GENERAL &

SYSTEMIC PATHOLOGY
o Explains the occurrence of Cardiovascular
P.02 CELLULAR ADAPTATION, CELL INJURY Diseases (CVD’s): Heart attack and/or stroke
AND CELL DEATH (PART 1) o Blocked or decreased blood flow to a tissue/
Dr. Ayochok | August 8, 2017 organ
o Cells deprived of oxygen and nutrients
- Can HYPOXIA occur without ISCHEMIA?
TOPIC OUTLINE YES
I. Pathology: Definition
- Can HYPOXIA occur with ISCHEMIA?
II. Divisions of Pathology
YES
III. Core of Pathology
IV. Cellular Adaptations of Growth and  INADEQUATE SUPPLY OF OXYGEN
Differentiation o Also known as as HYPOXIA which is the
eventual result of ischemia
I. PATHOLOGY o Anoxia – total lack of oxygen
o May occur without ischemia
 Literally means “Study of suffering” o Most commonly seen in the following:
o (from logos meaning study and pathos  Drowning
meaning suffering)  Damaged red cells
 Bridge between basic science and clinical practice
 It is divided into TWO DIVISIONS:  PHYSICAL AGENTS
o Radiant energy (x-ray, sunlight)
o GENERAL PATHOLOGY
o Extremes of temperature: too hot or too cold
o SPECIAL OR SYSTEMIC PATHOLOGY
o Electrical energy
o Trauma
II. DIVISIONS OF PATHOLOGY
 CHEMICAL AGENTS
 GENERAL PATHOLOGY
o Could be external and internal chemicals
o Basic reaction of cells and tissues to
o EXOGENOUS: introduced into the body
abnormal stimuli that underlie disease
through ingestion, inhalation, injection
o Study of how tissues react to any injurious
o ENDOGENOUS: from uncontrolled cellular
stimuli in any part of the body
metabolism
o More complex because it deals with “how”
 Waste products
and its approach is on a molecular level
 BIOLOGIC AGENTS
 SYSTEMIC PATHOLOGY o Viruses
o aka Special Pathology o Bacteria
o Specific responses of organs and tissues in a o Fungi
more or less WELL DEFINED STRUCTURE o Rickettsia
(e.g. body systems) in the presence of an o Protozoans
injurious stimuli o Helminths

III. CORE OF PATHOLOGY  IMMUNE REACTIONS

o Normally helpful in fighting infectious agents
A. ETIOLOGY attacking a person BUT could also harm the
o Refers to the CAUSE of the disease body into two ways:
o 2 major classes  Hypersensitivity reactions:
 Intrinsic or genetic overreacting immune system
 Meaning you were born with the  Autoimmune disorders: Antibody
cause ( like a defective gene) against one’s own

 DEFECTIVE GENES
 Acquired
o Abnormal accumulation of glycogen in cells
 Factors present in the environment
o Absence of enzyme that releases glucose
which could present as an injurious
from glycogen resulting to a disease called
stimuli.
glycogenosis
 eg chemical, mechanical, infectious)
o Missing gene carrying the code for Glucose-
A.1 GENERAL ETIOLOGY OF CELLULAR DAMAGE 6-phosphatase

 ISCHEMIA  INCREASED WORKLOAD ON CELL

o Deficient/ lack BLOOD FLOW OR BLOOD o Elevation in body temperature in
SUPPLY o Exercise

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 GENERAL &
SYSTEMIC
 Too much exercise can cause
damage to skeletal muscle cells
o Increase hormone secretion
 Like in hyperthyroidism
 AGING
o Less adaptable
o More prone to injury and death
 Due to the loss of the body’s
DEFENSE SYSTEM as a person
ages.
 LACK OF ESSENTIAL NUTRIENTS
Scurvy
o 
 Lack of Vitamin C
 Inadequate production of collagen
 Collagen is needed in
tissue repair. Inadequacy
therefore results to scurvy
B. PATHOGENESIS
o Refers to the MECHANISM/S of
DEVELOPMENT of the disease from the
time of exposure to the cause (genetic or
acquired) up until the time where the
disease expressed itself in the form of
symptoms.
o From the initial stimulus up to the
expression of the disease
o Tries to answer the questions “WHAT
HAPPENED” or “HOW DID THE
DISEASE HAPPEN?”
B.1 GENERAL PATHOGENESIS OF CELL DAMAGE
 DAMAGE TO CELL MEMBRANE
o Destructive material leak from organelles to
cytoplasm
o Unwanted substances cross the damaged
membrane
o May lead to cell death
PATHOLOGY
 ALTERED CELLULAR RESPIRATION
o Biochemical reactions which transform
glucose to carbon dioxide and water
generating energy in ATP
o Aerobic respiration
o Lactic acid accumulation
o Membranes and lysosomes deteriorate
C. MORPHOLOGIC CHANGES
o Refers to STRUCTURAL CHANGES or
ALTERATIONS in cells or tissues seen
under the microscope
Look for “clues” that could tell the
probable defect in the patient
o Characteristic of the disease
 Some morphologic changes when
grouped can be unique to a
particular disease
 e.g. Tuberculosis and
Cancer
o Diagnostic of the etiologic process
 How benign and malignant growth
is distinguished from one another
 How autoimmune reaction is
distinguished from a
hypersensitivity reaction
o Changes may overlap each other having 2 or
more alterations in the cell morphology
CLINICAL CORRELATION
TUBERCULOSIS: Unique morphologic changes
include:
 AFB positive
 Presence of granuloma
 Caseation necrosis

 MECHANISM OF MEMBRANE DAMAGE

o Replenishing components of cell membrane
depressed/ stopped (e.g. Endoplasmic
reticulum)
o Internal network of supporting tubules of cell
cytoskeleton (maintains cell integrity as to D. CLINICAL SIGNIFICANCE
shape and is responsible for movement) may o Also known as FUNCTIONAL
be damaged CONSEQUENCES/ DERANGEMENT of the
o Direct injury to cell membrane disease to the patient
o breakdown of internal molecules o Anticipated clinical manifestations in relation
to Etiology, Pathogenesis and Morphologic
 PRODUCTION OF HYPERACTIVE MOLECULE changes
o Unstable molecule or compounds o Influence on normal function
o Overproduction of TOXIC FREE o Determines the clinical features
RADICALS: Superoxide, H2O2, hydroxyl o Predict the course and prognosis or outcome
o React with cell membrane lipids thus of the disease
destroys membrane integrity  Patients diagnosed with
o Radiant energy injury nasopharyngeal carcinoma
o Metabolism of certain chemical drugs (eg (acquired from smoking)
acetaminophen and cancer drugs) theoretically has bad prognosis (di
na daw aabot ng dalawang taon...)

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 GENERAL &
SYSTEMIC PATHOLOGY
IV. CELLULAR ADAPTATIONS OF GROWTH AND
DIFFERENTIATION  COMPENSATORY HYPERPLASIA
‒ Response of cells to increased demand and external o Increase tissue mass after damage/ partial
stimulation resection to compensate for the loss of the
HYPERPLASIA & HYPERTROPHY tissue section (hence the name
‒ Reduced supply of nutrients and growth factors compensatory)
ATROPHY  In Nephrectomy (where one of the
‒ Change in cell type – true for epithelial tissues kidneys are removed), the other
METAPLASIA kidney will undergo hyperplasia to
compensate
 Hepatectomy (where lobes of the
liver are removed), the remaining
Adaptive tissue would undergo hyperplasia to
Changes
(Adaptation fill in the removed tissue section of
the organ.

MECHANISM OF PHYSIOLOGIC HYPERPLASIA

 Increase local production of growth factors
and these growth factors are necessary in
Normal Injury Reversible
changes order the cells to divide)
Cell (degenerative
 Increase levels of growth factor receptors on
Intensity changes)
Duration responding cells
 Activation of a lot intracellular signaling
pathways but not to a point where it
Irreversible becomes neoplastic (malignanat) in nature
changes
(Necrosis)
 Stem cell stimulation (ie partial
hepatectomy)

Cell may be subjected to injurious stimulus. Depending upon

the length or duration of exposure of the cell to the stimulus A.2 PATHOLOGIC HYPERPLASIA
and with the intensity as mild, moderate, severe, the cell ‒ May take place in the presence of EXCESSIVE
can enter into Adaptive phase, Degenerative phase and HORMONAL STIMULATION/ GROWTH FACTORS
Irreversible phase. ACTING ON TARGET CELLS

o Example
 Endometrial hyperplasia- due to
A. HYPERPLASIA estrogen production which is a
‒ INCREASE IN powerful mitogen;
NUMBER OF  causes abnormal
CELLS in menstrual bleeding
organ/ tissue
‒ Result: increase  Benign prostatic hyperplasia (BPH)-
volume of due to testosterone;
organ/ tissue  presented with acute
‒ Happens in cells blockage of urine
capable of
synthesizing
DNA ‒ Regression happens when hormonal stimulation is
‒ May be eliminated or withdrawn.
physiologic or
pathologic ‒ Fertile soil in which cancerous proliferation
may occur
A.1 PHYSIOLOGIC HYPERPLASIA
 HORMONAL HYPERPLASIA –
o influenced by the physiologic increase in the
concentration of hormone resulting in
INCREASE FUNCTIONAL CAPACITY
o Example: hyperplasia of female breast,
uterus

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 GENERAL &
SYSTEMIC PATHOLOGY
HYPERPLASIA: Photomicrographs CHECKPOINT! Test yourself!

Answer:
A - if item A one pertains to the stem but item B does not
B - if item B one pertains to the stem but item A does not
C – if both items pertains to the stem
D – if neither of the item pertains to the stem
___ 1. Ischemia
A. Loss of blood flow and supply
B. May be due to a blockage to a particular tissue

___2. Hypoxia
A. Total lack of oxygen in the tissues
B. The eventual result of ischemia
Specimen: Breast
Findings: Lobules and ducts are lined with several layers
___3. Chemical agents
A. Exogenous: from uncontrolled cellular
metabolism
B. Endogenous: from ingestion, inhalation and
injection of substance to the body

___4. Etiology
A. The cause of a certain disease
B. Answers the question “how did the disease
happened”

___5. Pathogenesis
A. From expression of diseases to initial stimulus
Specimen: Stomach B. Refers to the mechanism by which the diseases
Findings: Hyperplasia manifested by an increase in the number came about
of glands; aka hyperplastic polyp; crowding of parietal cells
___6. Responses where in a cell could till revert to the normal
state
A. Degenerative changes
B. Necrosis

___7. Response of cells to increased external stimulation

A. Hyperplasia
B. Hypertrophy

___8. Enlargement of female breast due to puberty

A. Hormonal physiologic hyperplasia
B. Compensatory physiologic hyperplasia
Specimen: Endometrium
Findings: Endometrial hyperplasia; due to exposure of too
___9. Pathologic hyperplasia
much estrogen
A. BPH
B. Suitable for neoplastic changes

___10. Regression is possible

A. Physiologic hyperplasia
B. Pathologic hyperplasia
c-b-d-a-b-a-c-a-c-c

Specimen: Prostate gland (glandular and fibromuscular organ)

Findings: Crowding of prostatic glands; prostatic hyperplasia

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