The document discusses general pathology, aiming to provide students with an in-depth understanding of disease mechanisms, including etiology, pathogenesis, morphological changes, and clinical manifestations. It outlines the importance of studying pathology and describes various types of cellular adaptations and injuries, leading to cell death through necrosis or apoptosis. Furthermore, it highlights the evolution of pathology and its diverse branches, including systemic and histopathology, contributing to clinical practice and patient care.

2. Unit I- General pathology

3. GENERAL OBJECTIVE
• At the end of the class the students will be able to gain in-depth understanding
about General Pathology and will be able to apply this knowledge in clinical
practice.

4. SPECIFIC OBJECTIVES
At the end of the class the students will be able to,
• Explain the basic concept of pathology
• Describe the Cellular & tissue changes.
• Describe the Infiltration and regeneration
• Elaborate the inflammation and infection

5. CONCEPT OF PATHOLOGY

6. IMPORTANCE OF STUDY OF PATHOLOGY
PATHOLOGY
PATHOS LOGOS DISEASE
(In Greek word)-
harm/
feeling/suffering
(disease)
Study
Dis + ease
(discomfort)- it is loss
of ease to the body

7. INTRODUCTION
• Thus pathology is a branch of biological sciences that deals with the study of all
structural and functional abnormalities (at the level of cells, tissues, organs and
body fluids) that take place as a result of a disease.
• Study of pathology began with Hippocrates (Greece) 460-377 B.C (The father of
Medicine) He Started the study of patient symptoms as method of diagnosis, & he
also dissociated disease from religious believes.

8. Pathology addresses 4 components of
diseaseomponents of disease:
PATHOGENESIS –
MECHANISMS OF
DEVELOPMENT
ETIOLOGY-
CAUSE
MORPHOLOGI
C CHANGES-
STRUCTURAL
ALTERATIONS
OF CELLS
CLINICAL
MANIFESTATIONS
- THE
CONSEQUENCES
OF CHANGES

9. Etiology of a disease means the cause of the disease.
• If the cause of a disease is known it is called primary
etiology.
• If the cause of a disease is unknown it is called
idiopathic.
There are two major classes of etiologic factors:
• Genetic
• Acquired (infectious, nutritional, chemical, physical
etc.)
1. Etiology

10. 2. Pathogenesis
• Means the mechanism through which the cause operates to produce the pathological
& clinical manifestations.
• The pathogenetic mechanisms could take place in the latent or incubation period.
Pathogenesis leads to morphologic changes.

11. Refer to the structural alterations in cells or tissues that occur following the
pathogenetic mechanisms.
The structural changes in the organ can not be seen with the naked eye or they may only
be seen under the microscope.
• Those changes that can be seen with the naked eye are called gross morphologic
changes (G/A- gross appearance ).
• Those that are seen under the microscope are called microscopic changes. (M/E-
microscopically examination.
• In addition, the morphologic changes will lead to functional alteration & to the
clinical signs & symptoms of the disease.
3. Morphological Changes

12. • The morphologic changes in the organ affect the normal function of the organ.by doing
so, they determine the clinical features (symptoms & sign), course and prognosis of
the disease.
4.The Consequences Of Changes

13. In summary, pathology studies:-
• Etiology > pathogenesis> morphologic changes > clinical features & prognosis of
all diseases.
• Understanding of the above core aspects of disease that is understanding
pathology will help one to understand how the clinical features of different
diseases occur & how their treatment work. This understanding will, in turn,
enable health care workers to handle & help their patients in a better & scientific
way.

14. HuPathology
1.General
pathology- it deals
with the general
principles of disease
2. Systemic pathology – it
deals with study of disease
pertaining to the specific
organs & body system.
3. Histopathology -(anatomic
pathology) surgical pathology
(biopsy), forensic pathology
(autopsy)- cytopathology.
4. Hematology-
deals with disease
of blood.
5. Chemical Pathology –
Analysis of biochemical
constituents of blood urine,
semen, CSF etc.
6. Immunology- detection of
abnormalities in the immune
system of the body e.g
autoimmune disorders.
7. Experimental Pathology- it is
production of disease in the
experimental animal & its study
8. Geographic pathology- deals
with study of frequency & type
of diseases in populations of
different parts of the world.
9. Medical genetics-
relationship between heredity
& disease e.g. inborn errors of
metabolism , chromosomal
aberration's etc.
10. Molecular pathology-
the detection &
abnormalities at the level
of DNA of the cells.

15. Definition of terms
• Etiology – cause of disease.
• Pathogenesis – Evolution of disease.
• Symptoms – felt by patient
• Signs- discovered by clinician.
• Diagnosis investigation & identifying disease.
• Prognosis – prediction of outcome of disease & course of a disease.
• Pus – liquid material contains broken down leukocytes & cells.
• Serous – relating to, containing, or producing serum or a substance having a
watery consistency.

16. • Oma – tumor e.g Sarcoma.
• Aemia – of the blood e.g anaemia , hypovolaemia.
• Ema – swelling e.g oedema.
• Polyp – any mass of tissue that bulges or projects outward or upward from the
normal surface level.
• Penia – decreased e.g. thrombocytopenia.
• Peri – around e.g peri bronchial.

17. Evolution of pathology
• Era of religious beliefs (1500 A.D)the practice of medicine began with
Hippocrates (460-377 BC) he first stressed study of patients symptoms and
described methods of diagnosis, according to him disturbances in equilibrium of
the body resulted in and illness.
• Era of gross pathology (A.D 1500 to 1800)
• Cellular pathology (AD 1800-1950)
• Modern pathology (1950- 21st century)

18. CELLULAR & TISSUE
CHANGES

19. • CELL: - The Cells From The Basic
Structural And Functional Unit Of A
Tissue/Organ. There Are About 210
Distinct Human Cell Types, There Are
Between 50 And 75 Trillion Cells In The
Human Body.

20. Cell injury and cell death
A cell is injured or damaged when it fails to adopt to the exposed damaging agents.
The cell injury may be caused by:
1. Infection agents, such as
• Viruses
• Bacteria
• Fungi
• Parasites
2. Hypoxia or deficiency of oxygen, e.g. cardiorespiratory failure.
3. Ischemia is loss of blood supply due to arterial or venous block e.g myocardial
infarction, gangrene of intestine.

21. 4.Physical injury e.g. Burn, Trauma, severe
cold, radiation.
5. Chemical injury e.g. Poisoning.
6. Drug injury e.g. Drug toxicity.
7. Immunologic injury e.g. anaphylactic
reaction.
8. Nutritional injury

22. Cellular reactions to injury:-
Cell injury underlies all diseases. So to understanding diseases one has to start by
knowing what cell injury is when a cell is exposed to an injurious agent. The
possible outcomes are:
1. The cell may adapt to the situation
2. The cell may acquire a reversible injury.
3. The cell may obtain an irreversible injury & may die. The cell may die via one
of two ways either by necrosis or by apoptosis

23. Mechanism of cellular injury

24. 1.Cellular adaptations:-
Different types of cellular adaptations are:
1.Hyperplasia
2.Hypertrophy
3.Atrophy
4. Metaplasia
• These cellular adaptations are reversible & the cell will return to normal state
when the stress is removed.

25. 1.Hyperplasia
• It is defined as increase in the number of cells in an organ/ tissue capable of
replication. Which in turn leads to increased volume of the organ.
Types:-
Physiologic Hyperplasia:-
• 1. Hormonal Hyperplasia- e.g. proliferation of glandular epithelium of female
breast during puberty/pregnancy.
• 2. Compensatory Hyperplasia – e.g. Regeneration of liver following
hepatectomy

26. Pathologic Hyperplasia:-
• Usually occurs due to excessive hormonal or growth factors stimulation.
• 1. Due to imbalance between estrogen & progesterone includes hyperplasia of the
endometrial tissue, resulting in abnormal menstrual bleeding, this patients are at
increased risk of endometrial cancer & with HPV (human papillomavirus)
infection leads to cervical cancer.
• 2. Hormone induced hyperplasia of prostate.

27. 2.Hypertrophy
• It is defined as increases in the size of the cells leads to increases in size of the
organ. In contrast to hyperplasia, there are no new cells but the existing cell
becomes larger due to increased amount of structural protein & organelles or
excessive secretion of growth factors. Hypertrophy usually occurs in non-dividing
cells
Types:-
Physiologic Hypertrophy:
• 1. Hypertrophy of the muscles due to exercise/workload.
• 2. Hypertrophy of uterus in pregnancy due to oestrogen stimulated smooth muscle
hypertrophy.
Pathologic Hypertrophy
• The enlargement of the left ventricle in hypertensive heart disease (LVH-left
ventricular hypertrophy. & aortic valve heart diseases.

29. 3.Atrophy
• It is defined as shrinkage in the size of the cell, by loss of cell substance.
• An atrophic cell has diminished function but they are not dead.
• Main mechanism of atrophy it is due to excessive degradation of structural
proteins or an imbalance between the protein synthesis & degradation.
Types:-
Physiologic Atrophy:
• Ageing, after menopause, atrophy of brain in aging.

30. Pathologic Atrophy:-
• DISUSE ATROPHY (decreased work load e.g. wasting of muscle of limb
immobilized in plaster cast.
• NEUROPATHIC ATROPHY (loss of nerve supply), poliomyelitis.
• ISCHEMIC ATROPHY loss of blood supply atrophy of brain due to cerebral
atherosclerosis.
• STARVATION ATROPHY inadequate nutrition protein energy malnutrition
• ENDOCRINE ATROPHY loss of endocrine stimuli atrophy of uterus, ovaries,
testis.
• PRESSURE ATROPHY prolonged pressure from tumours cause compression &
atrophy of tissues ex. Erosion of skull by meningioma arising from pia arachnoid.
• IDIOPATHIC ATROPHY

31. 4. Metaplasia
• Meta – transformation & plasia- growth
• It is defined as a reversible change of one type of epithelium into another.
Types:-
• SQUAMOUS METAPLASIA:-Change of columnar epithelium to squamous
epithelium.
• COLUMNAR METAPLASIA:-Change of squamous to columnar epithelium.
• The main mechanism is genetic reprogramming of the stem cells, this occurs due
to withstand the stress to which the cell is exposed, but metaplasia is reversible on
the withdrawal of stimulus
Cartilaginous Metaplasia: Ex. Take place in healing of fractures.
• REVERSIBLE CELL INJURY when the cells are subjected to severe stress , they
fail to undergo adaptation process, then cell injury occurs, there are two phases in
cell injury-initial reversible phase & final irreversible phase (cell death)

33. 2.Morphological patterns of reversible cell injury
• Cellular swelling: This occurs due to the loss of maintenance of the fluid and ionic
balance as a result of the defective functioning of the Na/k.
• Fatty change: This is accumulation of triglycerides inside parenchymal cells. It is
caused by an imbalance between the uptake, utilization & section of fat. Fatty
change is usually seen in the liver, heart or kidney.

34. 3.Morphological of irreversible cell injury (cell death)
• Irreversible cell injury leads to cell death, the major from of cell death occurs by
necrosis.
• Necrosis it is defined as focal tissue death along with degradation of tissue, mostly
induced by degradative action of the enzymes on the injured cell.
• The enzymes may be released from the same cell (autolysis) or from the adjacent
cells & inflammatory cells (heterolysis).
• Necrosis (greek meaning dead the stage of dying, the act of killing)

35. Cell damage: necrosis, apoptosis, General
Death
• Necrosis (from the Greek. Nekros - dead). It’s death of cells and tissues in living
organism. Necrosis may be in one cell, a group of cells, part of the body or organ.

36. Stages:-
1 - Preneсrosis or paranecrosis
2 - Necrobiosis
3 - Actually necrosis
4 - Autolysis
• Preneсrosis or paranecrosis- changes similar to necrotic, but reverse
• Necrobiosis-profound degenerative changes, in which the prevailing catabolic
over anabolic changes.
• Actually necrosis –cell death when the time of death cannot be established.

38. Classification of necrosis

39. Types of necrosis
1. Coagulative necrosis.
2. Liquefactive necrosis.
3. Caseous necrosis.
4. Fat necrosis.
5. Fibroid necrosis.
6. Gangrenous necrosis.

40. Coagulative necrosis
• Coagulative necrosis commonest type and is ischemic. It may happen in heart,
kidney, or adrenal organs and is firm in texture. In coagulative rot, engineering of
dead tissue is protected for a few days. It may happen due to denaturation of
proteins including enzymes.
• Gross Features: The necrosis area is swollen, firm and pale.

41. Liquefactive Necrosis
• Necrosis of big tissue with super included festering, with dark, foul-smelling
appearance is known as Liquefactive rot (dark or green color is due to breakdown
of hemoglobin).
• Gross Features: Soft and liquid.

42. Caseous necrosis
• It is cheese-like, as in tuberculosis. Granuloma is shaped with central cheesy
material rimmed by epitheloid cells & giant cells (outside body monster
cells/Langhan monster cells). Tuberculosis coagulative rot is altered by capsule of
lipopolysaccharide of Tb bacilli.
• Gross Features: Soft, granular, and friable as cream -cheesy appearance.

43. Fat necrosis
• In fat necrosis, there's central area of fat destruction (pancreatic lipase process cell
film & shape greasy corrosive + calcium white deposits).
• Gross Features: Opaque and chalky.

44. Fibroid necrosis
• Usually not a true degeneration but a unequivocally eosinophilic recolor like
fibrin.
• Location: interstitial collagen and blood vessels (small artery and arteriole)
• Nature: one kind of necrosis.
• Example : In allergic receptive infections: active rheumatism
• Gas gangrene Gas is created in necrotic tissue by anaerobic microbes, clostridium
perfringes.

45. • Conditions: profound sullied wounds in which there's impressive muscle harm by
gas shaping bacteria.
• Character: swollen clearly, gas bubbles arrangement. The contamination rapidly
spreads and there's associated extreme toxaemia. Only occasionally in civilian
practice but could be a genuine complication of war wounds.

46. Gangrenous necrosis
Wet gangrene Coagulative necrosis by ischemia + Liquefactive corruption by
superimposed infection.
• Conditions: Both blood vessel and venous hindrance; wet in environment;
• Character: damp, swollen, foul-smelling, dark or green.

47. Dry gangrene drying of dead tissue related with fringe vascular maladies.
• Necrosis is isolated from reasonable tissue by line of demarcation.
• Conditions: as it were happens on the skin surface taking after blood vessel
obstacle. It is especially at risk to influence the appendages, particularly the toes

49. Apoptosis
• Apoptosis is the process of programmed cell death (PCD).apoptosis is a
genetically programmed self-destruction (death) activated by various causes.
• It is a type of coordinated & internally programmed cell death in which the cells
are destined to die.
• Active & energy-dependent, reduced (shrinkage).

50. Pathogenesis:-
• Apoptosis is a multistep process triggered by the withdrawal of growth factors,
hormones, or due to toxin, free radical injury, etc. This may lead to the activation
of caspases. The activated caspases cause breakdown of its own nuclear DNA &
cytoplasmic proteins.