Cellular Reaction to Injury Flashcards by Heather Clark

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

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Cellular Swelling
Degeneration
Infiltration
Necrosis
Atrophy
Hypertrophy
Hyperplasia
Regeneration
Somatic Death

Cellular Changes

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Passive (worsen) cell alteration that may result in:
cellular swelling
degeneration
infiltration

Regressive Cellular Changes

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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

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Loss of color.

Pallor

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Cells become distended.

Turgor

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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)

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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

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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

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Jelly-like appearance of tissues.

E.g., lungs- anthracosis: lung dust disease due to inhalation of coal pigment.

Colloid degeneration

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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)

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Deposit of fat in tissues often due to poisons or diet, occurs mostly in the liver, kidneys, and heart.

Fatty Infiltration

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Coloration caused by deposit, or lack, or colored material in the tissues (increase or decrease in pigment deposit).

Pigmentation infiltration

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Pigment transmitted from outside the body.

Exogenous

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Carotene in blood; resulting in discoloration of the liver and skin.

Carotenemia

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Due to lead poisoning > discoloration to gums, damage to the brain and other internal organs.

Plumbism

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Pigment present inside the body

changes in the retina of the eye
melanosis
albinism
jaundice (icterus= bile pigments)

Endogenous

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Moles, melanomas, freckles

Melanosis

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Calcium deposits (lime salts) in tissue, usually surrounded by bacteria, necrotic cells, mucous, foreign materials.

Calcification

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Kidney stones

Renaliths (renal calculi)

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Bladder stones

Vesical Calculi

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Calcification in the intestines or appendix

Fecaliths

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Calcification in the nose

Rhinoliths

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Gallstones

Choleliths

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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

Cellular Reaction to Injury Flashcards

(69 cards)