CELL STRUCTURE & FUNCTION NORMAL PHYSIOLOGY READ AND REVIEW CHAPTER 3 CELL RESPONSES TO INJURY:

ALTERED CELLULAR FUNCTION CELL INJURY, AGING, & DEATH Chapter 4

REVERSIBLE CELL INJURY Hydropic swelling Malfunction of Na+-K+ pumps Suffix megaly (splemomegaly, hepatomegaly) Intracellular accumulations Excess of normal intracellular substances (fat, CHO, glycogen, proteins) Abnormal substances produced by cell (sorbital) Particles cell is unable to degrade (silicon, calcium salts) CELLULAR ADAPTATION Atrophy decreased cell size Hypertrophy increased cell size Hyperplasia increased cell number Metaplasia conversion of one cell type to another Dysplasia disorderly growth IRREVERSIBLE CELL INJURY NECROSIS Coagulative solid (proteins) Liquefactive abscess or cyst (brain) Fat from trauma or pancreatitis (saponification) Caseous clumpy cheese (lung) Gangrene Dry extremities Wet internal organs Gas bubbles of gas in muscle tissue (Clostridium) APOPTOSIS cell suicide, falling off ETIOLOGY OF CELLULAR INJURY: ISCHEMIA & HYPOXIC INJURY Ischemia reduced blood supply The most common cause of hypoxia Hypoxia lack of sufficient oxygen The single most common cause of cellular injury Anoxia total lack of oxygen NUTRITIONAL INJURY DEFICIENCIES Iron Vitamins A night blindness D Rickets in children, Osteomalacia in adults K bleeding disorders B1 Beriberi, Wernicke syndrome, ?Korsakoff B6(pyridoxine) peripheral neuropathy B12 Pernicious anemia C Scurvy Folate megaloblastic anemia, neural tube defects Niacin Pellagra (3 Ds: dementia, dermatitis, diarrhea)

 EXCESSES INFECTIOUS & IMMUNOLOGIC INJURY Direct effects of micro-organism (Polio virus) Indirect effects of triggering immune response (Hepatitis B) Exotoxins (Clostridium botulinum, Clostridium tetani, Cholera, Diphtheria) Endotoxins (Escherichia coli, Klebsiella pneumoniae) CHEMICAL INJURY Lead Carbon monoxide Carbon tetrachloride converted to highly toxic free radical by liver cells that causes liver failure OTC drugs acetaminophen, in high doses, may have similar toxic effects on liver LEAD Significant number of childhood poisonings Lead-based paint, old plumbing, contaminated soil Children absorb lead more readily thru intestines and toxic effects are enhanced if insufficient intake of Fe, Ca++, vit D EFFECTS OF LEAD ON ORGAN SYSTEMS: NERVOUS: Interference with neurotransmitters S/S: hyperactive, convulsions, delirium, paralysis of extremities HEMO: Inhibits enzymes for Hgb synthesis S/S: Anemia, hemolytic RENAL: Lesions cause tubular dysfunction S/S: glycosuria, aminoaciduria, hyperphosphaturia GI: S/S (less severe): nausea, loss of appetite, weight loss, abdominal cramping CARBON MONOXIDE Toxic asphyxiant directly interferes with cellular respiration Odorless, colorless, undetectable Produced by incomplete combustion of fuels such as gasoline Causes hypoxic injury: O2 deprivation Binds with Hgb (carboxyHgb) instead of oxygen S/S: HA, giddiness, tinnitus, N&V, weakness PHYSICAL & MECHANICAL INJURY EXTREMES OF TEMPERATURE FROSTBITE, BURNS ABRUPT CHANGES OF ATMOSPHERIC PRESSURE GAS EMBOLI, THE BENDS MECHANICAL DEFORMATION MILD ABRASION ---> SEVERE LACERATION ELECTRICITY DISRUPTING NEURAL & CARDIAC IMPULSES, BURNS IONIZING RADIATION FREE RADICALS

CELLULAR AGING Atrophy Decreased function Loss of cells Apoptosis active process of cellular self-destruction; dropping off Compensatory mechanisms of hypertrophy and hyperplasia of remaining cells, which can lead to metaplasia, dysplasia, and neoplasia

SOMATIC DEATH Death of the entire person Algor mortis postmortem reduction of body temperature Livor mortis purple discoloration from blood settling in dependent tissues postmortem Rigor mortis muscle stiffening within 6 hours after death