Cellular Reaction to Injury Flashcards
oxygen deprivation (hypoxia), nutritional deficiencies, chemical agents (prescription drugs, air pollutants, alcohol, asbestos, pesticides), autoimmune diseases and infections, genetic defects, aging process (cellular senescence).
Etiology of Cellular Changes
Cellular Swelling Degeneration Infiltration Necrosis Atrophy Hypertrophy Hyperplasia Regeneration Somatic Death
Cellular Changes
Passive (worsen) cell alteration that may result in:
cellular swelling
degeneration
infiltration
Regressive Cellular Changes
Increase in cell water content due to cell injury that allows intracellular sodium to rise.
- Entire organ or tissue experiences loss of color, cells that become distended.
Cellular Swelling
Loss of color.
Pallor
Cells become distended.
Turgor
The deterioration of tissues with corresponding functional impairment as a result of disease resulting in appearance of substances within the cell that are not normally present.
Degeneration (intracellular)
Deposit of abnormal amounts of fat in cells; e.g. , heart, liver, kidneys.
This is due to malnutrition, diabetes mellitus, obesity, or starvation.
Fatty Degeneration
Deposit of amyloid (starch like protein) giving tissues waxy, translucent, hyaline appearance.
e.g., liver, kidneys, adrenal glands
This is due to diabetes mellitus, poisons, often secondary to chronic rheumatoid arthritis, carcinoma, tuberculosis, osteomyelitis, Hodgkin’s disease.
Amyloid Degeneration
Jelly-like appearance of tissues.
E.g., lungs- anthracosis: lung dust disease due to inhalation of coal pigment.
Colloid degeneration
The process of seepage or diffusion into tissue of substances that are not ordinarily present; abnormal passing and deposit of substances in tissue.
Infiltration (intercellular)
Deposit of fat in tissues often due to poisons or diet, occurs mostly in the liver, kidneys, and heart.
Fatty Infiltration
Coloration caused by deposit, or lack, or colored material in the tissues (increase or decrease in pigment deposit).
Pigmentation infiltration
Pigment transmitted from outside the body.
Exogenous
Carotene in blood; resulting in discoloration of the liver and skin.
Carotenemia
Due to lead poisoning > discoloration to gums, damage to the brain and other internal organs.
Plumbism
Pigment present inside the body
changes in the retina of the eye
melanosis
albinism
jaundice (icterus= bile pigments)
Endogenous
Moles, melanomas, freckles
Melanosis
Calcium deposits (lime salts) in tissue, usually surrounded by bacteria, necrotic cells, mucous, foreign materials.
Calcification
Kidney stones
Renaliths (renal calculi)
Bladder stones
Vesical Calculi
Calcification in the intestines or appendix
Fecaliths
Calcification in the nose
Rhinoliths
Gallstones
Choleliths
Calcification in the lungs
Pneumoliths
Calcium deposits in the arteries
Arteriosclerosis
Stone baby, calcified fetus, usually in fallopian tubes.
Lithopedion
Primary chronic metabolic disorder (a common form of arthritis) associated with elevated blood uric acid level.
results in accumulation of uric acid and uric acid salts in joints (often the big toe), kidneys, external ear and eyelids.
Causes swelling, arthritic pain and deformed joints.
Gout
Cell degeneration that can lead to cell and tissue death without replacement.
Cellular Death
Mechanical injury, malnutrition, heat or cold, loss of nerve supply, low oxygen (hypoxia), or no oxygen (anoxia) delivered to tissues, drugs or bacterial toxins, or viruses.
Causes of cellular death
Programmed cell death
Apoptosis
Cell death caused by disease
Necrosis
Rare genetic diseases associated with early aging and short life span
Progeria and Werner’s syndrome
Degeneration of proteins; tissues becomes dry, firm, form yellowish mass that occurs due to ischemia, infarct, or heat. (most common)
Coagulative necrosis
Result of certain infections such as tuberculosis, tissue has a creamy-white, “cheesy” appearance (flaky, crumbly).
Caseous necrosis
Necrotic tissue softens, becomes wet; usually due to infections.
Liquefactive necrosis
Death of tissue due to lack of blood supply (common complication of healing). Tissue has a dry, firm, blackened, mummified appearance as in diabetics, or frostbite.
Ischemic necrosis
Necrosis of tissue, usually resulting from deficient or absent blood supply; most common in the lower extremities.
caused by infection, insufficient blood supply,
results in ischemia, putrefaction
Gangrene
Decomposition of organic matter, especially protein, by microorganisms, resulting in production of foul-smelling matter.
Putrefaction
Dry
Wet
Gas
Types of gangrene
Results from obstruction of ARTERIAL blood flow with or without invasion by bacteria, usually in extremities.
symptoms: tissue is dry, shrunken, dark black, resembles mummified flesh, as in diabetics.
Dry (Ischemic Necrosis) Gangrene
Results from inadequate VENOUS drainage, occurs in naturally moist tissue and organs suck as the mouth, intestines, lungs, cervix, and vulva; often in extremities or area of bedsores (sacrum, buttocks, heels)
Etiology: following ischemia, or infarction, invasion by saprogenic microorganisms (perfringes, fusiformis, putrificans).
Moist (wet) Gangrene
feed on dead organic matter
Saprogenic
swelling of tissue (edema), tissue site is cold and has no pulse, moist black skin under tension, liquefaction (tissue softens) > foul odor, condition spreads.
Symptoms of moist gangrene.
Similar to moist gangrene, but caused by anaerobic bacterium Clostridium perfringens.
symptoms: same for moist gangrene, crepitation, severe tissue necrosis, sepsis, toxemia
Gas Gangrene
Stretching of tissue due to gas production by bacteria.
Crepitation
Whole-body inflammatory state caused by infection.
Sepsis
Atrophy Hypertrophy Hyperplasia Metaplasia Regeneration
Adaptive responses to cellular injury
Wasting, decrease in size of organ or tissue
Atrophy
Normal decrease in size of an organ or tissue, resulting from conditions such as hormonal changes or senility (skin changes)
Physiological Atrophy
Decrease in the size of an organ or tissue due to disease.
caused by inadequate nutrition (insufficient blood supply), pressure on bones or other organs or disuse, loss of nerve supply, loss of endocrine stimulation.
Pathological Atrophy
The enlargement of an organ or part due to the increase in SIZE of cells composing it.
Hypertrophy
Normal adaptation to increase functional demand (like enlarging of the breast during lactation). The increased size of the cells enlarge the organ or part.
Physiological Hypertrophy
Enlargement of an organ or part due to enlargement of cells as a result of disease.
Pathological Hypertrophy
Absence of disease, increase in the size of an organ or tissue to counteract a structural or functional defect.
Compensatory Hypertrophy
The increased size of an organ or part due to the excessive but regulated increase in the NUMBER of cells.
Hyperplasia
Uterine hyperplasia at puberty is an example of this.
Physiological Hyperplasia
Prostatic hyperplasia that can lead to cancer or adrenal gland hyperplasia are examples of this.
Pathological Hyperplasia
The replacement of one type of tissue into a form that is not normally found there.
- this is normally replaceable, but may lead to cancer.
Metaplasia
The replacement of damaged cells with identical cells (except for nervous tissue)
Regeneration
Restoration of tissue elements under normal condition.
Physiological Regeneration
Replacement of lost tissue as a result of trauma or infection by connective tissue forming scars.
Pathological Regeneration
Cessation of vital activities of the body resulting in cell degeneration, necrosis, atrophy.
can lead to organ failure or system shutdown
results in somatic and cadaveric changes
Somatic Death
no heart sounds, no respiration, facial and eye changes due to lack of nervous stimulation and blood supply (sunken glazed eyes, pale ashen skin, thin nose, prominent lips), complete muscle relaxation.
Somatic Changes
Seen after somatic death
algo mortis, rigor mortis, livor mortis, putrefaction
Cadaveric Changes
Cooling of the body, the body reaches environmental temperature in approximately 24 hours post mortem.
Algor Mortis
Stiffening of the body, starts 4-12 hours after death with the eyelids, jaws, head, limbs; usually lasts 24-36 hours.
Rigor Mortis
“Bluish color”, accumulation of blood in organs leads to dark red discoloration in tissue (blood pooled in capillaries and diffused into tissue due to lack of heart action and gravity); starts 1-6 hours after death.
Livor Mortis
Due to autolysis of dead tissue and bacterial growth, begins in abdomen and affects the brain early.
Putrefaction
