CELLULAR ADAPTATION

Refers to changes made by a cell in response to adverse or varying environmental changes

(Permits survival and maintenance of cell function)
> May alter differentiation of genes enabling a cell to change size or form.
>The adaptation may be physiologic (normal) or pathologic (abnormal).
Normal adaptive is a response to an appropriate stimulus.
Abnormal cellular changes may also occur

Four types of morphological adaptations include:

 Atrophy
 Hypertrophy
 Hyperplasia
 Metaplasia

1. Atrophy (cells shrink)

environmental conditions
Is adaptive and reversible
results in a decrease in cell size

Types:
-Disuse atrophy (paralysis)
-Degeneration atrophy (MS)
-Ischemic atrophy (kidney, heart)
-Malnutrition atrophy (starvation)
-Loss of endocrine stimulation (uterine, breast)

2. HYPERTROPHY
D/T increase workload requirement of an organ part
 Causes an increase in cell size & cell function
 Results in an increase in tissue mass
 Seen in cardiac, skeletal, and muscle tissue
 These cells are not capable of mitosis (so, no  number or hyperplasia)
 May be a normal physiologic response
 as seen in an increase in muscle size with exercise

May be a pathological response as in myocardial hypertrophy from HTN or valve disease

 A PATHOLOGICAL HYPERTROPHY resulting in incrs size of heart d/t incrs workload caused by
HTN.
There is an increase in size but function is compromised
However, there is a LIMIT to the amount the tissue can enlarge

3. HYPERPLASIA (incrs # of cells)

Occurs d/t to a response from appropriate stimulus and ceases when stimulus is removed
An increase in NUMBER of cells
 Restricted to cells capable of mitosis
-epidermis, intestinal epithelium, and glandular tissue.
Physiological hyperplasia
- uterus and breast enlarge in pregnancy
4.HYPERPLASIA (cont)
May be a PHYSIOLOGICAL response and occur with hypertrophy (increase in both cell size &
number)
Hyperplasia is important in wound healing
May also be a non-physiologic hyperplasia
 Seen in prostatic hypertrophy (BPH), endometrial hyperplasia d/t increased hormone
stimulation, or thyroid enlargement

4. METAPLASIA
One cell type is replaced by another
May predispose to cancer
 Allows to cells to better survive in a hostile environment
Is REVERSIBLE
 Is a response to chronic irritation and inflammation
 Cells that are normally columnar or stratified may change to squamous.
Examples:
-With continued smoke exposure, ciliated columnar cells are changed to stratified squamous cells
-Cervical cells change when exposed to STDs or HPV
Think metamorphosis or change from one form to another
 Continued exposure may predispose to cancerous transformations.

5.DYSPLASIA*(ATYPICAL HYPERPLASIA)
Deranged cell growth resulting in cells of varying size, shape, and appearance
-May be associated with chronic irritation or inflammation
-May be reversible if offending agent is removed
Dysplasia is considered A STRONG PRECURSOR OF CANCER!!!
However, dysplasia is an adaptive process – may or may not lead to cancer
Decrease risk if irritation is removed or inflammation treated.

6.Anaplasia
-Cells differentiate to a more IMMATURE or embryonic form.
-Malignant tumors are characterized by anaplastic cell growth.

Cellular Infiltrations (carbon, triglycerides)

 Carbon can accumulate via inhaled coal dust. Can cause black lung disease (pneumonconiosis)
 Organs enlarged, i.e., “MEGALY”
Ex. spleenomegaly, hepatomegaly

Diseases d/t cellular accumulations MAY BE REVERSIBLE if d/t a correctable systemic disorder

CELLULAR ACCUMULATIONS: (lipids and edema)

If the offending cause is not or cannot be corrected
CELL DEATH may occur
Cellular swelling – extracellular water shifts into cells

Causes of cell injury

Chemical agents
Hypoxia
Free radicals
Infectious agents (bacteria, viruses, fungi)
Physical and mechanical agents
Genetic factors
Nutritional imbalances
CELLULAR INJURY
Cause: Mechanical Forces

Cellular injury may be reversible or irreversible determined by: the severity of the insult, blood supply,
nutritional status, and regeneration capability
-Physical Agents – trauma
-Electrical
-Temperature extremes
-Radiation

Injury from biological agents: viruses, bacteria, and parasites

 Biological agents are able to replicate and thus can continue to cause injury to cells
 Viruses incorporate themselves into the DNA of the cell
 Bacteria secrete exotoxins or endotoxins that interfere with cellular reproduction of ATP, or
release antitoxins that cause injury
 Parasites can cause direct injury to the cell

Injury from nutritional imbalances

 Nutritional excesses such as obesity and diets high in fats can predispose to atherosclerosis
leading to ischemia
 The body needs minerals, vitamins, certain fatty acids, and specific amino acids.
 Nutritional and vitamin deficiencies interfere with cell metabolism and delay wound healing

Cellular Death
Apopthosis
Is essentially “cell suicide” or programmed cell death
Apopthosis is the process that eliminates:
-Worn out cells (RBCs)
-Cells which have been produced in excess
ex. WBCs with infectious response with hepatitis)
-Cells which have developed improperly
ex. spontaneous abortion
-Cells which have genetic damage
Ex cancer

Necrosis- death of most or all of the cells in an organ or tissue due to disease, injury, or failure of the
blood supply.
 Interferes with cell replacement and tissue regeneration.
 Necrotic cells or tissue can:
Liquefication
cells becomes liquefied
Ex: abcess, brain tissue
May result in wet gangrene

INFARCTION
- cells die and become BLACK AND SHRIVELED

Gangrene
Gangrene is necrosis of a mass of tissue
 Death of many cells!
Results from severe hypoxia and subsequent ischemia (blood flow/oxygen- is restricted or
reduced in a part of the body.)
 Often seen with impaired circulation to lower extremities (Diabetes)
Three types of gangrene:
1.Dry Gangrene
Part of the tissue becomes dry and shrinks, the skin wrinkles and color changes to brown or
black
 Shriveled/mummified
 Spread is slow
 Results from chronic ischemia of tissue
 Symptoms not as marked as with wet gangrene

2.Moist or wet gangrene

Frequently occurs in internal organs (appendix)
 If on the skin, surrounding area is cold, swollen, and pulseless
- Skin in moist, black, and under tension
 Blebs form on the skin, liquefaction occurs, and foul odor develops from bacteria
No line of demarcation
Spread is rapid
Severe systemic symptoms may develop
-Changes in kidney function
-Death may occur
-Venous return is impaired, swelling is remarkable
-Bacterial invasion is present
- May affect extremities or internal organs
 Dry gangrene may become wet gangrene if a bacterial invasion occurs

3. Gas Gangrene
(destroys connective tissue and cellular membranes)
- Is a specialized type of wet gangrene
 Results from infection of clostridium bacteria, clostridium are often found in the soil.
- Gas gangrene is more prone to occur when there is trauma with a compound fracture
Gas gangrene
- Bacteria produce toxins which dissolve cell membranes causing:
 death of muscle cells
 massive spreading edema
 hemolysis (rupture or destruction) of RBCs
 renal toxicity (very harmful)
 Characteristic bubbles of hydrogen (sulfide gas) form in the muscle
-Can be fatal