Chapter 3 Cellular Adaptation, Injury and Death

cellular adaptation

cells adapt to changes in the internal environment

• atrophy

• hypertrophy

• hyperplasia

• metaplasia

• dysplasia

atrophy

cells revert to smaller size in response to decreased workload or adverse environmental conditions; require less oxygen and is a more efficient level of functioning when shrinking occurs

what are the causes of atrophy?

• disuse

• denervation

• loss of endocrine stimulation

• inadequate nutrition

• ischemia or decreased blood flow

hypertrophy

increase in cell size and an increase in the amount of functioning tissue mass; increased workload imposed on body part/ organ

• normal physiologic

• abnormal pathologic

physiologic hypertrophy

increased muscle mass associated w/ exercise

pathologic hypertrophy

result of disease conditions

• adaptive

• compensatory

hyperplasia

increase number of cells; occurs only in tissue/organs which are capable of mitotic division

physiologic hyperplasia

hormonal (stimulation in pregnancy-estrogen stimulation) or compensatory (regeneration of liver after partial hepatectomy)

non-physiologic hyperplasia

ex. benign prostatic hyperplasia

metaplasia

replacement of one cell type by another cell type; occurs in response to chronic inflammation or irritation (substitution of cells that are better able to survive)

dysplasia

cells vary in size, shape and organization; deranged cellular growth within a specific tissue (chronic inflammation of irritation)

intracellular accumulations

buildup of substances that cells cannot immediately use or eliminate; accumulate transiently or permanently (can be harmless or toxic)

cell injury

• physical agents

• radiation

• chemical

• biological agents

• nutritional imbalances

physical agent injury

trauma, mechanical forces, extreme temperatures, electrical

radiation injury

releases free radicals that destroy cells, interruptions of cell replication, genetic mutations

chemical injury

drugs or lead toxicity

biological agent injury

replicates, viruses, parasites, bacteria

nutritional imbalance injury

excess and deficiencies

what are the three mechanisms of cell injury?

1. free radical formation

2. hypoxia/ ATP depletion

3. disruption of calcium homeostasis

free radical injury

• free radicals

• reactive oxygen species (ROS)

• oxidative stress

free radicals

highly reactive chemical species that establish chain reactions that generate them

• damages cell membranes and tissues

  • DAMAGES DNA

reactive oxygen species

oxygen containing molecules; produced endogenously by normal metabolic processes; UV/ ionizing radiation

oxidative stress

generation of ROS exceeds the ability of the body to neutralize and eliminate ROS; implicated in cancer, cardiovascular disease, etc.

hypoxic cell injury

• deprives cell of oxygen; blood cannot deliver enough O2 to cells

  • brain cells dies within 4-6 minutes

  • interrupts generation of ATP

  • cells revert to anaerobic metabolism

  • acute swelling occurs

hypoxia

inadequate amount of oxygen

ischemia

impaired oxygen delivery and impaired removal of metabolic and products such as lactic acid

reversible cell injury

cellular changes due to ischemia are reversible if oxygenation is restored

apoptosis

cell death; designed to remove injured or aged cells (tissue regeneration)

two basic pathways of apoptosis

extrinsic and intrinsic

extrinsic pathway

activation of tumor necrosis factor (TNF) receptors

intrinsic pathway

activated by DNA damage, ROS, hypoxia, activation of p53 protein by DNA damage

necrosis

cell death in an organ or tissue that is still part of living organism

• causes loss of cell membrane integrity and triggers inflammatory process

liquefaction necrosis

cells undergo (soft center of abscess)

coagulation necrosis

transformed to gray firm mass (infarction)

caseous necrosis

cheesy material by infiltration of fatlike substances

gangrene

considerable mass of tissue undergoes necrosis

• dry= shrinks, brown, positive line of demarcation

• wet= cold, pulseless, moist, black, negative line of demarcation

gas gangrene

results from infection; prone to occur in trauma/ open-fractures with debris (bubbles of hydrogen sulfide gas form in muscle; potentially fatal)