Cellular Injury Flashcards
Cellular injury
-Most diseases begin with cell injury
-Cell unable to maintain homeostasis
-Injured cells may recover (reversible injury) or die (irreversible)
Dependent factors of cellular injury
-Cell being affected: type, nutritional state, level of differentiation, level of susceptibility, adaptive process of the cell
-Injurious agent: type, severity, duration of the stimulus
Mechanism of cell injury
-Hypoxia: lack of oxygen due to ischemia (low blood supply)
1. Vacuoles form in the mitochondria = low ATP
2. Na+/K+ pump of the cell membrane is disturbed: Na+ and Ca2+ into the cell, K+ flows out
3. Water follows = edema
4. Ribosomes detach from E.R. = protein synthesis diminishes
5. Reversible if oxygen is restored; if not = cell death
Free radicals
-Electrically uncharged atoms having an unpaired electron; in an attempt to become stable, they form chemical bonds with other molecules
Where do these free radical come from?
-Absorption of UV radiation, redox reactions (oxygen is reduced to water), enzymatic metabolism of chemicals/drugs
Damaging effects of free radicals
-Lipid peroxidation (H2O2): increases membrane permeability
-Attacks critical proteins (affects ion pumps)
-Fragmenting DNA (affects protein synthesis)
-Damaging mitochondria (increases calcium cytoplasm)
-Certain antioxidants (vitamins s E, C, cysteine, etc) and certain enzymes can combat free radicals
Chemical injury
-Biochemical interaction between a poison (toxin) and cell membrane
-General mechanisms of destruction: direct toxicity or formation of free radicals
-Ex: CCl4, arsenic, cyanide, CO, alcohol, lead, social drugs
Injuries (intentional and unintentional)
-Blunt force, contusion, abrasion, laceration, bone fractures, stab wounds, puncture wounds, gunshot wounds, asphyxial injuries, drowning
Blunt force
-Blows/impact causing tearing, shearing, crushing
Contusion (bruise or hematoma)
-Blow that squeezes soft tissue causing bleeding underneath skin/underlying tissue
Abrasion (scrape)
-Removal of superficial skin
Laceration
-Jagged or irregular tear/rip
Asphyxial injuries
-Suffocation, strangulation, chemical asphyxiants (CO, cyanide)
Infectious injuries
-Caused by any microbial agent that can survive and thrive in the body (bacteria, virus, protozoan, fungus, helminths)
Pathogenicity or virulence depends on
- Ability to invade and destroy cells
- Toxin production
- Production of hypersensitivity reactions in host
- Overall health of host (especially the condition of the immune system)
Cellular injuries
-Cellular swelling due to water infiltration (affects ion pump)
-Abnormal accumulation of lipids and carbohydrates in cells (spleen, liver, CNS); glycogen (diabetes), proteins, pigments (melanin and hemoproteins), calcium, and urate (uric acid)
Clinical manifestations of cellular injury
-Fever; acute inflammatory response
-Increased heart rate; increased metabolism due to fever
-Leukocytosis
-Release of cellular enzymes into extracellular fluid (type of enzyme depends)
Cellular death
-Necrosis: dense clumping of DNA and disruption of plasma and organelle membranes
-Autolysis: cellular self-digestion
-Karyolysis: nuclear dissolution
Types of necrosis
-Coagulative
-Liquefactive
-Caseous
-Fat
-Gangrenous
Coagulative necrosis
-Due to hypoxia
-protein denaturation (albumin hardens)
-Occurs in kidneys, heart, and adrenal glands
Liquefactive necrosis
-Ischemic injury to brain neurons
-Cells become digested by their own enzymes
Caseous necrosis
-Pulmonary infection (usually tuberculosis)
-Dead cells disintegrate but leave cellular debris
Fat necrosis
-Lipases destroy cells
-Breast, pancreas, abdomen
Gangrenous necrosis
-Severe hypoxia
-Bacterial infection
Apoptosis
-Programmed cell death
-Deletion of individual cells by fragmentation into membrane bound particles which are then phagocytized
-Both normal (needed for tissue turnover) and pathologic
Aging
-Normal wear and tear due to accumulation of small microinsults caused by UV light, mechanical insults, and metabolic reactions
-Many theories on aging: genetic and environmental factors, degenerative extracellular changes, changes in cellular control mechanisms
Somatic death
-Death of the entire person
-Postmortem change:
-Complete cessation of breath, circulation
-Falling body temp (algor mortis)
-Gravity causes blood to settle in lowest tissues causing purple color (livor mortis)
-Muscle stiffening starts within 6 hours (rigor mortis); entire body 12-14 hours
-Putrefaction 24-48 hours; then flaccid again
-Postmortem autolysis (microscopic putrefactive changes due to lytic enzymes)
