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Cellular Adaptation

 It is the ability of cells to respond to various types of stimuli and adverse environmental changes for its

survival and maintenance of cellular function.

 May alter differentiation of genes enabling a cell to change size or form.

 It includes atrophy, hypertrophy, hyperplasia, and metaplasia.

 Tissues adapt differently depending on the replicative characteristics pf the cells that make up the

tissue. Labile tissues such as the skin can readily replicate, and therefore can also regenerate after

injury.

 If cells are not able to adapt to the adverse environmental changes, cell death occurs physiologically in

the form of apoptosis, or pathologically in the form of necrosis.

Types of Cellular Adaptation

1. Atrophy

 It is the shrinkage in the size of the cell by loss of cell substance.

Mechanism:

a. Decreased protein synthesis

 Due to reduced metabolism

b. Increased protein degradation in cells

 Due to ubiquitin-proteasome pathway, degradation of intermediate filaments of the cytoskeleton.

The cytoskeleton is a structure that helps cells maintain their shape and internal organization, and it

also provides mechanical support that enables cells to carry out essential functions like division and

movement.

c. Autophagy of cellular components: generation of autophagic vacuoles which fuse with lysosomes to

breakdown cellular components

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Types:

a. Physiologic

 Normal embryonic development – thyroglossal duct atrophy.

b. Pathologic

 Atrophy of disuse (immobility) due to decreased muscular workload.

 Brain atrophy in Alzheimer’s Disease

o Atrophic cells loss endoplasmic reticulum, have fewer mitochondria, and myofilaments.

2. Hypertrophy

 Refers to an increase in cell size and cell function which results in increased tissue mass.

 It occurs in non-dividing permanent cells like cardiac, muscles and skeletal tissues which are not

capable of mitosis.

 Stimulation by hormones or growth factors lead to increased synthesis of structural components of

cells.

 It can be a normal physiologic response.

Types:

a. Physiologic

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 Skeletal muscle in bodybuilders.

b. Pathologic

 Enlargement of cardiac muscle due to hypertension.

3. Hyperplasia

 Increased number of cells in a tissue resulting in increased mass of the organ/tissue.

 It occurs due to a response from appropriate stimulus and ceases when stimulus is removed.

 It is restricted to cells capable of mitosis like epidermis, intestinal epithelium, and glandular tissue.

Types:

a. Physiologic

 Compensatory hyperplasia or liver cell proliferation after partial hepatectomy.

 Wound healing

 Uterus and breast enlargement in pregnancy.

b. Pathologic

 Endometrial hyperplasia due to hormone-driven-increased oestrogen level

 Benign prostatic hypertrophy.

 Thyroid enlargement.

 Skin warts in papillomavirus.

4. Metaplasia

 Reversible change from one mature or differentiated cell type to another.

 This maybe because certain cell types withstand adverse environment better than others.

 It involves reprogramming of undifferentiated stem cells.

 It is a response to chronic irritation and inflammation.

 It may lead to cancer like in Barrett esophagus.

 It produces new cell types caused by changes in cell signals generated by mixture of cytokines, growth

factors, extracellular matrix components in cell matrix.

Types:

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a. Squamous Metaplasia

 Chronic smoker – ciliated columnar epithelium of trachea and bronchi are replaced by stratified

squamous epithelial cells.

 Vitamin A deficiency – squamous metaplasia in respiratory epithelium; replacement of thin

squamous conjunctival lining with stratified keratinizing squamous epithelium (keratomalacia).

 Squamo-columnar junction of cervix – to hormone changes.

b. Columnar metaplasia

 Barrett esophagus – non-ciliated, mucin producing columnar metaplasia of distal esophagus

(normally lined by nonkeratinizing squamous epithelium suited to handle friction of food bolus)

due to chronic gastroesophageal acid reflux.

c. Myeloid metaplasia

 Proliferation of hematopoietic tissue outside bone marrow, eg. liver and spleen

 Occurs in chronic idiopathic myelofibrosis

d. Connective tissue metaplasia

 Formation of cartilage, bone, or adipose tissues that normally do not contain these elements.

Example – myositis ossificans (muscle changes to bone during fracture healing).

Other Similar Terms

1. Dysplasia

a. Referred to as atypical hyperplasia.

b. It is not a true adaptive process, but arises from pathological hyperplasia and metaplasia, like in

endometrial hyperplasia and Barrett esophagus.

c. Deranged cell growth resulting in cells of varying size, shape, and appearance which may be

associated with chronic irritation or inflammation and may be reversible if offending agent is removed.

d. Decrease risk if irritation is removed or inflammation treated.

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e. Dysplasia is not cancer but considered a strong precursor of cancer like cervical intraepithelial

neoplasia the precursor to cervical cancer dysplasia

2. Anaplasia

a. Cells differentiate to a more immature or embryonic form.

b. Malignant tumors are characterized by anaplastic cell growth.

c. The cell no longer functions as a part of the tissue that surrounds it.

d. As the cell undergoes mitosis, it produces cells that also display anaplasia. In this was, a malignant

tumor is born.

Examples:

a. Leiomyosarcoma vs leiomyoma

 Leiomyosarcoma is a malignant smooth muscle tumor.

 Leiomyoma is a benign smooth muscle tumor.

 The only difference between the two is the state of anaplasia that exist in the malignant form.

b. Adenoma to adenocarcinoma

 Adenoma is a benign glandular tumors, these benign cells can actually become a malignant

adenocarcinoma but most often they do not.

Summary:

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II. Cellular Injury

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 It is often caused by mechanical forces.

 It can be reversible or irreversible determined by the severity of insult, blood supply, nutritional status and

regeneration capabilities.

 Most common causes are physical agents, electrical, temperature extremes, radiation.

Causes:

1. Mechanical Injuries

a. Physical agents

 Resulting from lacerations, fractures, burns, injury to blood vessels, and disruption in blood

flow.

b. Electrical

 It can cause extensive tissue injury and disruption of neural and cardiac impulses causing

vessel degeneration creating thrombi or clots.

 The body acts as conductor of electrical current. The extent of injury is determined by the

amount of voltage and duration of exposure.

 Lightning and high voltage wires produce most damage.

c. Temperature extremes

 Heat stroke or partial thickness burns can cause cellular injuries.

 An increase in intensity of heat causes the blood vessels to coagulate and tissue protein loss

occurs, which is called the fried egg effect.

 Cold exposure increases blood viscosity and induces vasoconstriction which may cause tissue

hypoxia which leads to cell membrane disruption.

d. Ultraviolet Radiation

 Sunburn increases the risk of skin cancers.

 Damage to melanin-producing processes in skin and damage to DNA occurs.

 The risk of skin cancers increases with the number and severity of sunburn.

e. Radiation Injury

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 Beyond certain thresholds, radiation can impair the functioning of tissues and/or organs and

can produce acute effects such as skin redness, hair loss, radiation burns, or acute radiation

syndrome. These effects are more severe at higher doses and higher dose rates.

2. Chemical Injury

 A biochemical interaction between a toxic substance and the cell’s plasma membrane occurs and leads

to increased cell permeability.

 Examples are air and water pollution, tobacco smoke, some processed or preserved foods, carbon

monoxide, insecticides, trace metals such as lead and drugs.

a. Drugs

 It can cause direct or indirect cell injury whether prescription or over-the-counter drugs.

b. Lead Toxicity

 It is absorbed in GI tract or via the lungs into the blood.

 It causes demyelination of nerve cells in the cerebral and cerebellar matter

causing death of neural and cortical cells.

 It can cause a decrease in IQ and impaired behavioral development in children.

 It can cause peripheral neuropathy in adults.

3. Biological Agents

 Biological agents are able to replicate and thus can continue to cause injury to cells.

a. Viruses

 They incorporate themselves into the DNA of the cell.

b. Bacteria

 They secrete exotoxins and endotoxins that interfere with

cellular production of ATP, or release antitoxins that cause injury.

c. Parasite

 It can cause direct injury to cells.

4. Nutritional Imbalances

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 Nutritional excesses such as obesity and diets high in fats can predispose to atherosclerosis leading to

ischemia.

 Nutritional and vitamin deficiencies interfere with cell metabolism and delay wound healing.

5. Hypoxic or Ischemia

 The most common cause of cell injury.

 Generalized form of hypoxia is an inadequate supply of oxygen in the blood affecting the entire body.

 Localized form causes ischemia in tissues which can lead to infarction or death of tissues.

 Causes of hypoxia include decrease of oxygen in the air, respiratory disease, ischemia, anemia due to

decreased hemoglobin and edema.

III. Cellular Accumulations

 It is the buildup of substances the cells are unable to dispose of which is a result of cellular injury.

 It is often referred as cellular infiltrations.

 It occurs due to accumulation of normal cellular substance such as water, lipid, carbohydrates, protein and

abnormal substances such as exogenous and endogenous into tissues. Exogenous includes minerals or

product of infectious agents and endogenous include synthetic and metabolic products.

 It may be transient (reversible) or permanent.

 It may be harmless but occasionally harmful.

 It may be in the cytoplasm or the nucleus.

Causes:

1. Normal endogenous substances are produced at normal or increased rate but metabolism is inadequate.

2. Abnormal endogenous substances accumulate due to alteration in protein folding and transport.

3. Normal endogenous substances accumulate because of inherited defect in enzymes.

4. Abnormal exogenous substance accumulates because of defect in enzymatic mechanism and transport.

Types:

A. Lipid Accumulation

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 It is the abnormal lipid accumulation in cell. It may be of fatty acid (steatosis) and cholesterol.

1. Steatosis

 Abnormal accumulation of triglycerides in parenchymal cells.

 Example is a fatty liver disease.

Sites

 Liver (commonly), heart, muscles and kidneys.

Causes:

 Toxins, protein malnutrition, diabetes mellitus, obesity, anoxia and alcohol.

Morphology:

 Light microscopy reveals vacuoles in the cytoplasm displacing the nucleus to the periphery of the cell.

Rarely cell rupture and enclosed fat globules coalesce and forming fatty cyst.

 Grossly, fatty liver will be enlarged bright yellow, soft and greasy. Fatty change in liver fatty acid

vacuole displacing nucleus (basophilic) cell periphery.

2. Cholesterol and Cholesterol Esters

 Accumulations in the form of intracellular vacuoles, are seen in several pathologic processes.

a. Atherosclerosis

 Smooth muscle cells and macrophages filled with cholesterol and cholesterol ester forming

foam cells within intima layer of vessels.

b. Xanthomas

 Cluster of foam cells in subepithelial connective tissues of skin and in tendons producing

tumorous masses.

c. Cholesterolosis

 Accumulations of foam cells (cholesterol-laden macrophages) in the lamina propria of the

gallbladder.

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d. Niemann-Pick Disease Type C

 Lysosomal enzyme defect by mutation result in lysosomal storage disease causes cholesterol

accumulation in multiple organs.

B. Protein Accumulation

 Accumulation of protein droplets in proximal renal tubules.

 In renal disease with heavy protein leakage across the glomerular filter.

 Example is amyloidosis.

Morphology:

 Round eosinophilic droplets, vacuoles or aggregates in cytoplasm. May be amorphous or crystalline.

 Protein droplets in proximal renal tubules.

C. Glycogen Accumulation

Diabetes Mellitus

 Disorder of glucose metabolism, glycogen found in renal tubular epithelial cells.

Glycogen Storage Disorders or Glycogenoses

 Genetic disorder resulting in enzymatic defect in synthesis and breakdown of glycogen.

IV. Cellular Death

 It is characterized by the breakdown of cellular structures.

 It pertains to the events leading to the death of a cell either when they have completed a fixed number of

division cycles (around 60, the Hayflick limit) or at some earlier stage when programmed to do so, as in

digit separation in vertebrate limb morphogenesis.

 Whether this is due to an accumulation of errors or a programmed limit is unclear, some transformed cells

have undoubtedly escaped the limit.

Types of Cellular Death:

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1. Programmed Cell Death

 It is a kind of cell death that is regulated by an innate physiological system.

 The cell undergoes a natural process of death after completing a number of cell divisions.

 The cell ceases to carry out its functions and dies to be replaced by new ones.

 The programmed type of cell death is further categorized into type I cell death or apoptosis and type II

cell death or autophagy.

a. Apoptosis

 A programmed cell death involving an ordered sequence of biochemical events that result in cell

changes.

 It is signaled by the nuclei in normally functioning human and animal cells when age or state of

cell health and condition dictates.

 It is an active process requiring metabolic activity by the dying cell, often characterized by

cleavage of the DNA into fragments that give a so called laddering pattern on gels.

 Examples are blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation,

chromosomal DNA fragmentation.

b. Autophagy

 It is characterized by biochemical events leading to self-digestion through the destructive action

of enzymes produced by the cell itself, often as a defensive or self-preservation response.

 It is the process involving biochemical events catalyzed by enzymes produced within the cell that

leads to self-digestion.

2. Necrosis

 It is the death of the cell due to factors such as disease, injury, or the death of the organism.

 It is a term pertaining to the bodily injury characterized by the localized death of cells in a living tissue

or organ.

 It is different from apoptosis in a way that the former is a premature death of cells or tissues. 

Mark Emil U. Bautista Altered Cellular Structure and Function

MA in Nursing Advanced Medical-Surgical Nursing II