PATHOLOGY Progressive and severe Irreversible injury

Cell death
General Pathology- reactions of cells and tissues Necrosis
to abnormal stimuli and to inherited defects Apoptosis
(main causes of disease)
Metabolic Alterations, Genetic Intracellular
Systemic Pathology- alterations in specialized or Acquired; Chronic Injury Accumulation
organs and tissues (Proteins, lipids,
carbs);
Calcification
4 Aspects of a Disease Process: EPMC

Etiology or Cause
Cumulative Sublethal Injury Cellular Aging
o Genetic or Acquired
over Long Life Span
Pathogenesis
o the sequence of events in the response
of cells or tissues to the etiologic agent ADAPTATIONS
o from the initial stimulus to the ultimate
Reversible changes in size, number, phenotype,
expression
metabolic activity or fxns
Morphologic and Molecular Changes
o Structural alterations Hypertrophy
Clinical Manifestations
o Functional consequences of the increase in cellular contents increase in cell
o changes size LARGER organs
o Signs and symptoms encountered in cells w/c are not capable or
o Clinical course or outcome have limited capacity to divide
seen in heart (myocytes) and skeletal muscles
Adaptations- are reversible functional and structural no new cells
responses to more severe physiologic stresses may involve subcellular organelle hypertrophy
caused by increased functional demand or
Cellular Responses to Injury
hormonal stimulation
Nature of Injurious Stimulus Cellular Response can be reverted if the cause is removed
Classification: pathologic or physiologic
Altered Physiological Stimuli; Cellular o Physiologic: exercise
Some Nonlethal Injurious Adaptations o Pathologic: obstruction of heart valves
Stimuli (ex. STRESS) causing increased workload

demand, stimulation Hyperplasia, Hyperplasia

( ex. By growth factors, hypertrophy
hormones) increase in cell number in an organ or tissue
Atrophy LARGER organs
nutrients, stimulation seen in epithelium, blood cells and CT
Metaplasia no cell division!
Chronic irritation (physical or Occurs if the population is capable of
chemical) synthesizing DNA, permitting mitotic division
Classification
Reduced Oxygen Supply; Cell Injury o Physiologic: from normal stimuli
Chemical Injury; Microbial Hormonal:
Infection hyperplasia of breast
and uterus during
Acute and transient Acute reversible
pregnancy
injury
 menstrual
endometrium
Compensatory: regeneration of
liver following partial
hepatectomy
o Pathologic: stimulation of growth
factors
Excess hormonal stimulation
ACTH from pituitary
Viral infection (papilloma
viruses)
Lymphoid tissue hyperplasia
occurring after localized
inflammation
Diffuse: crowding of epithelial
cells forming papillary
projections (Graves Disease)
Nodular
Hyperplasia of psoriasis
Hyperkeratosis on the
epidermis (scaly
grossly)
o May give rise to neoplasms
Atrophy
Decrease in the size and metabolic activity of
cells
Shrinkage in the size of cell body by loss of cell
substance
Classifications:
o Physiologic
Due to decreased workload
size of uterus
following childbirth
Reduction of lymphoid tissue
o Pathologic
Primarily due to denervation of
muscle, diminished blood
supply, nutritional deficiency,
old age, disuse , and some are
idiopathic
Causes of Atrophy
Reduced Functional Atrophy of Disuse
demand (Disuse)
Lack of Trophic Endocrine Atrophy
Hormones
Malnutrition Starvation or Hunger
Atrophy
Loss of Innervation Denervation Atrophy
Diminished Blood Supply Vascular Atrophy
Aging Senile Atrophy
Pressure Pressure Atrophy
Adaptation Reversible injury Irreversible Injury
Cell death
Ex: Myocytes: in hemodynamic loads
o Adaptation: Myocardial Hypertrophy
Caused by blood flow
requiring greater mechanical
effort by myocytes
Leads to thickening of left
ventricular wall to >2cm
(N: 1-1.5cm)
o Reversibly Injured Myocardium
Generally only functional
effects, w/o any gross or
microscopic changes
o Necrosis: Acute Myocardial Infarction
Caused by reduced blood fow
(ischemia)
Cell Death
End result of progressive cell injury
A normal and essential process in
embryogenesis, development of organs and
maintenance of homeostasis
2 Principal Pathways of Cell Death:
Necrosis
Apoptosis
Nutrient deprivation- triggers autophagy cell death
Pathologic Calcification- calcium deposition in cell death
Adaptations
Reversible changes in size, number, phenotype,
metabolic activity or fxns