GENERAL PATHOLOGY

FOR UNDEGRADUATE

Dr. Hany M.Khattab

Professor Of Pathology
Faculty Of Medicine - Cairo University
2021
 Table of Contents

• Introduction 1
• Inflammation 2
• Repair 11
• Cell Injury and Cellular Accumulations 17
• Disorders of Vascular Flow 26
• Disturbances of Cell Growth 42
• Neoplasia (Tumours) 44
• Ionizing Radiations 71
• Environmental Pathology 72
• Bacterial Infections 77
• Viral And Fungal Infections 90
• Diagnostic Cytology 94
 INTRODUCTION
Pathology is the science which deals with the cause and nature of disease. This
study of diseases comprises:
1. Definition and Etiology (Causes).
‫ تكوين‬2. Pathogenesis: The mechanisms of development of disease.
3. Pathological features:
a. Gross or naked eye or macroscopic picture.
b. Microscopic or histopathological picture.
4. Fate and complications.

• Causes of Cell Injury (Causes of Diseases): All what effect Tissue

1. Living irritants as bacteria, viruses, parasites, fungi....
2. Non living irritants as:
a- Physical: cold, heat and irradiation.
b- Chemical: acids, bases, and poisons.
c- c- Mechanical: trauma, fractures and frictions.
3. Hypoxia (Decrease in oxygen supply) as in anemia.
4. Ischemia (Decrease in blood supply): as in arterial occlusion.
5. Immunological reactions.
6. Nutritional disturbances.
7. Genetic disorders.

• Mechanisms of cell injury:

1. Mitochondrial damage and lysis of endoplasmic reticulum.
2. Defective energy production and disorders of ions movement.
3. Defective enzyme functions and abnormal lysosomal changes.
4. Loss of integrity of cell membrane.

• Effects and consequences of cell iniuirv:

1. Inflammation and repair.
2. Degeneration (reversible cell injury) and necrosis (irreversible cell injury).
3. Intracellular accumulations as water, fat, protein, pigments....
4. Exracellular accumulations as calcification and amyloidosis.
5. Vascular disturbances as thrombosis and edema.
6. Cellular adaptations as atrophy, hypertrophy, hyperplasia and metaplasia.
7. Disturbances of cell growth as dysplasia and neoplasia.
 Chapter 1:
INFLAMMATION
Definition:
It is the reaction of living vascularized tissues in response to an irritant. This reaction
consists of vascular, lymphatic and cellular changes. It is a protective dynamic process aiming
at localization and removal of the irritant then healing of tissue. The suffix "it is" is added to
designate the inflamed organ or tissue e.g. tonsillitis, appendicitis, pancreatitis,

Causes:
All causes of cell injury, mainly the living irritants, such as bacteria, viruses and
parasites. The simplest classification of inflammation is acute and chronic inflammation.

ACUTE INFLAMMATION
- It has usually rapid onset and short duration
- The acute inflammatory reaction consists of:

• Local tissue damage:

- The central cells are killed (necrosis) due to maximal concentration of the irritant.
- The surrounding cells become sick (degeneration) due to disturbances in their
metabolism.
- Damaged cells release chemical mediators such as histamine, bradykinin and
prostaglandins.

• Local vascular reactions: (Vascular phase of the inflammatory response):

J. Transient vasoconstriction: due to direct action of the irritant on the vessel wall.
2. Vasodilatation: due to direct effect of released chemical mediators on the vessel wall.
3. Increased vascular permabilitv: Due to the action of chemical mediators.
4. Formation of inflammatory fluid exudates and vascular leakase:
- Mechanism of formation of fluid exudate: .
a. Increased capillary permeability mainly due to the action of chemical mediators.
b. Increased intravascular hydrostatic pressure due to vasodilatation.
 c. Increased extravascular osmotic pressure due to breakdown of large protein
molecules.
d. Increased fluidity of the ground substance.
‫ بنية‬- Composition of fluid exudate: Exudate is uid that leaks out of blood vessels into nearby tissues. The
a. High protein content 4-8 gm/dl. uid is made of cells, proteins, and solid materials. Exudate may ooze
from cuts or from areas of infection or in ammation. It is also called pus
b. High fibrinogen content.
c. High specific gravity above 1018.
d. High cellular content.
- Functions of fluid exudate:
a- Dilutes the irritant with its toxins and minimizes its effects.
any of various proteins (such as antibodies or complement)
b- Bring antibodies from blood: such as opsonins, antitoxins and bacteriolysins. that bind to foreign particles and cells (such as bacteria)
making them more susceptible to the action of phagocytes

c- Its fibrinogen content coagulates to fibrin and:

‫بينية‬
1. Localizes and surrounds the irritant and blocks interstitial tissue spaces and some
lymphatics.
Lymphangitis and lymphadenitis are
2. Forms network for phagocytic cells and repair cells to move on. d- both caused by an infection of the
lymphatic system. Lymphangitis is the
in ammation of the lymphatic vessels,
d- Brings nutrition to the cells and removes waste products. whereas lymphadenitis is the
in ammation of one or two lymph
nodes
- Fate of fluid exudate:
It is carried by lymphatics, with its bacteria and toxins and may cause lymphangitis and
lymphadenitis. Affected lymph nodes become enlarged, soft, painful and tender. If the
exudates carries bacteria and its toxins to the blood stream it leads to toxaemia,
bacteraemia or septicaemia. Septicemia is systemic infection in which bacteria get into the bloodstream and travel throughout the body. Toxemia refers to the presence of bacterial toxins in the blood.

5- The Inflammatory cellular exudates: (Cellular phase of the inflammatory

response):
a. Margination and Pavementation of leucocytes.
b. Emigration of polymorphs and monocytes.
c. Diapedesis of red cells.
d. Chemotaxis: orientation or movement of an organism or cell in relation to chemical agents
It is the unidirectional movement of polymorphs and macrophages towards the
irritant. They move on fibrin threads. Chemical products of bacteria, damaged
tissues and complement components, as C5a and C3a are chemotactic
involving, inducing, or exhibiting chemotaxis
substances.
The mechanism of chemotaxis involves the binding of chemotactic agents to
specific receptors on the surface of the leucocytes resulting in the hydrolysis and
activation of phospholipase C and release of calcium resulting in the activation
of extracellular and intracellular contractile proteins leading to cell movement.
 e. Phagocytosis:
It is the ingestion and destruction of bacteria and necrotic tissues by the phagocytic
cells, which are:
1. Microphages = Polymorphs = Neutrophils. Polymorphs and neutrophils are same
2. Macrophages: derived from blood monocytes and tissues histiocytes.
• The process of phagocytosis comprised:
a- Recognition and attachment: of bacteria to the cell surface of the
Phagocytic cells, in the presence of opsonins,
‫ غمر‬b- Engulfment: By extension of pseudopods around the attached opsonized
bacteria forming phagocytic vacuoles which fuse with lysosomes.
c- Degradation and destruction of bacteria, through oxygen dependent and
independent mechanisms.
* Factors influencing the efficiency of phagocytosis:
- Presence of opsonins and efficiency of chemotaxis.
:able to overcome bodily
- Type of bacteria: virulent bacteria resist phagocytosis.
defensive mechanisms :
markedly pathogenic

- Type of tissue: phagocytosis is weak in loose tissues.

• Chemical Mediators of Acute Inflammation:

I- Plasma factors: (Plasma proteases:
1. The kinin system (Bradvkinin): any of various polypeptide hormones that are formed locally in the tissues
and cause dilation of blood vessels and contraction of smooth muscle

- Causes increase in vascular permeability and vasodilatation.

2. The complement system
- C5a & C3a (Anaphylotoxins) have chemotactic and permeability increasing
properties, while C3b is an important opsonin.
3. The coagulation and fibrinolytic systems:
Bring the conversion of soluble fibrinogen to insoluble fibrin, increase vascular
a plasma protein that is produced in the liver and is
permeability and increase movement of leucocytes. converted into brin during blood clot formation

II- Factors released form tissue cells:

1. Vasoactive amines: amino
a- Histamine: causes vasodilatation and increased vascular permeability,
Released from mast cells, basophils and platelets,
b- Serotonin: Released from platelets.
2. Arachidonic acid metabolites:
a- Prostaglandins: Causes vasodilatation. Released from damaged cells,
b- Leukotrienes: cause chemotaxis for neutrophils and monocytes. Released from
damaged cells and neutrophils.

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 3. Lysosomal components: increase vascular permeability and chemotaxis for leucocytes.
Released from neutrophils.
lymphokine 4. Lvmohokines: In delayed hypersensitivity reactions and cause increase in permeability
and chemotaxis. Released from sensitized T lymphocytes.
5. Monokines: Like the lymphokines but released from macrophages.
Effects of Chemical Mediators:
1. Increased vascular permeability mainly by histamine and bradykinin.
2. Vasodilatation mainly by histamine, bradykinin and prostaglandins.
3. Chemotaxis mainly by the anaphylatoxins C5a and C3a.
The course and fate of acute inflammation;
‫ تسوية فض‬1. Resolution: Complete restoration of normal conditions due to minimal tissue damage,
rapid removal of irritant and good macrophage functions.
‫ انتكاسة تراجع‬2. Regression and healing: When the body overcomes the irritant. Healing occurs by

regeneration or by granulation (fibrosis).

‫ تفاقم‬3. Progression & spread: When the bacteria overcome the defense mechanisms,
inflammation spreads directly, by lymph or by blood.
chronic 4. Chronicitv: When the irritant and the body defense are about equal, the inflammation
continues for a long time.
The general changes in acute inflammation are:
a) Leucocvtosis: increase of blood leucocytes above 10.000 per cmm, and is caused by
leucocytosis promoting factor, IL-1 and TNF released from dead tissues which have
stimulating effect on bone marrow.
b) Fever (Pyrexia): dead leucocytes produce pyrogenic substances that cause increased
metabolism and rise of body temperature. producing or produced by heat or fever

c) High erythrocyte sedimentation rate (ESR).

The cardinal signs and symptoms of acute inflammation:

1.Hotness

2.Redness or flare

3.Swelling or wheal

4.pain and tenderness

5.loss of function
 The types of acute inflammatio
I- Suppurative inflammation.
II- Non-suppurative inflammation.

Suppurative is a term used to describe a disease or condition in which a

purulent exudate (pus) is formed and discharged
 I- Acute Suppurative Inflammation

Definition:
Severe acute inflammation characterized by pus formation, and caused by pyogenic
bacteria as: staphylococci, streptococci, gonococci and others.
Bacteria that cause pus are called pyogenic

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 and attract polymorphs. Many
polymorphs are killed and become pus cells. They release their proteolytic enzymes which
cause liquefaction of necrotic tissues and fibrin. This liquefied necrotic material mix with
inflammatory exudates forming pus. The dead polymorphs are called pus cells.
proteolysis : the hydrolysis of proteins or peptides with
formation of simpler and soluble products
• Composition of Pus:
1. Living and dead bacteria with their toxins and their pigments.
2. Liquified necrotic material mainly peptones. any of various water-soluble products of partial hydrolysis of
proteins

3. Inflammatory fluid exudate.

4. Inflammatory cellular exudate.

• Types of suppurative inflammation:

1- Localized suppurative inflammation:
A. Abscess: STAPH AUREUS
- 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 such as the (liver, lung, brain,
........................ ).

• Pathology of Abscess:
1. At first, abscess is formed of central necrotic zone and outer zone of acute
inflammation with cellular degeneration containing large numbers of
polymorphs and macrophages.
 Staphylococcus (staph) is a group of bacteria. There are more than 30
types. A type called Staphylococcus aureus causes most infections. Staph
bacteria can cause many different types of infections, including: Skin
infections, which are the most common types of staph infections

2. Later on it is formed of three zones due to liquefaction of necrotic tissues and pus
formation.
- Central zone: Necrotic core: gradually decreases in size.

fl
- Mid zone: Abscess cavity: Filled with pus.
- Outer zone: Pyogenic membrane: Acutely inflamed degenerated area.
3. The abscess enlarges due to more necrosis and liquefaction. Enlargement stops
when the staphylococci produce coagulase enzyme that helps fibrin formation and
localization.
4. Pus must be evacuated spontaneously or surgically followed by healing which
occurs by fibrosis or by granulation.

‫بثرة‬ B- Boil (Furuncle):

This is a small abscess related to hair follicles or sebaceous gland. Common sites
are face, back of neck and axilla.
‫ جمرة دمل‬C- Carbuncle Carbuncles are clusters of furuncles connected subcutaneously

- Definition: A localized suppurative inflammation characterized by multilocular

abscess cavity opening to the skin by multiple sinuses discharging pus.
- Cause: Staphylococcus aureus. More common in diabetics.
- Sites: Back of neck and 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.
Hyaluronic acid is a natural substance found in the uids in the eyes and joints. It acts as a cushion
and lubricant in the joints and other tissues.
2- Diffuse suppurative inflammation (The Cellulitis):
- Definition: Acute diffuse suppurative inflammation.
- Cause: Streptococcus haemolyticus which produces two enzymes:
1. Streptokinase = Fibrinolysin: dissolves and prevents fibrin formation.
2. Hyaluronidase = Spreading factor: breaks down tissue ground substance.
- Sites: Loose connective tissue such as orbit, pelvis and scrotum.
- Pathologv: Differs from abscess in:
1. Failure of localization with more serious spread.
2. Excess necrosis, with more toxaemia.
 Phlebitis means "in ammation of a vein
Thrombophlebitis (throm-boe- uh-BY-tis) is an in ammatory process that causes a
blood clot to form and block one or more veins, usually in the legs. The affected vein
might be near the surface of the skin (super cial thrombophlebitis) or deep within a
muscle (deep vein thrombosis, or DVT).

* Complications of Suppurative Inflammations:

1. Change to chronic.
2. Blood spread: Toxaemia, septicaemia and pyaemia.
3. Lymphatic spread: Acute lymphadenitis and lymphangitis.
4. Complications of healing such as chronic ulcer, sinus, fistula or keloid.
5. Septic thrombophlebitis.
6. Putrefaction and gangrene.

II- Acute Non Suppurative Inflammation

‫التهاب االنف‬ Rhinitis is a reaction that happens in the eyes, nose, and throat when allergens in the air trigger histamine to be released in the body

1. Catarrhal Inflammation:
- Definition: Mild acute non suppurative inflammation of mucous membranes
characterized by excess mucous secretion.
- Examples: rhinitis, bronchitis, appendicitis, .........
2. Membranous = Pseudomembranous inflammation:
- Definition: Sever acute non suppurative inflammation of mucous membranes
characterized by the formation of a pseudomembrane.
dysentery :disease characterized by severe
diarrhea with passage of mucus and
- Examples: Diphtheria and bacillary dysentery. blood and usually caused by infection

- Pathogenesis: Bacteria produce powerful exotoxins which cause focal then diffuse
necrosis. The exotoxins spread from necrotic mucosa to submucosa causing acute
inflammation and to blood stream causing severe toxaemia.
3. Serofibrinous inflammation:
- Definition: Acute inflammation characterized by excess fluid exudates rich in
fibrinogen. It affects serous membranes (pleura, pericardium and peritoneum).
4. Fibrinous inflammation:
Characterized by exudates with excess fibrin, e.g. lobar pneumonia.
5. Serous inflammation:
Characterized by excess serous exudates, e.g. burn and herpes simplex.
6. Haemorrhagic inflammation:
Characterized by exudates rich in red blood cells due to damage of vascular wall, e.g.
smallpox.
7. Necrotizing inflammation:
Characterized by marked tissue necrosis, e.g., cancrum oris nad Vincent angina.
8. Allergic inflammation:
Due to antigen-antibody reactions, e.g., allergic rhinitis. It is rich in eosinophils.
 CH RO NI C I NF LA M M A TI ON
General Characters:
1- Mild irritant with gradual onset and long duration.
‫الدرن‬
2- May follow acute or start chronic as in tuberculosis. TB
condition marked by increase of
3- Progressive tissue necrosis and gradual replacement by fibrosis. interstitial brous tissue
4- The blood vessels show gradual thickening of the wall and gradual narrowing of the
lumen end arteritis obliterans).
5- Inflammatory fluid exudates is scanty.
6- Inflammatory cellular exudate is formed of:
Lymphocytes.
- Plasma cells.
Macrophages.
- Multinucleated giant cells.
Eosinophils.
- 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,
‫ الزهري‬syphilis, bilharziasis.

G RA N U LOM AS ‫األورام ألحبيبيه‬

Definitions
A type of chronic specific inflammation that begins as multiple small granules that
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 and fibroblasts.
Types:
1. Infective granuloma: ‫برص‬

- Bacterial: tuberculosis, leprosy, syphilis.

- Parasitic: Bilharziasis.
- Fungal: madure foot.
2. Non-infective granuloma:
- Silicosis and asbestosis.
- Foreign body granuloma around talc powder, silk suture ....
3. Granuloma of unknown etiolosv: e.g. Crohn's disease and sarcoidosis.
 ABSCESS CELLULITIS

Localized form of suppurative inflammation. Diffuse form of suppurative inflammation.

Caused by Staphylococccus aureus. Caused by Streptococcus haemolyticus.
Mainly in subcutaneous tissues Localized due Mainly in loose connective tissues
to coagulase secretion. Diffuse due to streptokinase and
hyaluronidase secretion.
Small necrotic centre Pus is thick and Extensive necrotic tissues Pus is thin and
yellowish Less toxaemia Less spread bloody More toxaemia More spread

ACUTE INFLAMMA TION CHRONIC INFLAMMA TION

Rapid onset and short duration Gradual onset and long duration Infiltration
Infiltration by polymorphs, pus cells and by lymphocytes, plasma cells, macrophages,
macrophages. giant cells and fibroblasts.
Eosinophils may be seen in allergic types. Eosinophils may be seen in parasitic types.
Blood vessels show dilatation and congestion. Blood vessels show endarteritis obliterans.
Connective tissue shows edema and fibrin Connective tissue shows fibrosis.
threads.

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 Chapter 2:
REPAIR

Definition:
Repair (Healing) is the replacement of damaged tissues 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:
The type of repair depends on the type of cells and their ability to divide and
proliferate. Three types of cells are known:
Continually undergoing chemical,
physical, or biological change or a- Labile cells: These cells can proliferate continuously throughout life and have
breakdown : UNSTABLE
good power of division. They include:
stratum = layer - Stratified squamous epithelium of skin and mucous membranes of mouth,
pharynx, larynx, vagina....
- Transitional epithelium of urinary tract.
- Columnar epithelium of G.I.T., respiratory tract, endometrium,...
- Haemopoetic and lymphoid cells.
‫ فى العادة ثابته‬b- Stable cells: These cells can proliferate only when needed and have limited power

of division, so that regeneration follows minor injury and fibrosis follows major
injury:
parenchymal - Parenchymatous cells: liver, pancreas, glands and renal tubules.
- Mesenchymal cells: osteoblast, chondroblast
chrondroblast and fibroblast,
c- Permanent cells: These cells cannot proliferate at all and include:
- Muscle cells: cardiac and skeletal. mesenchymal stem cells (mscs)
Central Nervous system
- Nerve cells: in brain and spinal cord.
• Examples of repair by regeneration:
1- Regeneration of skin (labile cells):
- Epidermis alone: regenerates easily.
- Dermis: heals by granulation tissue (fibrosis).
2- Regeneration of liver cells (stable cells): ‫سليمة‬
- Mild cell injury with intact fibrous framework: perfect regeneration.
- Severe cell injury with destroyed fibrous framework: irregular fibrosis and
liver cirrhosis. ‫تليف الكبد‬

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3- Repair in nervous system:
a. Central nervous system (permanent cells):
No regeneration can occur. The necrotic cells are removed by microglia and
then replaced by proliferating neuroglia cells. This process of healing is
called gliosis. =
b. Peripheral nerves: Regeneration can occur:
- Following nerve injury, the nerve cells swell, the Nissel granules disappear,
the nuclei become eccentric and the myelin sheath and axis cylinder
disintegrate.
- The Schwann cells proliferate and form continuous neurilemmal rube.
- New axons grow from the proximal end.
- Reformation of myelin sheath occurs finally.
* N.B.: If the 2 ends of the cut nerve are not in direct opposition to each
other, the Schwann cells and the growing axons mix together forming a
painful mass called traumatic (stump or amputation) neuroma.
4- Healing of bone fracture:
- Haematoma with acute inflammation and cellular debris forms at the fracture
site and growth factors are released.
- The haematoma is gradually invaded by fibroblasts, osteoblasts and new
capillaries with formation of soft callus or procallus.
- The procallus is converted to fibro-cartilagenous callus, then osteoid callus
and finally to hard bony (osseous) callus by progressive endochondral
ossification.
- The un-needed callus (the external and internal) are removed by osteoclasts
followed by remodeling of the intermediate callus with deposition of calcium
phosphate and carbonate.
- The bone marrow regenerates later on.
Bonv union may fail to occur because of:
1. Improper immobilization leading to fibrous union.
2. Impaired blood supply.
3. Infection at site of fracture.
4. Interference of soft tissue with bony ends.
5. Impaired nutrition and old age.
6. Diabetes mellitus and glucocorticoid therapy.

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 catarrh

ammation of a mucous membrane

especially : one chronically affecting the human nose and air passages

protein ‫ بيحوش‬tissue ‫ال‬

Suf x indicating condition, status, process, whether normal or diseased, or sometimes
an increase.
 E - Pig ments A ccu mul ation s
I- Endogenous Pigmentation
1- Melanin Pigment
Definition:
Yellow to brown pigment formed by melanocytes from tyrosine by the action of tyrosinase
enzyme. It is present in skin, iris and choroid.
• Disturbance is either:
1. Deficiency in melanin pigment:
a. Albinism. albino ‫أبرص او أمهق‬

b. Leucoderma.
2. Increase in melanin pigment:
a. Addison's disease.
b. Benign and malignant melanomas.
c. Chloasma: brown skin patches during pregnancy.
d. Direct prolonged exposure to sun, and ultraviolet rays.

3- L i p o c h r o m e P i g m e n t s L i p o f u s c i n P i g m e n t s )
Definition:
Yellowish brown pigment of lipid origin and it is normally present in corpus luteum, testis,
suprarenal cortex and heart muscles.
Brown atrophy of heart showing
1.Reduced size and weight. 2-Dark brown in colour.
3- Tortuous coronaries. 4-Soft flabby muscles.

4- H a e m o g l o b i n D e r i v e d P i g m e n t s
A- Haemosiderin Accumulation: Haemosiderosis:
Definition:
Pathological accumulation of haemosiderin in tissues.
Types: 1- Localized haemosiderosis: due to
a. Chronic venous congestion of liver, lung and spleen.
b. Around infarctions and varicose veins.
2- Generalized haemosiderosis:
c. Repeated blood transfusions.
d. Haemolytic anaemias.

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B- Haemochromatosis = Bronzed diabetes:
Definition: Just iron

An inborn error of iron metabolism leading to excess absorption of iron in diet. It affects
middle aged males (females do not develop the disease because of the regular loss,of blood and iron
in the menstrual cycles).
Effects:
1. Skin = bronzed colouration.
2. Pancreas = diabetes mellitus.
3. Heart = heart failure.
4. Liver = pigmentary cirrhosis.
2- Exogenous Pigmentation
1. Inhalation: carbon causes anthracosis of lung.
2. Ingestion: chronic lead poisoning causes blue line on the gums.
3. Inoculation: tattooing (India ink in subcutaneous tissues).

II- EXTRACELLULAR DEPOSITIONS

A- PATHOLOGICAL CALCIFICATION
1- Dystrohpic Calcification 2- Metastatic Calcification
- More common. - Less common.
- Deposition of calcium salts in -Deposition of calcium salts in living tissues.
degenerated and necrotic tissues.
- Blood calcium level is normal. -Blood calcium level is elevated.
- Cause is relative alkalinity or increased -Cause is increased calcium absorption,
phosphatase activity in these tissues. increased calcium mobilization from bone,
hyper-parathyroidism, hypervitaminosis D,
bone metastases and chronic renal failure.
Sites: Sites:
1. Areas of degeneration: 1. Renal tubules.
- Atherosclerosis and Hyalinosis. 2. Wall of stomach.
2. Areas of necrosis: 3. Lung alveoli.
- Thrombosis. 4. Walls of blood vessels.
- Tuberculosis.
- Fat necrosis.
Gross: Affected area is opaque white, hare and has granular cut surface.
Micro: Calcium stains blue with H & E.

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 3- Stone formation: Deposition of calcium salts in some organs, e.g., urinary tract, biliary tract,
salivary tract....
4- Idiopathic calcinosis: Rare with unknown etiology, may affect skin, subcutaneous tissue with the
formation of nodular masses called tumoural calcinosis.

B - A M Y L O I D D E P O S I T I O N ( A M Y L O I D O S I S } Definition;
It is the pathological deposition of pale, pink, homogenous, refractile, structureless protein
material. It is deposited in various tissues, mainly extracellular, in the wall of blood vessels and in the
basement membranes.

Staining of Amyloid Material:

‫كبير‬
1. Gross stainins:
- Dark red with Lugol's iodine that is transformed into blue after the addition of diluted sulphuric
acid.
2. Microscopic staining:
- Pale pink with H & E stain.
- Rose red with methyl violet or gentian violet stains.
- With congo red stain, the amyloid shows apple green briefrengence when observed by the polarizing
fl
light.

• Types and Causes of Amyloidosis:

Disease of blood
A- Systemic (Generalized! Amyloidosis:
1. Immunocvte dvscrasias with amyloidosis (Primary Amyloidosis):
It results from deposition of immunoglobulin light chain (AL) produced by abnormal B
lymphocytes and plasma cells. It is usually associated with plasma cell myeloma and
malignant lymphomas.
2. Reactive systemic amyloidosis (Secondary Amyloidosis):
It results from protracted breakdown of cells (AA deposition) associated with chronic
inflammatory disorders such as chronic suppurations, chronic osteomyelitis, tuberculosis and
rheumatoid arthritis. in ammation of joints due to infectious, metabolic, or constitutional causes

-26-
 ‫غسيل كلوي غسيل الدم‬
3. Hemodialysis associated amyloidosis:
It affects some patients with chronic renal failure subjected to repeated hemodialysis. The
deposited protein is B2-microglobulin.
‫متوارث‬
4. Hereditary amyloidosis:
Several types as in familial Mediterranean fever (AA deposition) and familial amyloidotic
neuropathy (transthyretin deposition). Hereditary amyloidosis is a condition in which abnormal protein deposits (called amyloid) form in
almost every tissue in the body. Harmful deposits most often form in the heart, kidneys, and
nervous system. These protein deposits damage the tissues and interfere with how organs work.

B- Localized amyloidosis:
1. Senile cardiac or senile cerebral amyloidosis. Which produce Thyroxine + Calcitonin
2. Tumors of endocrine glands with amyloid deposits such as medullary carcinoma of thyroid
(procalcitonin deposition).
:arising 3. Idiopathic localized amyloid deposits: nodular deposits of AL may affect the lung, larynx,
spontaneously or
from an obscure or tongue, skin and urinary bladder.
unknown cause

Gross Picture of Affected Organs in Amyloidosis:

1. Large size, and heavy weight.
2. Tense capsule.
3. Firm consistency and sharp cut edges.
4. Flat refractile waxy brownish cut surface.

Microscopically:
Amyloid appears as extracellular deposition of pale, pink, homogenous, structureless,
refractile material on the basement membranes and blood vessels leading to thickening of the wall, and
narrowing of the lumen with pressure atrophy on surrounding cells.

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Chapter 4

DISORDERS OF VASCULAR FLOW

(CIRCULATORY DISTURBANCES^
HYPERAEMIAfACTIVE HYPERAEMIA^

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

VENOUS CONGESTION fPASSIVE HYPERAEMIA^

Definition:
Increased venous blood in an organ or tissue due to obstruction of its venous return. Types:
I- General Venous Congestion

A-Acute General Venous Congestion:

- In acute heart failure and it is rapidly fatal.

B- Chronic General Venous Congestion:

- It is due to chronic right sided heart failure resulting from causes in:
1- The heart: mitral stenosis, left ventricular failure and myocardial fibrosis.
2- The lung: emphysema, tuberculosis, pneumoconiosis, bilharziasis and fibrosis.

Pathology and Effects:

1. Dyspnea, cyanosis and hypoxia.
2. Congested neck veins.
3. Cardiac edema.
b- The luns: is affected in all cases of left sided heart failure and with mitral stenosis.
• Gross: 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.

• Micro:

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 - Alveolar capillaries are dilated and congested.
- Alveolar septa are thickened and fibrosed.
- Alveolar lamina contain red blood cells and heart failure cells (macrophages engulfing
brown hemosiderin granules).

c- The liver:
• Gross: The liver shows the 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- Later on, the liver become shrunken, and firm with irregular surface.

• Micro:
- Central vein and central sinusoids and dilated and congested with red blood cells.
- Central liver cells are atrophic.
- Peripheral liver cells show fatty degeneration.

d- The spleen:
• Gross: Congestive splenomegaly.
1. Large size, heavy weight and firm consistency.
2. Sharp cut edges and flat cut surface.
II- Local Venous Congestion
A- Acute Local Venous Congestion:
- Causes: Sudden venous occlusion by thrombosis, ligature, strangulation, or torsion. B- Chronic
Local Venous Congestion:
- Causes: Gradual compression of veins by tumour mass, enlarged lymph node, pregnant uterus, liver
cirrhosis and bilharzial hepatic fibrosis. Mitral stenosis causes blood stasis in left atrium and lungs.

THROMBOSIS
Definition:
A thrombus is a compact mass formed of constituents of circulating blood, inside vessel or heart
during life.
Causes:
1. Damase to the vascular endothelium: (Endothelial injury)-.
- Mechanical: trauma, pressure, ligature.
- Inflammatory: phlebitis, arteritis, endocarditis.

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 - Degenerative: atherosclerosis, aneurysm, myocardial infarction.
2. Slowins of blood stream (Stasis):
During slowing the platelets cross the plasmatic zone and adhere to the vascular endothelium as
in: - Leg veins in chronic heart failure and varicose veins. ‫الدوالي‬
- Left atrium in chronic heart failure and varicose veins.
- Left atrium of heart in mitral stenosis.
- Areas of acute inflammation.
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: (Hvvercoaeulabilitv 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.
- Cases of hyperlipidemia, nephritic syndrome and advanced cancer.
- Use of contraceptive pills.
- Inherited deficiency of antithrombin III, protein C/S and fibrinolysin.

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 • Classification and Types of Thrombi:
1. Pale thrombus = Platelets thrombus:
- It is the first to be formed, and consists mainly of platelets and fibrin.

2. Red thrombus
- It is formed of platelets, excess fibrin and red cells.
- It occurs mainly in venous thrombosis.

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. Because these lines more fibrin is deposited entangling red and white cells.
- If the alternating platelets and fibrin lamellae are perpendicular to the vessel wall, it is called
coralline thrombus.
- If the alternating platelets and fibrin lamellae are parallel to the vessel wall, it is called laminated
thrombus (mainly in aneurysms).
- If the thrombus occludes the vessel partially it is called mural thrombus. while if it occludes the
vessel completely it is called occluding thrombus.

4. Propagating thrombus:
- Occurs mainly in veins of lower limbs.
- The blood proximal to an occluding thrombus is stagnant and it clots . This clot affects the whole
column of blood till the next tributary.
- Opposite the opening of a tributary the blood is circulating and a thrombus is formed till it
occludes the vessel completely. The process is repeated resulting in alternating thrombi and clots
known as propagating thrombus.

• Sites of Thrombus Formation:

1. Thrombosis in the heart:
More common in the left side, types are:
a- Mural thrombi: over myocardial infarction.
b- Vegetations: pale thrombi over valves in rheumatic valvulitis and bacterial endocarditis.
c- Auricular thrombi: usually in left auricle in cases of mitral stenosis.
d- Agonal thrombi: pale thrombi in right ventricle at time of death.

propagating thrombus

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 2. Thrombosis in veins: more common than in arteries because blood stream is slow and vein has thin
wall. Two types:
a- Thrombophlebitis: thrombosis initiated by inflammation may be:
- Septic thrombovhelbitis: occurs in veins draining areas of acute inflammation as appendicular vein
in acute appendicitis and uterine veins in puerperal sepsis.
- Aseptic thrombophelbitis: occurs in veins exposed to irradiation.

b- Phlebotrombosis: thrombosis initiated by other factors: , there is no in

- In varicose veins.
- In veins of feet and calf: in chronic heart failure, patients with prolonged recumbency and
compression of veins against bed mattress.
- In pelvic veins after labour or operations: with prolonged bed rest and absence of muscular
movements leading to stasis.

3. Thrombosis in arteries:
Less common than in veins, because blood stream is rapid and artery has thick wall. Causes are:
a- Atherosclerosis causing roughness of the intima. b- Arteritis causing ammation
damage to the endothelium, c- Aneurysms causing stasis and disorders of
blood stream.

• Fate and Complications of thrombosis:

A. Septic thrombus', may be fragmented by the proteolytic enzymes into septic emboli —> pyaemic
abscesses.
B. Aseptic thrombus:
‫ انحالل‬1. Lysis, fragmentation and embolization. But Without abscess
2. Fibrosis, or fibrosis and canalization.
3. Dystrophic calcification.
4. Propagation.
Danger danger
5. Arterial occlusion (ischaemia) or venous occlusion (congestion).
6. Incorporation of arterial thrombi into atheroma.

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 EM BO LIS M
Definition:
Embolus is an absolute 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 (thrombo-embolism): a. Course
and site of impaction of emboli:
- From systemic vein or right side of heart, the emboli pass to the pulmonary artery and impact
in the lung: Pulmonary embolism.
- From systemic artery or left side of the heart, the emboli impact in any organ (spleen, brain,
kidney, ....): Systemic embolism.
- From portal veins, the emboli impact in the liver: Portal embolism. a. Effects:
- Aseptic embolus: - Poor collaterals —*■ ischaemia and infarction.
- Good collaterals —*■ insignificant effect.
- Septic embolus: Pyaemic abscesses.
2. Air embolism: (Gas embolism):
- May be due to:
a. Injury of large neck veins.
b. Faculty techniques of artificial pneumothorax or blood transfusion under pressure.
c. Caisson's disease in divers.
3. Fat Embolism:
- May be due to:
a. Fractures of long bones.
b. Burns or inflammation of fatty areas.
4 Amniotic Fluid Embolism:
Strong uterine contractions may tear foetal membranes and push amniotic fluid in opened
maternal uterine veins causing fatal pulmonary embolism to the mother.

5- Tumor emboli.
6- Parasitic emboli.
7- Bacterial emboli.
8- Foreign body emboli.

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 IS CH AEMI A

Definition:

Decrease blood supply to tissue or organ due to occlusion of its arterial supply.

Types:
1- Sudden or acute (complete) ischaemia:
- Causes:
a. Thrombosis
b. Ligature of an artery.
c. Torsion or twisting of movable vessels in intestine or ovary.
d. Arterial spasm as in ergot poisoning.

- Effects: - No collaterals or poor collaterals —* infarction or gangrene.

- Good collaterals —> insignificant effect.

2- Gradual or chronic (incomplete) ischaemia:

- Causes:
a. Atherosclerosis.
b. Endarteritis obliterans as in syphilis.
c. Pressure from outside by enlarged lymph nodes, tumor mass....

Effects:
- Poor (inefficient) collaterals —•» ischaemic atrophy and fibrous replacement as in myocardial
fibrosis due to coronary atherosclerosis.
- Good (efficient) collaterals —> insignificant effect.

I NF A RCTI O N

Definition:
An areas of coagulation necrosis caused by sudden ischaemia. It is liquifactive in the brain.
Aetiology:
1) Mainly thrombosis or embolism causing arterial occlusion.
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 subscapular, and peripheral.
- Shape: pyramidal or triangular in shape with the base on the surface and the apex towards
the center, due to distribution of the blood supply.
- Surface: raised when recent (edema) and depressed when healed (fibrosis).
- Surrounded: by a red zone of hyperaemia.

• Types:
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 venous occlusion, in organs with congested
vessels or having double blood supply as lung or intestine. It is dark, moist and soft.

2. Micro
- Early: Cells show post necrotic changes after 12 h.
- Next: loss of cellular details and preservation of general architecture (ghosts of original
structure) after 36 h.
- Later: necrotic area appears as pink granular region surrounded by acute inflammatory
reaction, after 72h.

3. Fate:
a. Small infarct: phagocytosed by macrophages and replaced by fibrosis.
b. Large infarct: encapsulation and dystrophic calcification.

• Examples of Infarctions in Different Organs:

1. Kidnev.
- Due to thrombosis or embolism of a branch of renal artery.
- The infarct is usually pale in colour affecting mainly the cortex.
- Clinically: painless hematuria.
2. Spleen:
- Due to thrombosis or a branch of splenic artery.
- Clinically: left hypochondrial pain because capsule is affected (perisplenitis).

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3. Heart:
- Due to thrombosis or embolism of a coronary artery on top of atherosclerosis, usually present with
severe chest pain.
- It is pale and affects mainly the left ventricle.
4. Liver:
- Infarction of the liver is very rare (double blood supply).

5. Intestine: due to
- Thrombosis or embolism of mesenteric vessels.
- Strangulated hernia, volvulus and intussusception (Twisting of vessels).
* Gross:
The infarct is haemorrhagic. The affected loop and its mesentery are swollen, dark red, covered
by fibrin and the peritoneal cavity contains hemorrhagic effusion.
- Clinically: - Acute intestinal obstruction gangrene and septic peritonitis.

6. Brain: Due to
- Thrombosis or embolism of cerebral arteries.
* Gross:
- The infarction is liquifactive and may be pale or hemorrhagic.
- The covering meninges are thick and adherent.
- Healing takes place by gliosis.
* Micro:
- The myeline dissolves into fat globules which are phagocytosed by microglia which are called
compound granular corpuscles.
- Clinically: - Hemiplegia if infarct affects internal capsule.

7. Lungs: 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.
* Gross:
The infarction is hemorrhagic, may be multiple and usually subpleural, and covered by fibrinous
pleurisy.
* Micro:
- Ghosts of original structure are seen.
- Alveolar spaces are filled with blood and heart failure cells.
- Surrounding lung tissue shows chronic venous congestion.
- Clinically: - Haemoptysis and chest pain.

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 G A N G REN E

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 hydrogen sulphide. This hydrogen sulphide gives the gangrenous tissues a foul
odour and black colouration (by forming iron sulphide with the iron of hemoglobin).
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 Raynaud's disease, Buerger's disease, or ergot poisoning.
4. Surgical ligature of artery.
There is cut of arterial blood supply while the venous and the lymphatic drainages 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.
- Tissue necrosis starts usually in the big toe and the area is pale and cold.
- Putrefaction starts by saprophytic bacteria, the area becomes black & offensive.
- The toxic products irritate the surrounding healthy tissues causing thrombosis and more necrosis
and putrefaction. The gangrenous process spreads proximally and slowly along the limb.
- When gangrene reaches an area of good blood supply it stops, and a red line of acute
inflammation is seen between healthy and gangrenous parts known as line of demarcation.
- From the healthy side granulation tissue grows and separates the gangrenous part below and
appears as groove known as line of separation.

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2- Moist gangrene:
It usually affects internal organs due to sudden occlusion of both arterial and venous blood
supply. There is no evaporation and 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.

A. Moist gangrene of the intestine:

- Seen in strangulated hernia, intussusceptions or volvulus. Patient suffers from acute intestinal
obstruction, septic peritonitis & severe toxaemia.

B. Moist gangrene of the limb:

May follow severe crushing injury or tight tourniquet.

C. Bed sores:
Skin ulcers cover bony prominences as sacrum and greater trochanter due to prolonged
recumbency in bed in cases of paralysis and coma. They result from stasis, ischaemia necrosis and
secondary bacterial infection.

D. Diabetic gangrene:
Diabetics usually have atherosclerosis, trophic ulcers due to sensory loss, hyperglycemia,
low immunity and increased susceptibility to infection.
• Pathological features: It begins usually in big toe after mild injury. Tissue hyperglycemia
helps putrefaction followed by inflammatory occlusion of all vessels, arteries and veins. It
spreads rapidly with poorly developed line of demarcation, severe toxaemia and no self-
separation. It is a combination of moist and ineffective types.
Comparison between dry and moist gangrene
Dry Gangrene Moist Gangrene
Gradual arterial occlusion, by athero- Sudden arterial & venous occlusion, by
sclerosis or arterial spasm. crush injuries, bed sores or tight
Tourniquet.
Affects exposed parts. Affects internal organs.
Slow putrefaction & spread. Rapid putrefaction & spread
Tissue mummification. Tissue edema.
Line of demarcation and self-separation, are Poor line of demarcation and no self
Usually present. Separation.
Mild toxaemia. Severe toxaemia

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3. Infective Gangrene
A subtype of moist gangrene in which pathogenic bacteria cause tissue necrosis and
saprophytic bacteria cause tissue putrefaction.
Types:
a. Cancrum oris: Infective gangrene of oral mucosa of weak malnourished children. It is caused
by Treponema vincenti and Bacillus fusiformis. There is severe toxaemia and may be
complicated by aspiration bronchopneumonia.
b. Necrotizing fasciitis.
c. Synergistic gangrene.
4. Gas gangrene: highly fatal toxic gangrene occurring in deep wounds
Contaminated with anaerobic gas producing bacteria. The organisms are:
1- Saccharolytic bacteria
2-Proteolytic bacteria.

ED EM A
Definition:
Pathological accumulation of excess fluids in interstitial tissue spaces, serous sacs and body
cavities.
Causes and Pathogenesis:
1. Increased capillary hydrostatic pressure: in chronic venous congestion and hypertension.
2. Increased capillary permeability: in acute inflammation, toxins or hypoxia.
3. Decreased colloidal osmotic pressure of plasma: When total proteins fall below 2.5 gm or
albumin below 1.5 gm.
4. Sodium and water retention: in chronic heart failure and renal disorders.
5. Lymphatic obstruction: It is due to:
- Acute lymphangitis and lymphadenitis.
- Filarial lymphangitis and lymphadenitis.
- Pressure on lymphatic vessels by tumour.
- Congenital hypoplasia of lymph nodes.
- Metastasis in lymph nodes.

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* Types of edema: May be localized or generalized A- Localized:
1. Allergic edema: due to histamine released and increased capillary permeability.
2. Inflammatory edema: in acute inflammation.
3. Venous obstruction: leads to edema in area drained by obstructed vein, as in:
- Liver cirrhosis and bilharzial fibrosis —* intestinal edema and ascitis.
- Acute left sided heart failure —> acute pulmonary edema.
- Pressure of pregnant uterus on iliac veins —> edema of lower limbs. 5. Venous
obstruction: see local venous congestion.
B. Generalized Edema:
1. Cardiac edema: occurs with chronic right sided heart failure.
2. Renal edema: of two types:
a- Nephritic edema: Occurs in acute diffuse glomerulonephritis, b- Nephrotic edema. Occurs in
crescentic & membranous glomerulonephritis.
3. Nutritional edema:
Caused by hypoproteinaemia resulting from:
- Prolonged protein deficiency.
- Decreased plasma protein formation in chronic liver disease.
- Interference with food intake, passage, digestion or absorption.

H EM O RRHA G E
Definition:
Escape of blood outside vessels or heart.

Causes:
1. Traumatic: accidental or surgical injury of vessel wall.
2. Spontaneous: may be due to:
a. Degenerative conditions of vessel wall: atheroma and aneurysm.
b. Destruction of vessel wall by tumour or peptic ulcer.
c. Inflammation of vessel wall: arteritis or phlebitis.
d. Increased intravascular pressure: venous congestion and hypertension.
e. Haemorrhagic blood diseases: haemophilia and leukaemia.
f. Vitamin C or vitamin K deficiency.

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Types of haemorrhage:
1. External haemorhase: Escape of blood outside the body:
- Epistaxis: bleeding from the nose.
- Haemoptysis: coughing of blood from lung or bronchi.
- Haematemesis: vomiting of blood from oesphagus, or stomach.
- Melena: dark digested blood in stools from.
- Bleeding per rectum: fresh red blood in stools.
- Haematuria: blood in urine.
- Menorrhagia: excessive or prolonged menstrual bleeding.
- Menorrahagia: excessive or prolonged menstrual bleeding.
- Metrorrhagia: irregular uterine bleeding not related to the cycles.
2. Internal haemorrhage: Escape of blood inside a body cavity:
- Haemothorax: blood in pleura.
- Haemopericardium: blood in pericardium.
- Haemoperitoneum: blood in pericardium.
- Haematocele: blood in tunical vaginalis.
- Haemarthrosis: blood in joint cavity.
3. Interstitial haemorrhaee: Escape of blood in interstitial spaces:
- Petechiae: small amount of capillary blood.
- Ecchymosis: moderate amount of blood.
- Haematoma: large amount of blood causing swelling.

Effects of Haemorrhage:
1. Small amount for one time: no effect.
2. Repeated small amounts: microcytic hypochromic anaemia.
3. Moderate amount (less than 750 cc): there is compensation by:
- Reflex tachycardia.
- Reflex vasoconstriction of skin, muscles and splanchnic area.
- Increased catecholamines release from suprarenal medulla.
- Additional of proteins from liver.
- Addition of red and white cells from bone marrow.
4. Massive amount: (more than 1000 c.c.): causes hypovolaemic shock.

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 S H OCK
Definition:
Depression of vital functions due to decrease in cardiac output or acute
circulatory failure.
Clinically:
- Patient is usually quite but may be restless.
- Pale cold skin covered by cold sweat.
- Rapid weak pulse.
- Low blood pressure.
- Shallow rapid respiration.
- Oligouria or anuria.
• Types of hemorrhage:
1. Hvpovolaemic shock:
Due to reduction in blood volume as in:
- Severe hemorrhage as in trauma or surgical operations.
- Extensive vascular exudation as in burns.
- Dehydration due to severe diarrhea, vomiting or sweating.
2. Cardiogenic shock:
Due to acute cardiac lesion causing sever fall in cardiac output:
- In extensive myocardial infarction.
- Hemopericardium.
- Rupture of valve cusp.
- Massive pulmonary embolism.
- Severe arrhythmias.
3. Septic (Endotoxic) shock:
It is caused by the effects of endotoxins released in the course of serious
bacterial infections. These endotoxins produce cell membrane injury,
endothelial damage and stimulate the release of chemical mediators such as
histamine, kinins and prostaglandins causing peripheral vasodilatation,
increased vascular permeability and disseminated intravascular coagulation
(DIC). Septic shock may complicate septicaemia, peritonitis, infected
operations and infected burns.
4.Nerogenic shock:
Due to anaesthesia and spinal cord injury causing peripheral vasodilation.
5. Other causes:
Poisons, anaphylaxins and perforated peptic ulcers.

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Post Mortem Picture of Shock: (Pathological Features of Shock):
- Congestion of viscera and edema of soft tissues.
- Petechiae in serous membranes.
- Depletion of lipids from suprarenal gland, and may be adrenal haemorrhage
(stress response).
- Degeneration and necrosis of parenchymatous organs.
- Kidney lesions may be extensive (acute tubular necrosis) and cause oliguria
and uraemia.
- The brain may show multiple infarctions.
- The lungs show diffuse alveolar damage leading to adult respiratory distress
syndromes.

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Chapter : Chapter :
ENVIRONMENTAL PATHOLOGY

1. Chemical Iniurv

Methyl alcohol: Is found in solvents, and paint. Its metabolites, formic acid and formaldehyde,
are toxic to the retina of the eye and nerve cells.

Insecticides: There are readily absorbed through the skin, respiratory tract and gastrointestinal
tract. They may cause CNS disturbances, muscle twitches, paralysis, cardiac arrhythmias,
impotence and infertility.

Carbon monoxide (CO): It prevents the hemoglobin from binding to the oxygen and causes
respiratory depression.

Lead: It may cause chronic nephritis, peripheral neuritis, cerebral edema and gingival lead line
formation.

2.Physical Iniurv

Frostbite: Exposure to severe cold causes arteriolar spasm and blood stasis. This causes
ischaemia and gangrene of the fingers, toes, nose and ear.

Heat stroke: Results from exposure to heat. It causes excessive sweating, generalized
vasodilatation, hypotension and hypoxia.

Electrical injury: It may cause:

Skin burns;

Injury to internal organs;

Bone fractures;

Rupture of small vessels with focal haemorrhage;

Sudden death.

3. Air Pollution

The inhalation of pollutants may cause:

Acute or chronic inflammation, e.g., chronic bronchitis.

Allergic and immunologic reactions, e.g, bronchial asthma.

Granulomatous reactions, e.g, pneumoconiosis.

Some malignant tumors, e.g., bronchogenic carcinoma.

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4.Cultural Factors

Tobacco smoking: Predisposes to:

Coronary atherosclerosis and ischemic heart diseases.

Chronic obstructive lung diseases.

Bronchogenic carcinoma.

Peptic ulcers.

Alcohol intake: Predisposes to:

Fatty change in the liver, alcoholic hepatitis and cirrhosis.

Cardiomyopathy and hypertension.

Acute gastritis, chronic gastritis and pancreatitis.

Testicular atrophy and infertility.

Peripheral neuropathy.

Carcinoma of the oral cavity, pharynx, esophagus and liver.

Street drugs:

Bango: May lead to:

Adverse behavior and psychological reactions.

Deterioration of pulmonary, reproductive and immunologic functions.

Cocaine: May lead to:

Euphoria.

Tachycardia, hypertension and arrhythmias.

Heroin: Addiction may result in:

Meningitis and brain infections.

Peripheral neuropathy.

Transmitted infections by infected needles may cause AIDS, hepatitis

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5- Vitamin Deficiencies

Vitamin D Deficiency

1. Rickets

Definition:

Metabolic disorder characterized by failure of deposition of calcium and phosphorus in the

osteoid tissue of newly formed bone (failure of mineralization of osteoid tissue to osseous
tissue).

• Pathological Features;

Skeletal Lesions:

Skull:

Delayed closure of fontanelles and sutures.

Delayed eruption of teeth.

Bossing of frontal and parietal eminences causing square shaped skull.

Craniotabes: thin and flat occiput.

Chest:

Rosary chest: beading of costo-chondral junctions.

Pigeon chest: flattening of sides of chest and prominence of sternum.

Harrison sulcus: horizontal groove in lower part of the chest.

Vertebrae:

Kyphosis, lordosis or scoliosis.

Long bones:

Rachitic metaphysic, bowing of bones and pathological fractures.

Pelvis: Trifoil shaped contracted pelvis.

Somatic lesions:

Hyperplasia of lymphoid tissues with enlarged spleen.

Weak and skeletal muscles especially abdominal muscles.

General Lesions:

Overweight due to limited movements.

Delayed sitting, standing and walking.

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Bulging abdomen due to weak muscles, and enlarged spleen.

2. Osteomalacia

Occurs in adults due to vit. D deficiency and lack of sun exposure mainly in females with repeated
pregnancy.

Bones become thin, and soft with associated lumbar lordosis.

Pelvis is trifoil in shape, and femur & tibia are bent anteriorly.

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Vitamin K Deficiency

Pathological Features;

Increased tendency to bleeding due to hypoprothrombinemia.

Petechiae, ecchymosis and hematoma following minor trauma.

Persistant bleeding after any wound.

Vitamin C Deficiency {Scurvy}

Pathological Features:

Failure of osteoiod tissue formation, with pathological fracture.

Delayed wound healing and defective granulation tissue formation.

Defective teeth formation.

Bleeding from gums, internal haemorrhages and anaemia.

Vitamin A Deficiency

Pathological Changes:

Night blindness: due to inadequate formation of visual purpule.

Eye dryness (Xerophthalmia): due to keratinization of lacrimal glands.

Keratomalacia: opacity of the cornea.

Hyperkeratosis of skin.

Squamous metaplasia of mucous membranes.

Retardation of growth in children.

Vitamin B Complex Deficiency

1. Beri-beri: Vitamin B1 (Thiamine) deficiency.

Features:

Nervous lesions (Dry beri-berif: Degeneration of myeline sheath and fragmentation of axons.

Cardiac lesions (Wet beri-beri): right side of heart becomes dilated and causing right sided heart
failure.

Pellagra: Nicotinic acid (Niacin) deficiency, common in maize eaters.

Features:

Skin lesions (Dermatitis).

Gastro-intestinal lesions (Diarrhea).

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Nervous lesions (Dementia).

Riboflavin deficiency: glossitis, keratitis, conjunctivitis and dermatitis.

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Vitamin B6 (Pvridoxine) deficiency: Glossitis, stomatitis & peripheral neuropathy.

Vitamin B12 (Cobalamin) deficiency: megaloblastic anemia.

Folic acid deficiency: megaloblastic anemia.

Vitamin E Deficiency

• Pathological Features:

Degeneration of the axons in posterior columns of spinal cord.

Muscle hypotonia, and weakness

May cause infertility.

HYPERVITAMINOSIS

Hvpervitaminosis A: Headache, nausea, vomiting, anorexia and weight loss.

Hvpervitaminosis D: hypercalcemia and metastatic calcification.

Hvpervitaminosis C: Uricosuria and increased iron absorption.

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