GENERAL CONCEPTS:

1. Health and Disease

Dorland’s Medical Dictionary and Definitions

1.1. Health – a normal condition of body and mind.

i.e. with all parts functioning normally.

1.2. Disease – any departure from a state of health. Specifically, a

definite morbid process having a characteristic
train of symptoms, affecting the whole body or any of its parts.

Recently, the World Health Organization came up with a more

comprehensive definition of health stating that it is a “State of
complete physical, mental, emotional, and social well-being and not
merely the absence of disease or infirmity”.

Our purpose in medicine is not only to cure disease but more

importantly in the maintenance of health.

2. Causes of Diseases

The following are some common causes (Etymology) that could

alter the normal physiology, biochemistry and anatomy of the body.

2.1. Developmental and Congenital (Genetics) – anatomical

anomalies and
abnormalities.

2.2. Physical Agents – ex. Burns, heat stroke, heat exhaustion etc.

2.3. Chemical Agents – Chemical burns, inflammation etc.

2.4. Trauma – fracture, wounds, etc.

2.5. Microorganisms:

Bacteria – Bacterial diseases

Virus – viral diseases like mumps, influenza etc.
Rickettsia – Rickettsial diseases
Parasites – worms, protozoans, etc.

2.6. Fungus – (mycoses) plant – candidiasis, tinea, etc.

2.7. Newgrowth (Tumors)

Benign – apt. Fibroma etc.
Malignant – (cancer-sarcoma,carcinoma etc.)

2.8. Degenerative – atherosclerosis, arteriosclerosis etc.

2.9. Metabolic – diabetes, etc.

 2.10. Endocrine – Addison’s disease, Hyperthyroidism etc.

2.11. Deficiency – Beri-beri, scurvy, Ricketts, etc.

2.12. Unknown causes – (idiopathic diseases)

2.13. Inatrogenic

3. Fundamental Pathologic Processes:

A superficial idea of common pathologic processes as well as

nomenclature are hereby given because of the most common
reference to such processes and terminologies during
clinicoanatomical correlation.

A. INFLAMMATION

a.1. Definition – the response of the body to tissue injury involving

neurologic, vascular, humoral and cellular reactions within the site
of injury (Jobbins).

a.2. Clinical Manifestations (Signs and Symptoms)

2.1. Systemic – like fever, listlessness, loss of appetite

(anorexia) and certain degree of debility. These symptoms are
attributable to the release of humoral agents like pyrogens,
toxins, etc.

2.2. Local (cardinal signs)

2.21. Dolor – Pain

2.22. Rubor – Reddening
2.23. Calor – Heat
2.24. Tumor – swelling
2.25. Functio-laesea – loss in function

a.3. Inflammatory changes and reactions (Boyd)

3.1. Vascular changes – once an injurious agent gains a foot-hold

in any part of the body there is a brief constriction of the
arterioles followed by dilatation, resulting in increased arterial
blood in the capillaries. About half an hour later this is
followed by slowing of the blood flow and the blood cells
acquire a particular stickiness and sluggishness resulting in
STASIS.

This is accompanied by increasing PERMEABILITY of the vessel

walls due to loosening of the cement substance resulting in
EXUDATION of plasma into the surrounding tissue – EDEMA.

This exudation serves two all important functions:

a) Carry immunological substances as AGGLUTININS and
GAMMA GLOBULINS to the site of the conflicts.
b) Fibrin – is formed which may limit the spread of infection
serving at the same time as the scaffolding or framework
for future repair.
 3.2. With the slowing of the blood flow, the leukocytes fall out into
the periphery of the stream by virtue of their stickiness and
that of the endothelial lining, adhering to this layer, a
phenomenon called PAVEMENTING of the leukocytes.

3.2.1. Because of the looseness of the cement

substance of the vascular endothelium, the leukocytes
are able to push their way by ameboid movements
between the lining cells Emigration of Leukocytes.

3.2.2. They then become extravascular and the first

line of defense against infection, the polymorphonuclear
leukocytes now being able to perform their phagocytic
functions.

3.3. The factors responsible for an alarm reaction resulting in

these vascular changes are:

3.3.1. Histamine like substance

3.3.2. Leucotaxine (Menkin)

3.4. The motive power responsible for the emigration of

leukocytes seems to be a lowering of the surface tension of
the side next to the vessel wall by some diffusible chemical
agent as a result of which the leukocytes are drawn through
the vessel wall (CHEMOTAXIS).

3.5. The above mechanisms results in the production of an

INFLAMMATORY EXUDATE (Boyd) – which consists of cells and
plasma, the proportion of which varies according to the nature
and intensity of the irritant. They are partly derived from the
blood, partly from the tissues.

4. The cells of the inflammatory exudates are the following:

4.1. Polymorphonuclear Leukocytes – those are the cells of acute

inflammation and the chief element of ordinary pus, therefore
they are sometimes called PUS CELLS. These cells are actively
phagocytic for bacteria and they form the first line of defense.
They disintegrate, liberating proteolytic ferments which
liquefy the dead tissue.

4.2. Eosinophils – playsan important role in allergic inflammations

and infestations with parasites. On breaking down, they
release histamine which increases capillary permeability.

4.3. Lymphocytes – are the cells of chronic inflammatory

processes and the late stage of acute inflammations. They are
derived from both the blood and the tissues. They have no
phagocytic power but they either produce or store antibodies.
They have the potential of developing into large phagocytic
macrophages.

4.4. Plasma Cells – polygonal cells with abundant cytoplasma and

one of lymphocytic origin – they secrete antibodies and are
seen in long continued infections with marked immunological
response e.g. Syphillis.
 4.5. Macrophage or histiocyte – an important cell in the
inflammatory exudates because of its great phagocytic power,
removing debris dead cells and other foreign matter. Being a
tissue dweller the name histiocyte is given.

5. The above-mentioned cells of the inflammatory exudates collect

around the irritant in order to have the opportunity to exercise
their function of phagocytosis which removes debris from the
body. To these cells may be added the large mononuclear
leukocytes of the blood, the endothelial cells lining and blood and
lymphatic vessels, serous membranes and the wandering tissue
cells. They all help in removing dead cells from the tissues.

6. Plasma forms an important constituent of the inflammatory exudates.

6.1. Normally, it passes from the capillaries into the tissue as

LYMPH, to be absorbed into the lymphatics. In accumulating in
the tissues, it brings with it antibodies such as agglutinins,
bacteriolysins and opsonins. The amount varies greatly,
depending mainly on the site of inflammation. It is especially
abundant in loose subcutaneous tissue and serous sacs, but
even in such organs as the appendix, it may produce wide
separations between muscle fibers – inflammatory edema. It
is the chief cause of swelling in inflammatory conditions, and
in subcutaneous locations, the edema produced may be
recognized by the phenomenon of “pitting on pressure”.

6.2. Fibrin is formed as a result of the union of Thrombin (liberated

from prothrombin) with the fibrinogen of the plasma, and
consists of fine threads which may become interlaced. It is
especially abundant in serious surfaces such as the
peritoneum or pleura, or in the pharynx. In the latter site, it
frequently binds together the necrosed epithelial cells forming
a false membrane which usually become firmly adherent to
the surface. It is only present in small amounts in deep
inflammations and is not found, in an abscess where it has
been digested by proteolytic ferments of the leukocytes and
bacteria.

7. Objectives of Inflammatory Processes:

The main objective is the localization and containment of

infection. As a general rule, the more intense the reaction, the more
likely is the localization of infection.

Factors to be considered:

7.1. Infection due to certain bacteria remained localized

i.e. Staphylococci

7.2. Certain organism produce substances like HYALURONIDASE or

the spreading factor.

7.3. Fibrin forms a network around the site of infection (Menkin)

 7.4. The degree of absorption of bacteria and toxins from
the tissues.

8. Classification of Inflammation (Robbins)

8.1. According to Duration

8.11. Acute
8.12. Chronic
8.13. Subacute

8.2. Based on the character of the exudates

8.21. Serous
8.22. Fibrinous
8.23. Suppurative (purulent)
8.24. Hemmorrhagic

8.3. Based on the causative agent

8.31. Pyogenic
8.32. Reaction to spreading infections
8.33. Reaction to salmonella organisms
8.34. Viral and ricketsial
8.35. Granulomatous
8.36. Immunologic

8.4. Based on location

8.41. Abscesses
8.42. Ulcers
8.43. Membranous and pseudomembranous
8.44. Catarrhal

9. Nomenclature:

As a general rule (with exceptions) the term for an

inflammation of a specific tissue or organ, is derived by naming the
tissue or organ and adding suffix “itis” e.g. peritoneum – peritonitis,
tissue – cellulitis, colon – colitis, kidney (nephron) – nephritis, etc.

10. DEFINITIONS – various lesions of Inflammations:

10.1. Abscess – localized inflammation or collection of pus

10.2. Ulcer – a local defect or excavation of the surface of on
organ or tissue which is produced by the sloughing off
(shedding) of inflammatory necrotic tissue.
10.3. Cellulitis – a non-circumscribed, spreading tissue
inflammation.
10.4. Phlegmonous inflammation (Phlegma – a flame) – denotes an
angry spreading type of infection.
10.5. Boil or furuncle – an abscess located in a hair follicle or
sebaceous gland.
10.6. Carbuncle – the bacterial penetration of the deeper layers of
the skin and subcutaneous tissues.
10.7. Fistula – a tubular passage of tract connecting the skin with
a mucous surface or one mucous surface with another.
10.8. Sinus – a tubular ulcer which refuses to heal usually due to
the presence of dead tissues and is lined by granulation
tissue.
 10.9.Septicemia, bacteremia, Pyemia – presence of bacteria,
toxins, septicemboli, in the blood.

E. REPAIR (lobbins) – comprises the replacement of dead or damaged

cells by healthy cells. In man, this replacement only occurs in very
limited conditions. Repair of injury usually takes the form of
connective tissue scarring. Such repair restores morphologic
continuity but it usually replaces the specialized functioning cells.

I. FORMS OF REPAIR

1. Parenchymal regeneration by the following:

1.1. Labila cells – epithelial cells, lymphoid and

hematopoietic cells that are continuously proliferating.

1.2. Stable cells – parenchymal cells, connective tissue cells,

muscle cells. These cells repress mitotic processes in
the quiescent cell. Some are capable of functional
reconstitution.

1.3. Permanent cells – highly specialized and cannot

undergo mitotic division in post-natal life e.g. neurons.

2. Repair by connective tissue:

2.1. Primary union – healing by first intention

2.2. Secondary union – healing by second intention

3. Regeneration with connective tissue scarring.

C. NEOPLASMS (TUMORS)

1. Definition : An abnormal tissue mass, the growth of which is

uncoordinated and exceeds that of normal tissue, persisting
in the same excessive manner after the cessation of the
stimuli which evoked the change.

2. Kinds of Tumors:

2.1. Benign (Innocent)

2.11. Characteristics: Usually localized, slow growing,

does not invade surrounding tissues because it is
usually capsulated. They do not spread
(Metasteses). Involves both epithelial and
connective tissues. When completely removed
they do not recur. Symptoms are usually due to
pressure on surrounding tissues or organs.

2.12. Nomenclature: with some exceptions this tumors

are named after the tissue affected adding the
suffix “OMA” i.e. Fibrous tissue – fibroma; Lipoid
tissues – lipoma; Bone tissue – osteoma etc.