1. Altered Cellular and Tissue Biology
Paula Ruedebusch, ARNP, DNP

2. Cellular Adaptation

3. Cellular Adaptation Physiologic (adaptive) vs. pathogenic Atrophy
Hypertrophy
Hyperplasia
Metaplasia
Dysplasia

4. Atrophy The decrease or shrinkage in cellular size
Entire organ can shrink
Most often in: skeletal muscle, the heart, secondary sex organs and the brain.
Physiologic
Occurs with development
Thymus gland
Pathologic
Caused by: decreased workload, pressure, use, blood supply, nutrition, hormonal stimulation and nervous stimulation.

5. Atrophy

6. Hypertrophy Increase in size of cells and affected organ
Heart and kidney (commonly)
Increase in protein accumulation
Physiologic or pathologic
Physiologic: uterus and mammary glands in pregnancy
Pathologic: hypertrophy of heart secondary to hypertension or diseased valves

7. Hypertrophy

8. Hyperplasia
Increase in the number of cells resulting from an increased rate of cellular division.
Physiologic
Compensatory
Hormonal
Pathologic

9. Hyperplasia

10. Dysplasia
The abnormal changes in size, shape and organization of mature cells.
It is not really adaptive but is related to hyperplasia, and is often called “atypical hyperplasia”
Epithelial tissue, cervix and respiratory tract
Commonly associated with neoplasm or near cancerous cells.
It does NOT MEAN CANCER and may not progress to cancer.
If stimulus is removed, they are often reversible to normal cells

11. Dysplasia

12. Metaplasia
Reversible replacement of one mature cell type by another different cell type.
Reprogramming of stem cells
Example: bronchial metaplasia can be reversed if smoking is stopped.

13. Cellular Adaptation (cont’d)

14. Cellular Injury
Reversible
Irreversible

15. Cellular Injury (cont’d)

16. Cellular Injury Mechanisms
Hypoxic injury
Ischemia
Anoxia
Cellular responses:
Decrease in ATP, causing failure of sodium-potassium pump and sodium-calcium exchange
Cellular swelling
Reperfusion injury

17. Cellular Injury Mechanisms
Chemical injury
Lead
Carbon monoxide
Ethanol
Mercury
Social or street drugs (see table 3-6)

18. Lead A heavy metal that persists in the environment.
Children absorb readily through intestines
If exposed in pregnancy = learning disorders, hyperactivity and attention problems
Lead- based paint
Affects: nervous system, hematopoietic system, and kidneys
Symptoms: neurologic, renal lesions, hemolysis, decreased Hgb synthesis, GI symptoms (nausea, anorexia, weight loss, cramping)

20. Carbon Monoxide
Gasses can be classified according to their ability to asphyxiate or irritate
CO is a toxic asphyxiant
Odorless, colorless and undetectable
Produced – incomplete combustion of fuels (gasoline)
Produces oxygen deprivation
CO’s affinity for hgb is 300 x > than O2.
Prevents O2 binding
Symptoms:
Headache, giddiness, tinnitus, nausea, weakness, vomiting

21. Carbon Monoxide

22. Alcohol (ETOH) Primary choice among mood-altering drugs in U.S.
>10 million chronic alcoholics
Drug and food
Acute intake affects central nervous system (depressant)
Chronic intake causes structural alterations in all organs and tissues
Fatty liver, alcoholic hepatitis, cirrhosis, pancreatitis and gastritis

23. Fetal Alcohol Syndrome
Prenatal exposure to alcohol
Growth retardation, facial anomalies, cognitive impairment and ocular malformations
Amniotic fluid acts as a reservoir for alcohol, prolonging fetal exposure
Disrupts differentiation and growth

24. Unintentional and Intentional Injuries
Blunt force injuries:
Application of mechanical energy to the body resulting in the tearing, shearing, or crushing of tissues
Contusion (direct, blunt compressive force to a muscle) vs. hematoma (localized collection of blood outside the blood vessels)
Abrasion
Laceration
Fractures
Read “Health Alert” on page 75

26. Contusion vs Hematoma

27. Abrasion vs. Laceration

28. Unintentional and Intentional Injuries (cont’d)
Sharp injuries:
Incised wounds – longer than deep
Stab wounds – deeper than long
Puncture wounds
Chopping wounds

29. Unintentional and Intentional Injuries (cont’d)
Gunshot wounds:
Kinetic energy
Entrance wounds:
Look at characteristics to determine weapon and range
Exit wounds
Same appearance regardless of range.
Skin tough to penetrate – it can commonly stop just beneath skin.

30. Unintentional and Intentional Injuries (cont’d)
Asphyxial injuries:
Caused by a failure of cells to receive or use oxygen
Suffocation
Choking asphyxiation
Strangulation
Hanging, ligature, and manual strangulation
Chemical asphyxiants
Cyanide and hydrogen sulfide
Drowning

31. Infectious Injury Pathogenicity of a microorganism
Disease-producing potential
Invasion and destruction
Toxin production
Production of hypersensitivity reactions

32. Manifestations of Cellular Injury (cont’d)

33. Ecchymotic progression

34. Cellular Death Necrosis Apoptosis
Sum of cellular changes after local cell death and the process of cellular autodigestion
Apoptosis
Regulated or programmed cellular death

35. Coagulative Necrosis Coagulative necrosis
Kidneys, heart, and adrenal glands
Protein denaturation

36. Coagulative Necrosis (cont’d)

37. Liquefactive Necrosis
Neurons and glial cells of the brain
Hydrolytic enzymes
Bacterial infection
Staphylococci, streptococci, and Escherichia coli

38. Liquefactive Necrosis (cont’d)

39. Caseous Necrosis Caseous necrosis Tuberculous pulmonary infection
Combination of coagulative and liquefactive necrosis

40. Caseous Necrosis (cont’d)

41. Fat Necrosis Fat necrosis Breast, pancreas, and other abdominal organs
Action of lipases

42. Gangrenous Necrosis Gangrenous necrosis
Death of tissue from severe hypoxic injury
Dry vs. wet gangrene
Signs/Symptoms:
Dull ache, sensation of coldness and pallor of the flesh.
Can sometimes be reversed – vascular surgery

43. Gangrenous Necrosis (cont’d)
Gas gangrene
Clostridium

44. Apoptosis Programmed cellular death Physiologic vs. pathologic
See Figures 3-23, 3-29 and Table 3-12

45. Apoptosis vs. Necrosis

46. Apoptosis vs. Necrosis video

47. Aging vs. Disease

48. Life span and expectancy
Span: years old
Not much variation among populations
Expectancy: average number of years of life remaining at a given age.

49. Degenerative extracellular changes
Extracellular factors that affect aging:
Structural alterations of fascia, tendons, ligaments, bones and joints
Elastin disappears and causes wrinkling
Free radicals are formed

50. Free Radicals

51. Aging Cellular aging Tissue and systemic aging Frailty
Atrophy, decreased function, and loss of cells
Tissue and systemic aging
Progressive stiffness and rigidity
Sarcopenia
Frailty
Mobility, balance, muscle strength, motor activity, cognition, nutrition, endurance, falls, fractures, and bone density

52. Frailty

53. Somatic Death Death of an entire person Postmortem changes:
Algor mortis – post-mortem reduction of temp.
Livor mortis – blood settles in dependent tissues
Rigor mortis – muscle stiffening
Postmortem autolysis – enzymes begin decomposition.

54. Test Yourself!
Which of the following is the most common cause of cellular injury?
Hypoxia
Chemical injury from drugs
Free radical-induced injury
Chemical injury from pollutants

55. Test Yourself!
Which type of necrosis best describes death of a cell from hypoxia, generally as a result of ischemia in the lower extremities?
Fat
Coagulative
Liquefactive
Gangrenous

56. Test Yourself!
Which statement is TRUE with regard to cellular change due to aging?
The cellular changes are reversible.
DNA becomes less susceptible to injurious stimuli.
The cellular changes proceed slowly and in small increments.
Lipid, calcium, and plasma proteins are less likely to be deposited in vessel walls.