based on gross or microscopic morphology.
2- Choosing the most appropriate cost effective pathologic
diagnostic procedures
3- Selecting the necessary techniques for sample reception
& processing according to the nature of specimen received

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III-INTELLECTUAL SKILLS

By the end of the course, student should be able to :

1- Predict the signs and symptoms of a disease based on the

underlying gross & microscopic tissue changes
responsible for symptomatology and physical changes in
the patient
2- Interpreting in a professional manner a pathology report

lV- LIFE LONG LEARNING

By the end of the course, student should be able to :

1- Appreciate the importance of life long learning and show

a strong commitment to it
2- Use the sources of biomedical information to remain
current with the advances in knowledge & practice
3- Frame a question, search the literature, collect, analyze,
critically appraise and utilize the obtained information to
solve a particular clinical problem according to the
principles of evidenced based medicine

V- ETHICAL BEHAVIOUR:

By the end of the course, student should be able to :

1- Express themselves freely and adequately by improving
their descriptive capabilities and enhancing their
communication skills
2- Respond appropriately according to the seriousness of the
pathologic diagnosis in an acceptable human manner,
treating the patient as a whole rather than a lesion of
specimen

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 INFLAMMATION

Definition :

It is the reaction of living vascularised tissue against an

irritant in order to eliminate this irritant or its effect e.g. toxin
. This reaction consists of vascular, .lymphatic & cellular
changes. It is a protective process.
The suffix ''itis'' is added to designate the inflamed organ
or tissue e.g. tonsillitis, appendicitis...

Types :
1. Acute : rapid onset and short duration (days or weeks) .
2. Chronic : gradual onset and long duration (months or
years) .
3. Sub-acute : grade between acute & chronic .

Causes :
1. Living irritants : bacteria, viruses, fungus & parasites .
2. Non-Living irritants :
Physical (e.g. irradiation, excess heat or cold)
Chemical (e.g. acids)
Mechanical (e.g. trauma)
3- Tissue necrosis
3. Hypoxia .
4. Ischaemia causing tissue necrosis

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5. Immunological reactions .

ACUTE INFLAMMATION
The acute inflammatory reaction consists of 3
components:
 1- Local tissue damage :
o The central cells are killed (necrosis) due to maximal
concentration of the irritant .
o The surrounding cells become sick (degeneration)
due to disturbance in their metabolism .
o Damaged cells release chemical mediators such as
histamine, bradykinin & prostaglandins .

 2- Vascular Phase of the inflammatory response

:
1. Transient vasoconstriction : Remains for few seconds
or minutes and caused by direct action of irritant on
vessel wall .

2. Vasodilation :
- Caused by direct effect of released chemical mediators on
vessel wall mainly histamine
- This increases the blood flow to the inflamed area which
results in redness and hotness .

3. Increased vascular permeability due to the action of

chemical mediators leading to widening of capillary pores
between the endothelial cells by the effect of histamine and
bradykinin

4. Blood stasis :
Caused by increased blood viscosity due to plasma

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 extravasation and increased vascular permeability .

5. Inflammatory fluid exudate formation:

How it is formed ?

a- Increased capillary permeability mainly .

b- Increased intravascular hydrostatic pressure due to
vasodilatation and increased blood flow.
c- Increased extravascular osmotic pressure due to
breakdown of large protein molecules .
d- Increased fluidity of the ground substance
This exudate is rich in protein content (plasma) mainly
fibrinogen which differs from transudate (low protein and
lower specific gravity)

Functions of Exudate

1- Dilutes the irritant with its-toxins & minimizes its effects.

2- Brings antibodies from blood : such as opsonins, antitoxins
& bacteriolysins .
3- Its fibrinogen content coagulates to fibrin and :
a- Localizes & surrounds the irritant
b- Forms network fo phagocytic cells and repair cells to
move on
4- Brings nutrition to the cells and removes waste products .

Fate

It is carried by lymphatics, and may cause lymphangitis &

lymphadenitis (lymph nodes become enlarged, soft, painful)
If the exudate carries bacteria & its toxin to the blood stream
it leads to toxaemia, bacteraemia or septicaemia .

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3-Formation of The Inflammatory cellular exudate :

a- Margination &Adhesion of leucocytes :

Leucocytes mainly polymorphs and monocytes leave
the axial stream mainly due to blood stasis & adhere to
the sticky swollen endothelium helped by integrin

b- Emigration of polymorphs and monocytes :

They pass through the widened endothelial capillary
pores by pseudopods (amoeboid movement)

c- Diapedesis of red cells :

some red cells are pushed with leucocytes.

d- Chemotaxis :
It is the unidirectional movement of polymorphs and
macrophages towards the irritant. They move in fibrin
threads. Chemical products of bacteria, damaged tissues
and complement components, as C5a & C3aand
leukotriene are chemotactic substances.
The binding of chemotactic agents to specific receptors

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 occurs on the surface of the leucocytes resulting in
hydrolysis & activation of phospholipase C and release
of calcium resulting in the activation of cell movement
by activation of contractile proteins.

e- Phagocytosis :
It is the ingestion & destruction of bacteria and necrotic
tissues by phagocytic cells, which are mainly
polymorphs.

How phagocytosis is done?

a) Recognition and attachment: of bacteria to the cell

surface of the phagocytic cells, in the presence of
opsonins which coat the bacteria

b) Engulfment: by extension of cytoplasmic

pseudopods around the attached opsonized bacteria
forming phagocytic vacuoles (phagosomes) which
fuse with lysosomes with release of lysosomal
enzymes

c) Degradation and destruction of bacteria: through

oxygen dependent mechanism(formation of

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bactericidal hydrogen peroxidase) and oxygen
independent mechanisms by lysosomal enzymes

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Chemical Mediators of Acute Inflammation :

Effects of chemical mediators :

1- Increased vascular permeability mainly by histamine,
bradykinin & leukotrienes.
2- Vasodilatation mainly by histamine, bradykinin &
prostaglandins.
3- Chemotaxis mainly by the anaphylatoxins C5a & C3a,
lysosomal components and leukotrienes.

They consisted of:

I- Plasma factors: (Plasma proteases) :
1. The kinin system {Bradvkinin} : causes increase in
vascular permeability & vasodilatation also causes pain
sensation
2. The complement system :
- C5a & C3a INDUCE MAST CELLS TO RELEASe
histamine also C5 has chemotactic property.
- C3b an important opsonin activates phagocytosis
3. The coagulation and fihrinolvtic system :

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 Bring the conversion of soluble fibrinogen to insoluble
fibrin, increase vascular permeability & increase
movement of leucocytes.
II- Factors released from tissue cells :
1- vasoactive amines :
a- Histamine : causes vasodilatation and
increased vascular permeability, lasting 10-15
min. released from mast cells, basophils and
platelets.
2- Arachidonic acid metabolites :
a- Prostaglandins : causes vasodilatation.
released from damaged cells.
b- Leukotrines : cause chemotaxis for
neutrophils & monocytes. released from
damaged cells.
3- Lysosomal components : the lysosomal enzymes
destroy phagocytosed substances which are limited by
antiprotease present in plasma.and increase
chemotaxis for leukocytes
4- Lymphokines : in delayed hypersensitivity reactions
and cause increase in permeability and chemotaxis.
released from sensitized T lymphocytes. They
comprise IL-1, TNF & IL-8. and stimulate fever in

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 acute inflammation
5- Monokines: like the lymphokines but released from
macrophages.

What is the end of acute inflammation?

1- Resolution : complete restoration of normal conditions

due to minimal tissue damage, rapid removal of irritant
and good macrophage functions.
2- Healing : when the body overcomes the irritant. Healing
occurs by regeneration or by granulation (fibrosis)
3- Spread : when the bacteria overcome the defense
mechanisms, inflammation spreads directly, by lymph or
by blood.
4- Chronicity : when the irritant & the body defense are
equal.

Systemic changes in acute inflammation are :

1- Leucocytosis :
is caused by leucocytosis promoting factor, 1L-1 &
TNF released from dead tissues which have
stimulating effect on bone marrow.

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 Fever :
TNF & IL1 that cause rise of body temperature due to
stimulation of hypothalamus associated with rapid
pulse and weakness.

The five cardinal signs and symptoms of acute

inflammation :

1. Hotness.
2. Redness.
3. Swelling.
4. Pain & tenderness.
5. Loss of function.

What are the types of acute inflammation?

I- Suppurative inflammation:
a- localized b-Diffuse
II- Non-Suppurative inflammation:
a- Catarrhal
b- Pseudomembranous

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 c- Fibrinous
d- Serous
e- Serorfibrinous
f- Others

I- Acute Suppurative Inflammation

Definition: acute inflammation characterized by pus

formation, and caused by pyogenic bacteria as:

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 staphylococci, streptococci, gonococci and others

What is pus? It is the thick, alkaline fluid caused by pyogenic

bacteria and characterizes suppurative
inflammation.

Pathogenesis and mechanism of pus formation : pyogenic

bacteria cause marked tissue necrosis & attract excess
polymorphs. Many polymorphs are killed during this struggle
& become pus cells. They release their proteolytic enzymes
which cause liquifaction of necrotic tissue & fibrin. This
liquified material mix with inflammatory exudate forming
pus.

 Composition of pus :
1- Living & dead bacteria with their toxins & their pigments.
2- Liquified necrotic material mainly peptones.
3- Inflammatory fluid exudate.
4- Inflammatory cellular exudate.
 Types of suppurative inflammation :

1- Localized suppurative inflammation :

A- Abscess:

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Definition : a localized suppurative inflammation
characterized by an irregular cavity filled with pus. It is
caused usually by Staphylococcus aureus. It affects usually
subcutaneous tissues, but may occur in any organ (liver,
lung, brain, .......)

 Pathology :
1- At first, abscess is formed of central necrotic zone & outer
zone of acute inflammation and cellular degeneration
containing large numbers of polymorph & macrophages.

2- Later on it is formed of three zones due to liquifaction of

necrotic tissues & pus formation:
- Central zone: Necrotic core: gradually decreases in size.
- Mid zone: Abscess cavity: filled with pus.
- Outer zone: Pyogenic membrane: acutely inflammed

3- The abscess enlarges due to more necrosis and

liquifaction. Enlargement stops when the staphylococci
produce coagulase enzyme that helps fibrin formation &
localization
.

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4- FATE OF ABSCESS Pus must be evacuated
spontaneously or surgically followed by healing which
occurs by fibrosis

 Complications :

1- Change to chronic.
2- Blood spread: Toxaemia, septicaemia & pyaemia.
3- Lymphatic spread: Acute lymphadenitis & lymphangitis.
4- Complication of healing such as chronic ulcer, sinus,
fistula or keloid , haemorrhage and rupture
5- Septic thrombophlebitis.
6- Putrefaction and gangrene.
7- Compression.eg brain abscess

B- Boil (Furuncle) :

This is a small abscess related to hair follicle or

sebaceous gland. Common sites are face, back of neck and
axilla.

C- Carbuncle :

- Definition : a localized suppurative inflammation

characterized by multilocular abscess cavity opening to the
skin by multiple sinuses discharging pus.

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- Cause : Staphylococcus aureus. More common in
diabetics.
- Sites : back of neck & scalp.
- Pathology : multiple intercommunicating foci of pus in
subcutaneous tissue ,opening to the surface by multiple
sinuses discharging pus. Each focus develops as an
abscess and they are multiple because there are many
fibrous septa extending from deep fascia to the dermis.

2- Diffuse suppurative inflammation

a- Cellulitis:

- Definition : acute diffuse suppurative inflammation.

- Cause : Streptococcus haemolyticus which produces two
enzymes:
1- Streptokinase = Fibrionlysin : dissolves & prevents
fibrin formation.
2- Hyaluronidase = Spreading factor : breaks down tissue
ground substance.
- Sites : loose connective tissue such as orbit, pelvis &
scrotum.
- Pathology : differs from abscess in :
1- Failure of localization, and more serious spread.

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2- Excess necrosis.
3- Pus formation is slow, thin & sanguinous.
- Complication: the same as abscess.
b- Acute diffuse suppurative appendicitis

II- Acute Non Suppurative Inflammation

1- Catarrhal inflammation :

- Definition : Mild acute non suppurative inflammation of

mucous membranes characterized by excess mucous
secretion.
- Examples : rhinitis, bronchitis, appendicitis, ……..
- Gross :
- Early : mucous membrane is red, hot & swollen.
- Later : mucous membrane is covered by watery mucoid
discharge.
- Microscopic Picture :
1. Mucosal cells are swollen & may rupture or separate.
2. Submucosa shows dilated congested blood vessels, fibrin
threads and few acute inflammatory cells, such as
polymorphs, macrophages and pus cells.

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2- Membranous = Pseudomembranous
inflammation :

- Definition : Severe acute non suppurative inflammation of

mucous membranes characterized by the formation of a
pseudomembrane .
- Examples : diphtheria & bacillary dysentery .
- Pathogenesis : bacteria produce powerful exotoxins
which cause focal then diffuse necrosis. The exotoxins
spread from necrotic mucosa to submucosa causing acute
inflammation & to blood stream causing severe toxaemia.
- Gross :
Multiple small yellowish foci of necrosis, gradually
enlarge & fuse together forming a continuous membrane.
This membrane is grayish yellow and adherent. If it is
removed by force, it leaves a bleeding ulcerating surface
& reforms again (false membrane).
- Microscopic Picture :
1. Pseudomembrane is formed of necrotic mucosal cells,
bacteria, acute inflammatory cells & fibrin network .
2. Submucosa shows dilated congested blood vessels, edema,
fibrin and many acute inflammatory cells, such as
polymorphs, macrophages and pus cells .

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3- Serofibrinous inflammation :
- Definition : Acute inflammation characterized by excess
fluid exudate rich in fibrinogen. It affects serous
membranes (pleura, pericardium and peritoneum) .
- Gross :
Visceral and parietal layers are thickened, opaque &
covered by fine fibrin threads. When fibrin is in excess, it
is called dry (fibrinous) type . When fluid is in excess with
scanty fibrin, it is called wet (serous) type .
- Microscopic Picture :
a) Serosal cells of both visceral & parietal layers are swollen,
rounded degenerated and shedded.
b) Subserosa shows dilated congested blood vessels, edema,
fibrin and acute inflammatory cells .

4- Fibrinous inflammation :
Characterized by exudate with excess fibrin e.g. lobar
pneumonia .leading to bread and butter appearance
fibrin form threads

5- Serous inflammation :
Characterized by excess serous exudate, e.g. burn &
herpes simplex

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 It occurs mainly in pleura , pericardium and
peritoneum .

6- Haemorrhagic inflammation :
Characterized by exudate rich in red blood cells due to
damage of vascular wall e.g haemorrhagic cystitis
&acute haemorrhagic pancreatitis

7- Allergic inflammation :
Due to antigen-antibody reactions e.g. allergic rhinitis.
The exudate is rich in eosinophils .

CHRONIC INFLAMMATION
General characters :
1- Mild irritant, gradual onset & long duration .
2- May follow acute or starts chronic as in
tuberculosis(persistent infection difficult to eradicate) .
3- Progressive tissue necrosis & gradual replacement by
fibrosis .
4- The blood vessels show gradual thickening of the wall and
gradual narrowing of the lumen (end arteritis obliterans)
.
5- Inflammatory fluid exudate is scanty .

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6- Inflammatory cellular exudate is either diffuse or
perivascular arrangement & is formed of :
- Lymphocytes produce lymphokines .
- Plasma cells : produce antibodies .
- Macrophages: phagocytose necrotic debris & form
giant cells .
- Multinucleated giant cells : result from fusion of many
macrophages or multiple divisions of nuclei without
division of cytoplasm. They phagocytose foreign materials
.
- Eosinophils in allergic and parasitic types .
- Fibroblasts.

* TYPES :
1. Chronic non-specific :
It may follow acute inflammation without characteristic
microscopic picture e.g. chronic abscess .
2. Chronic specific :
Each irritant produces specific characteristic microscopic
picture e.g. tuberculosis, syphilis, bilharziasis.…

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 GRANULOMAS
Definition :
A type of chronic specific inflammation that begins as
multiple small collection (granule) of chronic
inflammatory cells gradually enlarge, fuse together
forming tumour like mass .

Microscopically :
There is focal accumulation of chronic inflammatory cells
such as macrophages, lymphocytes, plasma cells, giant
cells & fibroblasts .
In granuloma of certain organisms, hypoxia and free
radical injury lead to a central zone of necrosis which
appears cheesy and granular called caseous necrosis as in
tuberculosis
Types :

1. Infective granuloma :

- Bacterial : tuberculosis, leprosy, syphilis .

- Parasitic : bilharziasis .
- fungal : madura foot .

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2. Non-infective granuloma :
- Silicosis & asbestosis .
- Foreign body granuloma around talc power, silk
suture….

3. Granuloma of unknown etiology : e.g. Crohn's disease &

sarcoidosis .

QUIZ 1

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 ABSCESS CELLULITIS
Localized form of Diffuse form of
suppurative inflammation suppurative inflammation.

.
Caused by Staphylococcus Caused by streptococcus
aureus. haemolyticus
.
Mainly in subcutaneous Mainly in loose connective
tissues and any organ tissues.

Diffuse due to
Localized due to streptokinase and
coagulase enzyme hyaluronidase secretion.
secretion.

Pus is thick and yellowish. Pus is thin and sanguinous

Less toxaemia. More toxaemia.

Less spread. More spread

Acute inflammation Chronic inflammation

Rapid onset and short duration. Gradual onset and long
duration

Infiltration by polymorphs, pus Infiltration by lymphocytes,

plasma cells, macrophages,giant
cells and macrophages
cells and fibroblasts

Eosinophils may be seen in

Eosinophils may be seen in parasitic types
allergic types.
Blood vessels show dilatation Blood vessels show endarteritis
and congestion. obliterans

Connective tissue shows edema Connective tissue shows

and fibrin threads. fibrosis

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 REPAIR
Definition
Repair (Healing) is the replacement of damaged tissue by
healthy new one.

Types :
1. Repair by regeneration : replacement of damaged cells by
new healthy cells of same type.
2. Repair by granulation or fibrosis : replacement of
damaged cells by granulation tissue which matures into
fibrous tissue.

 Factors determining the type of repair :

I- The Type of cells:
The type of repair depends on the type of cells and their
ability to divide and proliferate.
Three types of cells are known :
a- Labile cells : These cells can proliferate continuously
throughout life & have good power of division.
They include :
- Stratified squamous epithelium of skin & mucous
membranes of mouth, pharynx, larynx, vagina ….

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 - Transitional epithelium of urinary tract .
- Columnar epithelium of G.I.T.. respiratory tract,
endometrium, etc …
- Haemopoietic & lymphoid cells.

b- Stable cells : These cells can proliferate only when needed

& have limited power of division, so that regeneration
follows minor injury and fibrosis follows major injury :
- Parenchymatous cells : liver, pancreas, glands & renal
tubules.
- Mesenchymal cells : osteoblast, chondroblast &smooth
muscle cells

c- Permanent cells : These cells cannot proliferate at all &

are irreversible resulting in a scar these include :
- Muscle cells : cardiac & skeletal .
- Nerve cells : in brain & spinal cord .

II-Factors controlling repair :

1- Contact inhibition: cells present in close contact inhibit

cell division of each other by stimulation of inhibitory
receptors on the cell surface.

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2 -Chalones: These are chemical factors formed by healthy
cell which can inhibit mitosis in adjacent cells. When cells
are damaged, the absence of chalones and the absence of
contact inhibition allow proliferation of neighboring cells to
divide and restore the damage.
3 -Presence of growth factors: These factors can help
cell division, migration, proliferation, angiogenesis and
stimulate DNA synthesis.they promote entry of the cells to
the cell cycle (from G0 to G1) They are produced from
damaged cells, platelets, macrophages, lymphocytes and
fibroblasts. They include:
a. Epidermal growth factor (EGF): it is mitogenic
for epithelial cells and fibroblasts.
b. Fibroblast growth factors (FGF): they control
all steps necessary for new blood vessels
formation (angiogenesis).
c. Platelet derived growth factor (PDGF): it
causes migration and proliferation of
fibroblasts, smooth muscles & monocytes.

d. Transforming growth factor alpha (TGF-): it

is mitogenic for epithelial cells & fibroblasts.

e. Transforming growth factor beta (TGF-): It

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 is the main fibrogenic factor . It stimulates
collagen synthesis and inhibits collagen
degradation . It is also a growth inhibitor for
most epithelial cells when repair is completed.
f. IL-1 & TNF: mitogenic & chemotactic for
fibroblasts and stimulate collagen synthesis.

4- Cell-Matrix interaction: extracellular matrix proteins as

fibronectin and laminin play important roles in cell division,
proliferation, maturation and differentiation. Disorders in
these interactions may lead to abnormal fibrosis.

III-General and local factors delaying repair:

General factors: old age, ischemia, deficiency of
proteins, vitamins or minerals, diabetes mellitus,
excess glucocorticosteroids and cytotoxic drugs.
Local factors: type of tissue , local infection which is
the most important cause of delay healing, foreign
body ,and mechanical pressure which can compress
the blood supply.

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* Examples of repair by regeneration :

1. Regeneration of skin (labile cells) :

- Epidermis alone : regenerates easily .e.g. abrasion
- Dermis : heals by granulation tissue (fibrosis)
e.g.skin wound.

2. Regeneration of liver cells (stable cells) :

- Mild cell injury & intact fibrous framework : perfect
regeneration .
- Severe cell injury & destroyed fibrous framework
irregular fibrosis and liver cirrhosis e.g. chronic
hepatitis.
3. Regeneration of kidney tissue (stable cells) :
- Tubular necrosis is usually followed by regeneration .
- Glomerular necrosis is usually followed by fibrosise.g.
glomerulonephritis.

 Healing by fibrosis :

- Mechanism of fibrosis :
The process comprised the formation of granulation tissue

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 which consists of proliferating fibroblasts and
anastomosing capillaries, which matures into fibrous
tissue through the following steps :
2. Migration of fibroblasts: to the injury site followed by
fibroblastic proliferation under the effect of PDGF and
FGF from macrophages
1. Angiogenesis (Neovascularization) : migration and
proliferation of endothelial cells towards the area of injury
leading to the formation of anastomosing capillary
loops.by the effect of vascular endothelial growth factor
a(VEGF) and fibroblast growth factor(FGF
).3. Fibroblasts secrete extracellular matrix substances:
proteins & collagen type I & III .
4. Remodeling & maturation of the granulation tissue:
by progressive synthesis of collagen, resorption of
capillaries and decrease in number of fibroblasst and
myofibroblasts contraction leading to the decrease of
size of the scar .Finally the scar is pale and mostly
avascular

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Healing of wounds :

Primary union of wounds Secondary union of wounds

(Healing by first intention) (Healing by second intention)
- Occurs in non-infected incised - Occurs in infected wounds with
wounds with minimal tissue destruction excess tissue destruction and gaping
and approximated edges (surgery) edges (accident)

- Basal cells on both sides proliferate, - Basal cells on both sides proliferate
cross the gap & then form the whole but cannot cross the gap until it is filled
epidermis (day 1-2) by granulation tissue, which is
infiltrated by polymorphs &
macrophages

- Macrophages start phagocytosis - Phagocytosis takes long time

(day 3)
- The basal layer covers the thick
- The gap is filled with granulation granulation tissue & form the whole
tissue, (day 4-5) but the skin adnexa do epidermis without adnexa within weeks
not regenerate
- Maturation of granulation tissue occurs
- Maturation of granulation tissue occurs resulting in thick irregular fibrous scar
resulting in thin avascular fibrous scar within 1-2 months
within 3-4 weeks

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Healing of wounds :

Healing by first intention

Healing by second intention

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Complications of wound healing :
1. Chronic ulcer : persistent loss of continuity of the
covering skin or mucous membrane .
2. Chronic sinus : a blind tract between deep wound (or
abscess) and the skin. It is lined by infected granulation
tissue & is caused by presence of foreign body or infection
3. Chronic fistula : a tract between two surface epithelia or
hollow organs (oesophagus and trachea) .
4. Keloid : large projecting scar covered by thin stretched
skin, due to excessive repair caused by foreign body
reaction resulting from hairs, keratin, cotton fibers, etc,…
unknown etiology is common. Seen especially in burns of
negros and certain families. It usually shrinks by
irradiation, but it may recur after surgical removal .
5. Interference with movement : due to excess scar
contraction at joints causing limitation of movement
6. Implantation epidermoid cyst : epithelial cells may
become trapped in the dermis where they proliferate &
form a cyst lined by stratified squamous epithelium &
filled with keration .
7. Malignant transformation : may develop rarely in old
scars especially burns Marjolin ulcer
8- Cosmetic deformities with extensive scar

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 CELL INJURY
(DEGENERATION AND NECROSIS)

Definition:if the cell is exposed to stresses or stimuli that

the cell cannotalter their normal functionthis lead to cell
injury which can be reversible or irreversible
Degeneration (Reversible cell injury) means
morphologic and metabolic changes in living cells resulting
from non fatal injury. These changes occur in the cytoplasm
while the nucleus remains within normal and these changes
can return to normal if the stimulus is removed
If severe stimulus occurs leading to nuclear damage,
cell death (necrosis& apoptosis) developed (irreversible cell
injury)
Parenchymatous cells with high metabolic rate (liver,
heart & kidney) suffer degenerations more than other
mesenchymal cells.
Causes of Cellular Injury
1. Hypoxia: Is a main cause in cell injury. Decrease
oxygen supply is caused by:
a. Ischemia e.g. arterial occlusion and
atherosclerosis.
b. Inadequate oxygenation e.g. cardiac and

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 pulmonary disease.
c. Decreased oxygen carrying capacity of the red
blood corpuscles e.g. anemia and carbon
monoxide poisoning.
2. Physical agents: Trauma, excess heat, excess cold,
radiation and electric shock.
3. Infectious agents: Bacteria, Viruses, fungus,
rickettsia and parasites.
4. Chemical agents: mercury, arsenic, insecticides, air
pollutants, asbestos.
5. Immunologic reactions: Reaction to drugs or
endogenous self antigens (autoimmunity).
6. Genetic derangements: sickle cell anemia (HBS)
7. Nutritional imbalances: decreased proteins,
decreased vitamins and increased lipids.

Mechanism of cell injury

The injurious agent eg hypoxia leads to:
1- decrease mitochondrial function and inhibition of
oxidative phosphorylation occurs with reduction of energy
production (ATP formation) resulting in:
- reduction of activity of sodium pump leading to exit of
potassium and entry of sodium and water causing swelling of
cell
-interference with protein synthesis
-increase intracellular calcium

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2- Accumulation of free radicals which interact with lipids in
cell membranes ,cellular proteins and DNA (oxidative stress)

2- Disrurbances of membranes functions

The injurious agent cause influx of calcium ions into
the cell with activation of phospholipases that destroy
the cell membrane, protease that break cellular proteins
and DNAs which cause DNA damage

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- 38 -
 HYDROPIC DEGENERATION

Definition :
Mild cellular degeneration characterized by
intracellular accumulation of water.
Pathological features :
- Gross picture : the affected organ shows:
- Increase in size, and weight, with tense capsule.
- Soft consistency and pale colour.
- Microscopically :
- Cells are swollen & rounded.
- Cytoplasm contains appear pale & vacuolated .e.g.
hydropic degeneration of renal tubules in nephritis
FATTY CHANGE = FATTY DEGENERATION
= STEATOSIS

Definition :

Pathological accumulation of excess neutral fat in

parenchymatous cells. It mainly affects the liver, heart &
Kidneys.
Causes : mainly due to hypoxia or toxic effects or other
causes of cell injury

In the liver : there are additional causes:

- 39 -
 a. Excess intake of fats & carbohydrates, as in obesity.
b. Fast & excess mobilization of fat from fat stores as in
case of starvation and diabetes mellitus
c. Liver diseases as viral hepatitis.
d. Deficiency of lipotropic factors as choline &
methionine.
e. Hepatotoxins as alcohol.
Gross picture : the affected organ show:
1. Increase in size, and weight with tense capsule.
2. Soft in consistency, and yellowish in colour.
3. Rounded cut edges & bulging greasy cut surface.

* Microscopically :
- Cells are swollen & rounded.
- Cytoplasm contain multiple small fat globules they
enlarge, fuse together into one big fat globule that
compresses the nucleus at one side (signet ring
appearance).

Organs affected:
Liver : it is the commonest organ affected
- Diffuse: in severe toxaemia & severe anaemia.

- 40 -
 - Patchy: in chronic venous congestion (nutmeg liver)
Heart:
- Diffuse: in severe toxaemia ( diphteritic toxic
myocarditis).
- Patchy: in severe hypoxia. The myocardium shows
yellow streaks alternating with brown spots. This is called
tabby cat , or tigroid appearance.
Kidneys: Fat accumulates in the convoluted tubules & foamy
fatty casts.

NECROSIS

Definition :
Irreversible cellular injury causing death of tissues or
group of cells in the living body. It may occur directly or
follow severe degeneration.there is destruction of cell
constituents which are leaked into the surrounding tissue
resulting in inflammation
Grossly :
Necrotic area is opaque whitish yellow &surrounded by
a zone of hyperaemia due to inflammation and may be

- 41 -
swollen.
Microscopically
1. Nuclear changes :
a. Pyknosis: small, irregular deeply stained nucleus.
b. Karyorrhexis: fragmentation of nuclear components.
c. Karyolysis: fading then disappearance of nuclear
fragments.

2. Cytoplasmic changes :
The cells are more eosinophilic (denaturated protein s
bind to eosin) and swollen (cytomegaly). The cell membrane
is lost & the affected cells appear as structureless pink mass
(ghost cells) in which the general architecture may be

preserved while the cellular details are lost.

- 42 -
Types of necrosis :
1. Coagulative necrosis :
Usually caused by ischaemia, and tissues are opaque and
firm due to coagulation of cellular proteins. It occurs in all
organs except brain eg. Myocardial infarction

2. Liquifactive necrosis :
Necrotic tissue is soft and rapidly liquifies, it is seen in brain
& spinal cord infarction due to high lipid & fluid content,
necrotic area is surrounded by glial tissue and form a cyst like
area

- 43 -
3. Caseation necrosis :

Type of allergic coagulative necrosis followed by slow partial

liquefaction by proteolytic enzymes released from
tuberculoprotein in case of tuberculosis
The tissues are dry, pale yellow & cheesy( casein like)

4. Fat necrosis : of two types :

A- Enzymatic fat necrosis : in cases of acute haemorrhagic

pancreatitis where the lipase enzyme escapes from

ruptured ducts & acts on fat of omentum & mesentery,

splitting it into fatty acids & glycerol. The later is

absorbed & fatty acids is deposited with calcium as dull

opaque white patches. Fat cells appear cloudy & are

surrounded by foreign body giant cell reaction, fibrosis

- 44 -
 & dystrophic calcification. The released trypsin causes

destruction of capillary walls and focal haemorrhage.

B- Traumatic fat necrosis : results from trauma to the

female breast or subcutaneous fat. There is self
digestion of fat cells after their rupture by intracellular
lipase. Grossly, the breast shows an irregular firm grayish
yellow nodule with central necrosis.
Microscopically, central necrotic fat cells are seen,
ssurrounded by lipid laden histiocytes, foamy cells,
polymorphs and giant cells. Foreign body granulomas &
fibrosis usually occur.
4- Fibrinoid necrosis: seen in immune reactions involved
blood vessels

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Programmed cell death which involves deletion of single
cells or clusters of cells ,without destruction of their
membranes thus there is no inflammatory reaction in
the surrounding tissues

Examples:
PHYSIOLOGICAL:
1- Focal elimination of cells during embryonic
developments
2- Endometrium during menustruation
3- Normal turnover of cells

PATHOLOGICAL:
1-Liver cells in viral hepatitis
2-Elimination of cancer cells
4- Cell injury caused by cytotoxic T-lymphocytes as in
organ rejection

Morphologic features:

1-the cytoplasm condenses and the cell shrinks but

with intact emembrane
3- Shrinkage and fragmentation of nucei
4- Formation of membrane blebsfollowed by
separation forming apoptotic bodies
5- 5 Apoptotic become removed by adjacent cells or
macrophages

QUIZ 2

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 DISORDERS OF VASCULAR FLOW
(CIRCULATORY DISTURBANCES)

HYPEREMEIA

Definition :
Increased blood flow to organ or tissue due to
vasodilatation of its arterioles & capillaries.
Types : - Physiological : muscular exercise.
- Pathological : acute inflammation.

VENOUS CONGESTION

Definition :
Increased venous blood in organ or tissue due to
obstruction of its venous return.
Types :
I - General Venous Congestion
A- Acute general venous congestion:
In acute heart failure & it is rapidly fatal.

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B- Chronic general venous congestion:
- It is due to chronic right sided heart failure resulting from
causes in:
5- The heart: mitral stenosis, left ventricular failure &
myocardial fibrosis.
6- The lung: emphysema, tuberculosis, pneumoconiosis,
bilharziasis and fibrosis.
Pathology and effects :
1. Dyspnea, cyanosis and hypoxia
2. Increased blood volume and congested neck veins.
3. Cardiac edema : edema caused by right sided heart
failure. It begins in the lower limbs around ankles, then
becomes generalized. It is due to:
a- Increased intravascular hydrostatic pressure.
b- Increased capillary permeability (hypoxia).
c- Sodium & Water retention (kidney congestion).
4. Congestion of different organs :
a- The heart: in case of mitral stenosis, the left atrium
is dilated and hypertrophied followed by the right
side.
b- The lung: is affected in all cases of left sided heart

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 failure and with mitral stenosis.
* Gross picture:
The lungs show brown induration :
1. Large size and heavy weight.
2. Brown colour.
3. Firm indurated consistency.
4. Sharp cut edges, and flat cut surfaces.
* Microscopic picture:
- Alveolar capillaries are dilated & congested.
- Alveolar septa are thickened and fibrosed.
- Alveolar lumina contain red blood cells and
macrophages engulfing brown haemosiderin
granules called heart failure cells.
- Homogenous pink transudate is seen in some alveoli.
c- The liver:
Gross picture:
The liver shows nut-meg appearance :
1. Large size, heavy weight and firm consistency.
2. Dark red spots of congestion against yellow
background of fatty degeneration.
3. Sharp cut edges and flat cut surfaces.
4. Finally the liver becomes shrunken & irregular

- 49 -
 * Microscopic picture:
- Central vein and central sinusoids are dilated &
congested with red blood cells.
- Central liver cells are atrophic.
- Peripheral liver cells show fatty degeneration.
- Haemosiderin granules are seen inside kupffer cells.

d- The spleen:
* Gross: congestive splenomegaly.
1. Large size, heavy weight and firm consistency.
2. Sharp cut edges & flat cut surface.
* Micro:
- Blood sinusoids are dilated & congested.
- Littoral cells are loaded with haemosiderin granules.
- Lymph follicles are atrophic.

II - Local Venous Congestion

A – Acute local venous congestion :

- Causes: Sudden venous occlusion by thrombosis, ligature,
strangulation, or torsion .
- Effect: rapid severe distention of veins & capillaries,

- 50 -
 leading to edema, haemorrhage and rarely infarction (v
B – Chronic local venous congestion:

1- Gradual compression of veins by tumor mass, enlarged

lymph node( veins proximal to obstruction are dilated &
congested with gradual opening of collaterals, edema,
haemorrhage & may be thrombosis
2- Pregnant uterus (compression of iliac veins causing
congestion of leg veins)
3-liver cirrhosis & bilharzial hepatic fibrosis
(compression of portal vein causing congestion of splenic
and mesenteric veins).
4- Mitral stenosis causes blood stasis in left atrium &
congestion of pulmonary veins .

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 THROMBOSIS

Definition:
A thrombus is a compact mass formed of constituent of
circulating blood, inside vessel or heart during life .It
consists of platelets with clotted blood (fibrin entangling
RBCs)

Causes:
1. Damage to the vascular endothelum: (Endothelial injury)
:
- Mechanical : trauma, pressure, ligature .
- Inflammatory : phlebitis, arteritis, endocarditis .
- Degenerative : atherosclerosis, aneurysm, myocardial
infarction .
2. Slowing of blood stream (Stasis):
During slowing the platelets cross the plasmatic zone &
adhere to the vascular endothelium as in :
- Leg veins in chronic heart failure and varicose veins
.
- Left atrium of heart in mitral stenosis .
- Areas of acute inflammation .

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3. Disorders of blood stream: (Turbulence) :
Distortion of lumen by aneurysm, atheroma or pressure
from outside causes turbulence and allows the platelets to
come in contact with the vascular endothelium .
4. Changes in blood composition: (Hypercoagulability of
blood) :
- Increase in platelets : after operation .
- Increase in fibrinogen : during pregnancy .
- Increase in red cells : in polycythaemia .
- Increase in white cells : in leukaemia .
- Decrease in plasma volume : in dehydration and extensive
burns .
- Use of contraceptive pills .
- Inherited deficiency of antithrombin III, and fibrinolysin .
- Advanced cancer , hyperlipidemia and severe burns

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 Mechanism of thrombosis :

1- The surface of normal endothelium is completely resistant

to thrombosis, but when injured or damaged, it can promote
thrombosis .
2- Under normal conditions, the endothelium cells possess on
their surface both antithrombotic factors and thrombotic
factors. These opposing properties are in balance and a non
thrombogenic surface is usually maintained .
3- Injury to endothelial cells will expose highly
thrombogenic subendothelial connective tissue particularly
collagen to which the platelets adhere and undergo contact
activation .
4- Adhesion of platelets to the exposed collagen is mediated
by the von Willebrand factor (factor VIII), released from
injured endothelial cells, which acts as a bridge between
platelet surface receptors and collagen .
5- Platelet release reaction : with activation, platelets
secrete a variety of products stored in their granules such
as ADP, fibrinogen, & others. ADP is a potent mediator
for platelet aggregation. Early, this platelet aggregation is
reversible (primary temporary hemostatic plug). Later
on, with increasing amounts of released ADP, the
secretion of thromboxane A2 from platelet and the release

- 54 -
 of thrombin, these will lead to the formation of a mass of
irreversibly aggregated platelets called secondary
permanent hemostatic plug .
6- the conversion of prothrombin to thrombin, is increased
and activated. Thrombin helps the transformation of
fibrinogen to fibrin .
7- The deposition of fibrin into and about the platelet
aggregation stabilizes and strengh it. Thus, the end result
will be a platelet-fibrin plug or thrombus .

 Classification and types of thrombi :

I- According to the color
1. Pale thrombus = Platelets thrombus :
- It is the first to be formed, and consists mainly of platelets
& fibrin .
2. Red thrombus :
- It is formed of platelets, excess fibrin and red cells .
3. Mixed thrombus :
- It is mixed because it is formed of platelets and other blood
elements .
- The platelets become deposited perpendicular to blood
stream forming reddish violet lines known as lines of Zahn.
Between these lines more fibrin is deposited entangling red
& white cells .

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II- According to the degree of obstruction:

- If the thrombus occludes the vessel partially it is called

mural thrombus,
- If it occludes the vessel completely it is called occluding
thrombus.

III- According to the Sites of thrombus formation :

1. Thrombosis in veins : more common than in arteries
because blood stream is slow & vein has thin wall.
Two Types :
a-Thrombophlebitis: thrombosis initiated by
inflammation may be :
- Septic thrombophlebitis : occurs in veins draining areas of
acute inflammation as appendicular vein in acute
appendicitis & uterine veins in puerperal sepsis .
- Aseptic thrombophlebitis : occurs in veins exposed to
irradiation .
b-Phlebothrombosis: thrombosis initiated by other
factors:
- In varicose veins .
- In veins of feet & calf : in chronic heart failure patients

- 56 -
 with prolonged recumbency and compression of veins
against bed mattress.
- In pelvic veins after labour or operations : Increase in
number, adhesiveness of platelets, prolonged bed rest and
absence of muscular movements leading to stasis .
2. Thrombosis in arteries :
Less common that in veins, because blood stream is rapid
& has thick wall. Causes are :
a- Atherosclerosis causing roughness of intima .
b- Arteritis causing damage to endothelium .
c- Aneurysms causing stasis & disorders of blood stream .

3. Thrombosis in the heart :

More common in the left side, types are :
a- VentricularMural thrombi : over myocardial
infarction .
b- Valvular Vegetations : pale thrombi over valves in
rheumatic valvulitis .
c- Atrial thrombi : usually in left atrium in mitral stenosis
.

- 57 -
 Fate and complications of thrombosis :
A- Septic thrombus : may be fragmented by the proteolytic
enzymes into septic emboli ---> pyaemic abscesses .
B- Aseptic thrombus :
1- Lysis, fragmentation & embolization .
2- Fibrosis, or fibrosis & recanalization .
3- Dystrophic calcification .
4- Propagation .
5- Arterial occlusion (ischaemia) or venous occlusion
(congestion) .
6- Incorporation of arterial thrombi into atheroma .

Fate of thrombosis

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 EMBOLISM

Definition :

Embolus is an insoluble material circulating in blood.

Embolism is the process of impaction of an embolus in a
blood vessel .

 Types of emboli :
1. Emboli of thrombotic origin (thromboembolism) :

a- Course and site of impaction of emboli :

- Pulmonary embolism From systemic vein or right
side of heart, the emboli pass and become impacted in the
lung
- Systemic embolism
From systemic artery or left side of the heart, the emboli
impact in any organ (spleen, brain, kidney, ….)

- Portal embolism
From portal veins, the emboli impact in the liver

- Paradoxical embolism : an embolus from systemic

vein impact into a systemic artery and not in the lung

- 59 -
 because it passes from right to left side of the heart through
atrial or ventricular septal defect. The thrombus may also,
be very small & can pass through lung capillaries to left side
of heart .

b- Effects :
- Aseptic embolus :
- Poor collaterals  ischaemia and infarction .
- Good collaterals  insignificant effect .

- Septic embolus : Pyaemic abscesses .

2. Air emboli (Gas embolism) :

May result from :
a- Injury of large neck veins causing suction of
atmospheric air forming air bubles in the SVC to right
ventricle
b -Caisson's disease in divers (may cause multiple emboli)
due to high atmospheric pressure .
- May lead to :
- Small amount : no effect .
- Large amount : (50 – 100c) : causes acute heart failure .

- 60 -
3. Fat embolism :
- May be due to : 1- Fractures of long bones .
2- Burns
3- severe fatty liver
- Results in pulmonary or systemic embolism .
- Rarely the fat embolism syndrome develops causing
respiratory distress, tachycardia & coma

4. Amniotic fluid embolism :

A rare condition in which strong uterine contractions
may tear foetal membranes & push amniotic fluid in opened
maternal uterine veins causing fatal pulmonary embolism to
the mother. It may be related to the high contents of
thrombogenic factors in the amniotic fluid .

5. Tumour emboli .
6. Parasitic emboli .
7. Bacterial emboli.
8. Foreign body emboli

- 61 -
 ISCHAEMIA

Definition :

Decrease blood supply to tissue or organ due to

occlusion of its arterial supply .

Types :
1- Sudden or acute (complete) ischaemia :
- Causes :
i. Thrombosis or embolism which are the 2 most
common causes
ii. Ligature of an artery.
iii. Torsion or twisting of movable vessels in intestine or
ovary.
iv. Arterial spasm as in ergot poisoning.
v. Buerger disease
- Effects :
- No collaterals or poor collaterals  infarction or
gangrene.
- Good collaterals  insignificant effect .
2- Gradual or chronic (incomplete) ischaemia :
- Causes :
a. Atherosclerosis.

- 62 -
 b. Endarteritis obliterans as in syphilis.
c. Pressure from outside by enlarged lymph nodes,
tumour mass ….
- Effects :
- Poor (Inefficient) collaterals  ischaemic atrophy &
fibrous replacement as in myocardial fibrosis due to
coronary atherosclerosis.
- Good (Efficient) collaterals  insignificant effect .

INFARCTION

Definition :

An area of coagulative necrosis caused by sudden

ischaemia. It is liquifactive in the brain.

Aetiology :
1) arterial occlusion mainly caused by thrombosis or
embolism (99% of cases)
2) Rarely surgical ligature, arterial spasm or twisting of
vessels.

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 General features of infarction :
1. Gross :
- Size : depends upon size of occluded vessel.
- Site : always subcapsular, and peripheral.
- Shape : pyramidal or triangular in shape with base
on surface & apex towards center.
- Surface : raised when recent (edema) & depressed
when healed (fibrosis).
- Surrounded : by a red zone of hyperaemia.
- Colour:
a- Pale (white) infarct : seen mainly with arterial
occlusion in organs as heart or kidney. It is pale, dry
and firm.
b- Red (Haemorrhagic) infarct : seen mainly with
congested vessels or having double blood supply as
liver, lung or intestine. It is dark red , moist and soft.
2. Micro :
- Early: Cells show post necrotic changes after 12hr
- Next: loss of cellular details & preservation of
general architecture (ghosts of original structure)
after 36hr
- Later: necrotic area appears as pink granular region

- 64 -
 surrounded by acute inflammatory reaction, after
72hr
3. Fate :

a. Small infarct: phagocytosed by macrophages &

replaced by fibrosis.
b. Large infarct: encapsulation & dystrophic
calcification.

 Examples of infarcts in different organs :

1. Kidney :

Due to thrombosis or embolism of a branch of renal artery.

- The infarct is usually pale in colour affecting mainly the
cortex.
- Clinically : painless haematuria.

2. Spleen :
- Due to thrombosis or embolism of a branch of splenic
artery.
- Clinically : left hypochondrial pain because capsule is
affected .

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3. Heart :
- Due to thrombosis or embolism of a coronary artery on top
of atherosclerosis.
- It is pale and affects mainly the left ventricle.

4. Liver :
Infarction of the liver is very rare (double blood supply).

6. Lung : due to:

- Thrombosis or embolism of pulmonary artery in lung
diseased by chronic venous congestion. In healthy
lung, no infarction develops because the lung has
double blood supply.
- Inefficient bronchial blood supply in case of chronic
lung congestion.
*Gross :

The infarction is haemorrhagic, may be multiple and

usually subpleural, and covered by fibrinous pleurisy.

- 66 -
* Micro :
- Ghosts of alveolar walls are seen.
- Alveolar spaces are full of blood.
- Surrounding lung tissue shows chronic venous
congestion.
- Clinically : Haemoptysis & chest pain.

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 GANGRENE

Definition :
Massive tissue necrosis with superimposed putrefaction.
Causes :
1. Necrosis : usually caused by ischaemia or bacterial
toxins .
2. Putrefaction : caused by saprophytic bacteria which
breakdown proteins of necrotic tissue liberating H2S. This
hydrogen sulphide gives the gangrenous tissue a foul
odour & black coloration (by forming iron sulphide with
the iron of haemoglobin) .
Types :
1. Dry gangrene :
It usually affects limbs with poor collaterals when a
main artery is occluded by :
1. Thrombosis usually on top of atherosclerosis .
2. Embolism .
3. Arterial spasm as in Raynauld's disease, Buerger's
disease, or ergot poisoning .
4. Surgical ligature of artery .

- 68 -
 There is cut of arterial blood supply while the venous
and the lymphatic draining are normal helping dryness of
affected limb. Also, there is evaporation from overlying skin.
The best example is :

 Senile gangrene :
- Usually affects old aged males, with atherosclerosis,
weak cardiac action and low body resistance .

Pathological features :
- Arterial occlusion may be either spontaneous or as a result
of injury by tight shoes .
- Tissue necrosis occurs usually in big toe and the area is
pale & cold. Evaporation, venous & lymphatic drainages
lead to shrunken mummified appearance .
- Putrefaction starts by saprophytic bacteria, and the area
becomes black & offensive .
- The toxic product irritate the surrounding healthy tissue
causing thrombosis and more necrosis & putrefaction.
The gangrenous process spreads proximaly & slowly
along the limb .
- When gangrene reaches an area of good blood supply, the
process stops and a red line of acute inflammation is seen

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 between healthy & gangrenous parts which is known as
line of demarcation .
- From the healthy side granulation tissue grows &
separates the gangrenous part below and appears as
groove know as line of separation. This groove gradually
deepens until it separates the gangrenous part completely
leaving a conical stump .

- 70 -
2. Moist gangrene :
It usually affects internal organs due to sudden
occlusion of both arterial & venous blood supply. There is no
evaporation & no drainage by veins or lymphatics, so the
organ retains its fluids which help rapid putrefaction, rapid
spread, severe toxaemia without line of demarcation and
no self separation .
Examples of moist gangrene include:
a- Moist gangrene of the intestine :
- Seen in strangulated hernia, intussusception or volvulus.
- There is venous congestion &tissue rich in fluids (edema)
at first .
- Then the artery is occluded leading to necrosis which is
soon invaded by intestinal saprophytic bacteria causing
putrefaction .
- Patient suffers from acute intestinal obstruction, septic
peritonitis & severe toxaemia .

b- Bed sores :
Skin ulcers over bony prominences as sacrum & greater
trochanter due to prolonged recumbency in cases of paralysis
& coma. They result from stasis, ischaemic necrosis and
secondary bacterial infection .

- 71 -
c- Diabetic gangrene :
Diabetic patients usually have atherosclerosis, trophic
ulcers due to sensory loss, hyperglycaemia, low immunity
and increased susceptibility to infection

 Pathological features : It begins usually in big toe after

mild injury. Tissue hyperglycaemia helps putrefaction
followed by inflammatory occlusion of all vessels,
(arteries and veins). It spreads rapidly with poorly
developed line of demarcation, severe toxaemia & no self
separation but surgical limb amputation may be done to
save life .

Comparison between dry and moist gangrene

Dry Gangrene Moist Gangrene

Arterial occlusion by Arterial & venous
atherosclerosis or arterial occlusion, by crush
spasms . injuries, bed sores or tight
tourniquet .

Affects exposed parts . Affects internal organs .

Slow putrefaction & spread Rapidputrefaction& spread
. .
Tissue mummification . Tissue edema .

Line of demarcation & self Poor line of demarcation &

separation . no self separation .

Mild toxaemia Severe toxaemia

- 72 -
3. Infective gangrene :

A subtype of moist gangrene in which pathogenic

bacteria cause tissue necrosis and saprophytic bacteria cause
tissue putrefaction .
Example:
a. Cancrum oris : infective gangrene of oral mucosa of weak
malnourished children. It is caused by Treponema vincenti
& Bacillus fusiformis. There is severe toxaemia & may be
complicated by aspiration bronchopneumonia .

- 73 -
 BACTERIAL INFECTIONS

Definition :
Invasion of body tissues by pathogenic bacteria &
development of pathological state.
It may be exogenous (inhalation, ingestion ,inoculation
etc…) or endogenous (bacteria normally present in the body).

Mechanisms of tissue injury by bacteria :

1. Cell death by direct adhesion to host cells .
2. Production of exotoxins and endotoxins .
3. Hypersensitivity reactions .

Effects of infection :
Inflammation, toxaemia, bacteraemia, septicaemia,
pyaemia, immunity & hypersensitivity .

- 74 -
 BACTERAEMIA
Definition :
Transient presence of some bacteria in blood without
toxic manifestations .

Pathogenesis :
Bacteria enter the blood from a septic focus e.g.
tonsillitis, sinusitis, or may follow tooth extraction or during
the incubation periods of infections .

Fate :
1. Usually bacteria are engulfed by phagocytic cells .
2. Uncommonly it may localize and produce acute
osteomyelitis, renal abscess or subacute bacterial
endocarditis on top of rheumatic valvulitis .

- 75 -
 TOXAEMIA
Definition :

Bacterial toxins circulating in the blood. These toxins

can be :
- Endotoxins : produced mainly by gram negative bacteria
- Exotoxins : produced mainly by gram positive bacteria,
Manifestations :
- Constitutional signs & symptoms : fever, rigors,
headache, weakness & loss of appetite.
- Degenerations :cloudy swelling & fatty degeneration of
parenchymatous organs.
- Necrosis & haemorrhage of suprarenal gland : may
cause fatal adrenal insufficiency .
- Anaemia : due to bone marrow depression .
- Septic shock .

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 SEPTICAEMIA

Definition :
Circulation and multiplication of large numbers of
virulent bacteria and their toxins in the blood. It is a highly
fatal condition. It is caused by highly virulent bacteria such
as strepococcus haemolyticus, pneumococcus, bacillus
anthrax ….
Aetiology :
Infected operations, septic wounds, puerperal sepsis,
abscess and cellulitis. Invasion is common with lowered body
resistance .

- 77 -
 PYAEMIA

Definition :
Circulation of septic emboli in the blood with their arrest
in different organs resulting in multiple small abscesses. It is
a highly fatal condition, associated usually with septicaemia
Types :
1.Systemic pyaemia :
- Septic emboli originate from cases of pulmonary
infections, lung abscess, infective bacterial endocarditis...
- They are arrested in the kidneys, spleen, brain,....
2.Pulmonary pyaemia :
- Septic emboli originate from cases of puerperal sepsis,
osteomyelitis,cellulitis, ….
- They are arrested in the lungs
3.Portal pyaemia :
- Septic emboli originate from cases of suppurative
appendicitis, acute cholecystitis, infected piles,.…
- They are arrested in the liver .

 Pathological features :
Multiple, nearly equal, paravascular abscesses, present
on the outer & cut surfaces and surrounded by hyperaemia.

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