cell lecture notes

7/29/2019 Cell Lecture Notes

1/3

ALTERED CELLULAR FUNCTION

CELL INJURY, AGING, & DEATH

Chapter 4

CELL STRUCTURE & FUNCTION

NORMAL PHYSIOLOGY

READ AND REVIEW CHAPTER 3

CELL RESPONSES TO INJURY:

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)


2/3

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 liverLEAD

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 oFe, 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


3/3

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

cell lecture notes

Documents