INTRODUCTION TO

PATHOLOGY
Dr. Michael P. Custodio
(IIIMMM BBBAAACCCKKK!!!)
MISSED YOU PEOPLE SO MUCH

The study of the origin and development of

a disease
Pathologists investigate etiology and
pathogenesis
By way of morphology (morphe = form)
Using techniques of histology (histo = tissue)
as well as biochemistry and molecular biology
With goal of easing clinical signs and
symptoms
Where the clinician begins

Language
Pathos = suffering, feeling
Logus = study
Genesis = origin, birth, development
Eti from aeiti = cause
Medical terms are compounded from
prefixes, roots, and suffixes that are
frequently Greek or Latin

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What is pathology?

Study of diseases that can cause abnormalities

in the structure or function of various organ
systems
Pattern of body response to injury
Disease may reflect alterations in cell
growth as in tumors, iatrogenic (caused by
physicians and their treatment or even idiopathic

Start with cellular alterations

Rudolf Virchow, the father of modern
pathology, pioneered the use of microscopes
in modern (mid 1800s) medical education
Omnis cellula e cellula every living cell
arises from a prexisting living cell
One of the pioneers of The Biogenesis Theory
Disease caused by patterns of injuries
(lesions) to cells, extracellular matrix, tissue,
organ, person

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What is acute inflammation?

It is the initial response of the body to local
injury
Examples are blunt, penetrating, trauma,
infectious organism or irritating chemical
substances

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Events in acute inflammation

Earliest response- dilation of arterioles, venules

and capillaries leading to increased bloodflow
in and around injured site
1. Alteration in blood flow and vascular
permeability
2. WBC migrates to injured site
3. Phagocytosis and enzymatic digestion of dead
cells
4. Repair of injury by regeneration

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Hyperemia produces heat and redness

due to increased blood flow
EXUDATE

TRANSUDATE

Protein rich

Protein poor

Produces swelling
associated with
inflammation and puts
pressure on sensitive
nerve endings resulting
to pain

Seen in pulmonary
edema

 In cases of Pneumococcal pneumonia, lesion is

repaired by normal anatomy and function of
tissue is restored
In post myocardial infarction, tissues are not
normally restored instead are replaced by
granulation tissues and finally a scar
Keloids are accumulation of excessive amounts
of collagen resulting in a protruding tumorlike
lesion
In cases of liver injuries due to alcoholism, the
liver regenerate and scar formation is observed
wherein irregular lobules of regenerated liver
cells are surrounded by bonds of scar

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5 CLINICAL SIGNS OF ACUTE INFLAMMATION

1. Calor heat
2. Rubor redness
due to increased blood flow
3. Tumor swelling
4. Dolor pain
result of an exudate causing increase in
interstitial fluid and pressure on nerve
5. Functio laesa loss of function

endings

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Systemic manifestations of acute inflammation

FEVER associated with the spread of

microorganisms into the bloodstream
Leukocytosis increase in circulating WBC
Some bacteria induce inflammation by releasing toxins
that damage tissues. ( Staphylococci and Streptococci )
TERMS REFERRING TO INFLAMMATION
1. Pyogenic produces thick yellow fluid containing dead
WBC, inflammatory exudate and bacteria
2. Suppurative inflammation associated with large
production of pus
3. Abscess when implanted beneath the skin or solid
organ/ localized collection of pus

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4. Bacteremia capable of invading blood vessels

and involving other tissues or organs
5. Granulomatous - distinct pattern of inflammation
seen in TB, syphillis and sarcoidosis
- localized area of chronic
inflammation often with central necrosis
- characterized by accumulation of
macrophages that fuse to form giant cells

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edema
Accumulation of abnormal amounts of fluid in
the intercellular spaces or body cavities
Classified either as localized, inflammatory
reaction or generalized,as in pronounced
swelling of the subcutaneous tissues
throughout the body (anasarca)
localized as those from inflammation with the
escape of protein rich intravascular fluid to
intravascular tissue or obstruction to lymphatic
drainage caused by a parasitic worm

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generalized as seen in patients with CHF,

liver cirrhosis, and renal diseases
prominent on dependent parts of the body
due to gravity such as ambulatory patients
tend to develop edema around ankles and
lower leg while bed ridden patients develop
edema in the back and sacral areas including
the lungs.

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Ischemia interference with blood supply of

an organ thus cells and tissues are deprived
of oxygen and nutrients
Causes:
1. narrowing of arterial structures like
atherosclerosis
2. thrombotic or embolic occlusion
Major determinant: availability of alternative or
newly acquired route of blood supply
(collateral vessels)

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Other determinants:
1. rate of development of occlusion
2. vulneribility of a tissue to hypoxia
3. oxygen carrying capacity of blood
Ganglion cells of the nervous system and
myocardial muscles undergo irreversible
damage if deprived of blood supply for 3 to 5
mins

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Infarct localized area of ischemic necrosis

within a tissue or organ produced by
occlusion of either an arterial supply or a
venous drainage
Common forms are myocardial and
pulmonary
- Frequently caused by thrombotic or embolic
occlusion
- Infrequent causes include twisting of an
organ, compression of a blood supply in a
loop of bowel or hernial sac or trapping of a
viscus under a peritoneal adhesion

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Gangrene necrosis of toes or a large

segment of the foot due to arterial
disease of
lower extremities
Hemorrhage rupture of a blood vessel
Caused by trauma, atherosclerosis,
inflammation or neoplastic erosion of a
vessel wall
Hematoma accumulation of blood
externally so that blood is trapped within the
body tissues
HEMOTHORAX

HEMARTHROSIS

HEMOPERICARDIUM
HEMOPERITONEUM

HEMANGITIS

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Forms of hematoma:
petechia minimal hemorrhages in the skin
purpura slightly larger than a petechia
ecchymosis large subcutaneous hematoma
- also known as a bruise
- about 1 to 2 cm
Significance of a hemorrhage:
1. volume of blood loss
2. rate of loss
3. site of hemorrhage
* large amounts of blood loss will result in
chronic loss of iron

 Hypertrophy

Adaptive responses

hyper = above, more

trophe = nourishment, food

Hyperplasia
plastein = to form, shape, growth,
development

Dysplasia
dys = bad or disordered

Metaplasia
meta = change or beyond

Hypoplasia
hypo = below, less

Atrophy, Aplasia, Agenesis

a = without
nourishment, form, begining

Altered demand (muscle

activity)
Altered stimulation (growth
factors, hormones)
Altered nutrition (including
gas exchange)

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Types of atrophy:
1. disuse atrophy- immobilization of a
limb using a plaster cast
2. pathologic or irreversible atrophy
loss of innervation, hormonal
stimulation or decreased blood
supply
- stenosis of the renal artery may
cause atrophy of the kidneys,
shrinkage of nephrons and loss of
interstitial tissue

Alterations in cell growth/

Physiological hypertrophynormal

Physiological hypertrophynormal?

Normal

Abnormal

Hypertrophy resulting from

pathological injury (hypertension)

infarction scars

Mechanisms of muscle hypertrophy

Increased protein synthesis
increased cell size
increased organ size
Nondividing cells produce
more protein and membrane
without division
Mechanosensors, PI3K /Akt
signaling pathway important
in exercise-induced growth
Growth factors, vasoactive
agents, hormones mediate
stress-induced response
Unrelieved stress eventually
results in irreversible injury

*. Dysplasia: disordered pattern of growth

: premalignant

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Differences between hypertrophy and

hyperplasia

HYPERTROPHY
Seen in cells that cannot
multiply like myocardial,
striated and peripheral
muscles
ex. Loss of a kidney will
hypertrophy the other in order
to compensate for the loss
and continue adequate renal
function

HYPERPLASIA
ex. Proliferation of
granulation tissue in their
repair after an injury
increased cellularity of the
bone marrow in patients with
hemolytic anemia
enlargement of the
adrenal cortex due to
increased ACTH secretion
enlargement of the thyroid
gland due to increased
thyrotrophic hormone

Physiological, hormonal
hyperplasia

Thyroid hyperplasianodular goiter

Prostate normal vs. hyperplasia

Epithelial dysplasia

This is cellular dysplasia in the uterine cervix. The normal

cervical squamous epithelium has become transformed to a
more disorderly growth pattern, or dysplastic epithelium. This is
farther down the road toward neoplasia, but dysplasia is still a
potentially reversible process.

Skin dysplasiaactinic keratosis

Dysplasia

Metaplasia respiratory epithelium

Metaplasia of laryngeal respiratory epithelium has occurred

here in a smoker. The chronic irritation has led to an
exchanging of one type of epithelium (the normal respiratory
epithelium at the right) for another (the more resilient
squamous epithelium at the left). Metaplasia is not a normal
physiologic process and may be the first step toward neoplasia

Metaplasia of esophageal epithelium

Glandular, or Barretts,metaplasia of the normal esophageal

squamous mucosa has occurred here, with the appearance
of gastric type columnar mucosa, secondary to gastric
reflux.