1.

1 LEC: INTRODUCTION TO PATHOLOGY

HISTOPATHOLOGY I ADVANCE CLASS

BASIC HISTOLOGY INTRODUCTION TO GENERAL PATHOLOGY

 Histology – study of tissue and their structure  Pathology (pathos: suffering; logos: study)
o Study of diseases at cellular, tissue and organ
Group of cells that form during level
Germ layers embryonic development. The layers o Bridge between medicine and science; it is the
will eventually differentiate into scientific foundation of medicine
various tissues and organs.
forms the exoskeleton DIVISIONS OF PATHOLOGY
o Living cells (alveolar cell) Macroscopic
i Ectoderm o Thyroid cells I Gross Pathology examination of tissues
o Digestive cells (pancreatic and organs
cell) II Microscopic Pathology
develops into organ Surgical
o Cardiac muscle cells Anatomic Pathology Biopsy (living), autopsy
ii Mesoderm o Skeletal muscle cells (dead)  histopathology
o Tubule cells of the kidney Hematology
o RBC Microbiology
o Smooth muscle cells (in gut) Clinical Pathology Clinical Chemistry
forms the inner lining of the organ Immunology/ Serology
iii Endoderm o Skin cells of the epidermis Clinical Microscopy
o Neuron on brain Parasitology
o Pigment cells
 Rudolf Virchow – father of modern pathology
TYPES OF TISSUES  Hippocrates – father of medicine
Epithelial Covering epithelia: lines surfaces
Glandular epithelia: secrete substances
 Disease – any change from a state of health as a
Connective Most abundant; binds, protects, supports
result of certain forms of stimuli and stress, which
Main component: collagen leads to impaired physiological functioning
Muscular Highly specialized; movement
Main component: actin and myosin FOUR ASPECTS OF A DISEASE PROCESS
Nervous Sensation, integration, response Etiology Cause or origin of the disease; might
Main component: nerve and glial cells be genetic factors or acquired factors
Mechanisms of the development of
IMPORTANCE OF HISTOLOGY IN the disease
GENERAL PATHOLOGY Pathogenesis Sequence of events from initial
 Disease processes affect tissues in distinctive stimulus to ultimate expression of the
ways, which depend on the type of tissue, and the disease
disease itself. How etiologic factors trigger cellular &
 These processes may cause them to die, to molecular changes in a disease
change their shape, to divide, to move or to invade Morphologic Structural, biochemical and molecular
other tissues. Any of these changes also affect and Molecular alterations induced in the cells and
the anatomy of the tissue. Changes organs of the body as a result of the
 Understanding the changes that are disease
characteristic of a disease requires a detailed Clinical Functional consequence of the
knowledge of the normal histology of cells and Manifestations changes
tissues, and the range of normality. i Signs Effects that can be observed by
 Knowing the type of tissue and their composition is others
important in the selection of the appropriate ii Symptoms Effects apparent only to the patient
histopathologic technique and stain to be used.
 These changes within cells and tissues can be STAGES OF THE CELLULAR RESPONSE TO
visualized using histopathologic techniques. STRESS AND INJURIOUS STIMULI
1 Normal cells have defined structure and can perform
limited functions based on their specialization,
metabolism, and availability of metabolic substrates.
They can handle physiologic demands through
homeostasis.

Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease (10th ed.) 1

MATEO, J.R. E.
1.1 LEC: INTRODUCTION TO PATHOLOGY
HISTOPATHOLOGY I ADVANCE CLASS

Homeostasis – act of maintaining a steady state Always harmful for the Often beneficial, although
2 When there is a slightly severe stress, or some organisms abnormal activity may
pathologic stimuli, cells undergo adaptation in order cause disease
to survive and continue to function.
APOPTOSIS NECROSIS
Adaptation – reversible structural and functional Cell size Reduced Enlarged
response of cells to stress and stimuli Pyknosis (clumping)
3 But if the limits of adaptive response are exceeded, Fragmentation into  Karyorrhexis
or when cells are exposed to injurious stimuli (agents Nucleus nucleosome-size (fragmentation) 
or stress), or deprived of essential nutrients, cell fragments Karyolysis
injury occurs. (dissolution)
a. If the stimulus is mild and transient, the Plasma Intact Disrupted
injury is reversible. The cell may go back to membrane
its normal state. Cellular Intact Enzymatic digestion;
b. If it is severe and progressive, the injury is contents may leak out of cell
irreversible. Cells that undergo irreversible Cellular No (because Frequent (due to
injury will ultimately suffer cell death, which contents phagocytes rapidly leakage of cellular
may be pathological or physiological. devour the cells) contents)
Physiologic/ Physiologic Pathologic
OTHER TYPES OF STRESS CAN pathologic?
INDUCE RESPONSES Death by destiny Death by disease
Autophagy starved cells eat its own components
(self-eating) during nutrient deprivation INFLAMMATION
Intracellular accumulation of substances (such as  A protective universal response to tissue
proteins, lipids, hyaline, glycogen, pigments) damage (mechanical trauma, tissue necrosis,
Pathologic abnormal tissue deposition of calcium infection)
calcification salts  May be beneficial or harmful
Cellular aging progressive decline in the life span
and functional capacity of cells Functions:
 Contain damage and isolate injury
CELLULAR ADAPTATION  Destroy cause of injury (microorganism/toxins)
 Changes made by a cell in response to stress  Destroy resulting necrotic cells and tissues
or stimuli  Prepare tissue for healing and repair
 May be physiologic or pathologic
CARDINAL SIGNS
Hypertrophy Increased cell size  increased organ 1 Rubor redness
size 2 Calor heat
Hyperplasia Increased cell number  increased 3 Tumor swelling
organ mass 4 Dolor pain
Atrophy Decreased cell size and number  5 Functio laesa loss of function
reduce tissue/ organ size
Metaplasia Change in one cell type to another ABNORMALITIES IN CELL GROWTH
Dysplasia Abnormality of cell development Retrogressive changes – organs are smaller than the
normal
CELL DEATH i Developmental Defects
 Occurs after irreversible injury Aplasia incomplete development of the
organ
NECROSIS APOPTOSIS Hypoplasia failure of an organ to develop fully
Premature cell death Program cell death Agenesia complete non-appearance of an
A pathologic process organ
caused by external A naturally occurring Atresia failure of an organ to form an
agents like toxins, trauma, physiologic process opening
etc. ii Atrophy acquired decrease of the size of a
Phagocytized by Phagocytized by normally developed organ
phagocytes phagocytes or adjacent Progressive changes – organs become larger than
cells normal
i Hypertrophy increase of cell size
ii Hyperplasia increase in cell population

Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease (10th ed.) 2

MATEO, J.R. E.
1.1 LEC: INTRODUCTION TO PATHOLOGY
HISTOPATHOLOGY I ADVANCE CLASS

Degenerative changes – changes in the adult form of life; absence of respiratory sounds
cell and movements is indicative
means “disordered growth”; loss of coordination and reflexes;
i Dysplasia development of abnormal cell types 3 CNS failure absence of brain stem reflex, and/or
within a tissue (reversible) electroencephalogram (EEG) activity
replacement of one cell type of cells is indicative
ii Metaplasia to another type in the same site
(reversible) SECONDARY CHANGES OF DEATH
iii Anaplasia lack of differentiation of cells 1 Algor Mortis
(irreversible) Cooling of the body; decrease in temperature
means “new growth”; uncontrolled Equalizing of the body temperature to the external
iv Neoplasia proliferation of cells with no purpose; temp
due to carcinogens, or DNA Normal rate of cooling: 7F/hr
alteration (irreversible) Sped up by: cold environment,
malnutrition/dehydration, severe hemorrhage
 Tumor/ neoplasms – mass of neoplastic cells Slowed by: fever, extreme physical activity before
death
General Characteristics of Tumors: 2 Rigor Mortis
 May resemble and function like a normal cell Stiffening of muscles due to lack of ATP (ATP is
 Autonomous; non-responsive to normal growth responsible for driving calcium ions back to
factors sarcoplasmic reticulum of muscles)
 Parasitic nature; competes with cells for metabolic First appears in the involuntary muscles of heart
needs Observed in eyelids, followed by neck, then lower
extremities
PARTS OF TUMOR Starts 2-3 hrs post-mortem, completes 6-12 hrs
Parenchyma actively dividing cells postmortem; persists for 3-4 days
Stroma connective tissue framework and After 3 to 4 days, relaxation occurs due to breakdown
lymphatic and vascular channels of contracted muscles
Factors: muscle activity by the time of death;
CLASSIFICATION OF TUMOR Sped up by: warm environment; infancy; thin-layered
BENIGN MALIGNANT muscles
Usually does not Slowed by: cold environment; obese people
Death cause death Usually causes 3 Livor Mortis/ Suggillation
except for infants death Purplish discoloration of skin due to blood stasis
and brain tumors Lividity of the dependent portions of the body due to
Differentiation Well- Some lack of settling of blood to the lowest parts of the body at the
differentiated differentiation time of death
Usually Blood vessels dilate due to loss of muscle tone
Rate of progressive and Erratic; may be
Growth slow; may come slow to rapid Livor Mortis Ecchymosis
to a standstill or Cause Post-mortem Trauma
regress stasis of blood
Metastasis After
(spread of Absent Frequent application Discoloration No
tumor to of pressure disappears disappearance
other sites) (Blanching
test)
SOMATIC DEATH After No No oozing
 Refers to the complete cessation of metabolic incision disappearance
and functional abilities of an organism

PRIMARY CHANGES DURING DEATH

start of death when cardiac
1 Circulatory function ceases; flat
failure electrocardiogram (ECG), and/or
absence of heartbeat is indicative
2 Respiratory decrease O2 and increase CO2;
failure loss of all processes necessary for

Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease (10th ed.) 3

MATEO, J.R. E.
1.1 LEC: INTRODUCTION TO PATHOLOGY
HISTOPATHOLOGY I ADVANCE CLASS

4 Post-mortem Clotting
Occurs immediately after death; apparent only in
autopsy

Post-Mortem Ante-Mortem
Clot Clot
Upper layer is
clear (chicken
Appearance fat); RBC Has tangled,
settles at the irregular fibrin
lowest part of
the blood vessel
(currant jelly)
Assumes blood Seldom
Shape vessel shape assumes blood
vessel shape
Consistency Rubbery Non-rubbery

The next 3 stages of death occur simultaneously and

leads to the total digestion of cells:
5 Dessication
General drying and wrinkling of fluid-filled
organs;
Most evident in the cornea, and anterior chamber of
eye
6 Putrefaction
Decomposition of body carried out by microbial
action (normal flora from gut migrates to blood
vessels and spreads all over the body)
Principal agent: Clostridium welchii (gram-positive,
anaerobic, rod-shaped)
First external sign: greenish discoloration of skin
over the right iliac fossa due to bacterial hydrogen
sulfide reacting with hemoglobin, thus forming
sulphahemoglobin which stains the area green
Eventual production of foul-smelling gas due to
invasion of saprophytes, which leads to distension of
abdomen, swelling of face and genitalia, and
liquefaction of internal organs
Most resistant to putrefaction: prostate gland
7 Autolysis
“Self-destruction”; the self-digestion of the cells by
their own enzymes;
First external sign is the whitish appearance of
cornea

Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Robbins and Cotran pathologic basis of disease (10th ed.) 4

MATEO, J.R. E.