“Persistent pre-lethal stress leads to
cellular adaptation”
1-Adaptation of growth.
a) Increased growth and cellular activity e. g. Hypertrophy & Hyperplasia
b) Decreased growth and cellular activity e.g. Atrophy.
c-Disturbances of cellular differentiation and morphology e.g. Metaplasia
2-Intra and Extra cellular accumulations e. g.
a) Lipids as in fatty change & Cholesterol deposits.
b) Proteins as in Hyaline change& Amyloidosis.
c) Calcium as in Pathologic Calcification
d) Pigments as in Pathologic pigmentation.
 Endogenous
 normal substance produced at normal or increased rate/rate
of metabolism inadequate for removal (fatty liver)
 Exogenous
 cell cannot degrade substance (carbon)
Intracellular Accumulations
Intracellular Accumulations
 Fatty Change (Steatosis)
 the liver is one of the main organs of the body involved in pathways involving
metabolism of fats or lipids.
 Accumulation of lipids in hepatocytes is termed fatty change (also known as,
hepatic steatosis, fatty liver).
 Another example of accumulation of lipids in cells is atherosclerosis
characterized by the accumulation of lipid-laden foam cells in the walls
 of arteries. The significance of atherosclerosis in humans is obviously reflected
in the high incidence of myocardial and cerebral infarction (heart attack and
stroke).
Intracellular Accumulations
 Fatty Change (Steatosis)
 Liver
 increased weight, yellow color
fat vacuoles within
cytoplasm of hepatocytes
 Another example of accumulation of an endogenous
substance, is the accumulation of protein in tubular
epithelial cells of the kidney known as amyloidosis
 Glycogen:
Abnormal accumulation occurs in liver, muscles and
kidney in case of Diabetes mellitus ( hyperglycemia)
defect in metabolism of glucose or glycogen
 Pigment disorders:
 Pigments are colored substances, synthesized within
the body (endogenous) or coming from outside
(exogenous).
 Endogenous pigments: include melanin, lipofuscin and
Hemosiderin
Intracellular Accumulations
 Endogenous Pigments
 Lipofuscin (“wear and tear pigment)
It contains complexes of lipid and protein derived from
peroxidation of lipids by free radicals. insoluble brownish-
yellow granular intracellular material that accumulates in a
variety of tissues (particularly the heart, liver, and brain) as a
function of age or atrophy (ageing pigment), when appear in
tissue grossly it is called brown atrophy

Intracellular Accumulations
 Endogenous Pigments
 Melanin
 brown-black pigment produced in melanocytes
 It is synthesized exclusively by melanocytes located in the
epidermis and acts as a screen against harmful ultraviolet
radiation
 Albinism: absence of melanin. Such individuals have
melanocytes but are unable to synthesize melanin. These
patients are vulnerable to cancer.
 Albinism is an inherited condition that is present at birth. It is characterized
by a lack of melanin, the pigment that normally gives color to the skin, hair,
and eyes. Many types of albinism exist, all of which involve lack of pigment
in varying degrees. The condition, which is found in all races, may be
accompanied by eye problems and may ultimately lead to skin cancer .
 The most common type of albinism is oculo-cutaneous albinism, which
affects the eyes, hair, and skin. In its most severe form, hair and skin remain
completely white throughout life.
 Albinism is an autosomal recessive disease, which means that a person must
have two copies of the defective gene to exhibit symptoms of the disease. The
child therefore inherits one defective gene responsible for making melanin
from each parent. Because the task of making melanin is complex, there are
many different types of albinism, involving a number of different genes.
Hair and skin colour.
People with albinism often
have white or very light blonde
hair, although some have brown
or ginger hair. The
exact colour depends on how
much melanin their body
produces. Very pale skin that
burns easily in the sun and
doesn't usually tan is also
typical of albinism.
Intracellular Accumulations
 Endogenous Pigments
 Hemosiderin
 golden-yellow pigment accumulate in tissues when there is
local or systemic excess of iron
 Local excesses of iron and hemosiderin result from
hemorrhages or vascular congestion,. With lysis of the
erythrocytes, the hemoglobin eventually undergoes
transformation to hemosiderin.
Hemosiderin
 Hemosiderosis
 hemosiderin is systemically deposited in many organs and tissues [ liver, bone marrow,
spleen, and lymph nodes
 occurs in
1. increased absorption of dietary iron,
2. hemolytic anemias,
3. transfusions
 Hemochromatosis
 hereditary more extensive accumulations of iron with tissue injury including liver fibrosis,
heart failure, and diabetes mellitus.
Intracellular Accumulations
 Exogenous Pigments
 Carbon (anthracosis)
 When inhaled, it is phagocytosed by alveolar macrophages
and transported by lymphatics to lymph nodes
 mild accumulations usually are of no consequence--heavy
accumulations may induce a fibroblastic response
Exogenous pigments
 Most of these are dust particles in the inhaled air,
deposited in the lungs and associated lymph nodes.
 The dust particles act as mild irritants and induce
proliferation of fibrous connective tissue( FCT)-
(fibrosis) and collection of macrophages.

Cellular adaptation

  • 1.
    “Persistent pre-lethal stressleads to cellular adaptation” 1-Adaptation of growth. a) Increased growth and cellular activity e. g. Hypertrophy & Hyperplasia b) Decreased growth and cellular activity e.g. Atrophy. c-Disturbances of cellular differentiation and morphology e.g. Metaplasia 2-Intra and Extra cellular accumulations e. g. a) Lipids as in fatty change & Cholesterol deposits. b) Proteins as in Hyaline change& Amyloidosis. c) Calcium as in Pathologic Calcification d) Pigments as in Pathologic pigmentation.
  • 2.
     Endogenous  normalsubstance produced at normal or increased rate/rate of metabolism inadequate for removal (fatty liver)  Exogenous  cell cannot degrade substance (carbon) Intracellular Accumulations
  • 3.
    Intracellular Accumulations  FattyChange (Steatosis)  the liver is one of the main organs of the body involved in pathways involving metabolism of fats or lipids.  Accumulation of lipids in hepatocytes is termed fatty change (also known as, hepatic steatosis, fatty liver).  Another example of accumulation of lipids in cells is atherosclerosis characterized by the accumulation of lipid-laden foam cells in the walls  of arteries. The significance of atherosclerosis in humans is obviously reflected in the high incidence of myocardial and cerebral infarction (heart attack and stroke).
  • 4.
    Intracellular Accumulations  FattyChange (Steatosis)  Liver  increased weight, yellow color
  • 5.
  • 6.
     Another exampleof accumulation of an endogenous substance, is the accumulation of protein in tubular epithelial cells of the kidney known as amyloidosis  Glycogen: Abnormal accumulation occurs in liver, muscles and kidney in case of Diabetes mellitus ( hyperglycemia) defect in metabolism of glucose or glycogen
  • 7.
     Pigment disorders: Pigments are colored substances, synthesized within the body (endogenous) or coming from outside (exogenous).  Endogenous pigments: include melanin, lipofuscin and Hemosiderin
  • 8.
    Intracellular Accumulations  EndogenousPigments  Lipofuscin (“wear and tear pigment) It contains complexes of lipid and protein derived from peroxidation of lipids by free radicals. insoluble brownish- yellow granular intracellular material that accumulates in a variety of tissues (particularly the heart, liver, and brain) as a function of age or atrophy (ageing pigment), when appear in tissue grossly it is called brown atrophy 
  • 9.
    Intracellular Accumulations  EndogenousPigments  Melanin  brown-black pigment produced in melanocytes  It is synthesized exclusively by melanocytes located in the epidermis and acts as a screen against harmful ultraviolet radiation
  • 10.
     Albinism: absenceof melanin. Such individuals have melanocytes but are unable to synthesize melanin. These patients are vulnerable to cancer.  Albinism is an inherited condition that is present at birth. It is characterized by a lack of melanin, the pigment that normally gives color to the skin, hair, and eyes. Many types of albinism exist, all of which involve lack of pigment in varying degrees. The condition, which is found in all races, may be accompanied by eye problems and may ultimately lead to skin cancer .  The most common type of albinism is oculo-cutaneous albinism, which affects the eyes, hair, and skin. In its most severe form, hair and skin remain completely white throughout life.  Albinism is an autosomal recessive disease, which means that a person must have two copies of the defective gene to exhibit symptoms of the disease. The child therefore inherits one defective gene responsible for making melanin from each parent. Because the task of making melanin is complex, there are many different types of albinism, involving a number of different genes.
  • 11.
    Hair and skincolour. People with albinism often have white or very light blonde hair, although some have brown or ginger hair. The exact colour depends on how much melanin their body produces. Very pale skin that burns easily in the sun and doesn't usually tan is also typical of albinism.
  • 12.
    Intracellular Accumulations  EndogenousPigments  Hemosiderin  golden-yellow pigment accumulate in tissues when there is local or systemic excess of iron  Local excesses of iron and hemosiderin result from hemorrhages or vascular congestion,. With lysis of the erythrocytes, the hemoglobin eventually undergoes transformation to hemosiderin.
  • 14.
    Hemosiderin  Hemosiderosis  hemosiderinis systemically deposited in many organs and tissues [ liver, bone marrow, spleen, and lymph nodes  occurs in 1. increased absorption of dietary iron, 2. hemolytic anemias, 3. transfusions  Hemochromatosis  hereditary more extensive accumulations of iron with tissue injury including liver fibrosis, heart failure, and diabetes mellitus.
  • 15.
    Intracellular Accumulations  ExogenousPigments  Carbon (anthracosis)  When inhaled, it is phagocytosed by alveolar macrophages and transported by lymphatics to lymph nodes  mild accumulations usually are of no consequence--heavy accumulations may induce a fibroblastic response
  • 16.
    Exogenous pigments  Mostof these are dust particles in the inhaled air, deposited in the lungs and associated lymph nodes.  The dust particles act as mild irritants and induce proliferation of fibrous connective tissue( FCT)- (fibrosis) and collection of macrophages.