1. A LTERED C ELLULAR AND T ISSUE B IOLOGY Paula Ruedebusch, ARNP, DNP

2. 2 C ELLULAR A DAPTATION

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

4. 4 A TROPHY 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. 5 A TROPHY

6. 6 H YPERTROPHY 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. 7 H YPERTROPHY

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

9. 9 H YPERPLASIA

10. 10 D YSPLASIA 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. 11 D YSPLASIA

12. 12 M ETAPLASIA 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. 13 C ELLULAR A DAPTATION ( CONT ’ D )

14. 14 C ELLULAR I NJURY Reversible Irreversible

15. 15 C ELLULAR I NJURY ( CONT ’ D )

16. 16 C ELLULAR I NJURY M ECHANISMS Hypoxic injury Ischemia Anoxia Cellular responses: Decrease in ATP, causing failure of sodium-potassium pump and sodium-calcium exchange Cellular swelling Reperfusion injury

17. 17 C ELLULAR I NJURY M ECHANISMS Chemical injury Lead Carbon monoxide Ethanol Mercury Social or street drugs (see table 3-6)

18. 18 L EAD 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)

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20. 20 C ARBON M ONOXIDE 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 O 2. Prevents O 2 binding Symptoms: Headache, giddiness, tinnitus, nausea, weakness, vomiting

21. 21 C ARBON M ONOXIDE

22. 22 A LCOHOL (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. 23 F ETAL A LCOHOL S YNDROME 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. 24 U NINTENTIONAL AND I NTENTIONAL I NJURIES 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

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26. 26 C ONTUSION VS. H EMATOMA

27. 27 A BRASION VS. L ACERATION

28. 28 U NINTENTIONAL AND I NTENTIONAL I NJURIES ( CONT ’ D ) Sharp injuries: Incised wounds – longer than deep Stab wounds – deeper than long Puncture wounds Chopping wounds

29. 29 U NINTENTIONAL AND I NTENTIONAL I NJURIES ( 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. 30 U NINTENTIONAL AND I NTENTIONAL I NJURIES ( 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. 31 I NFECTIOUS I NJURY Pathogenicity of a microorganism Disease-producing potential Invasion and destruction Toxin production Production of hypersensitivity reactions

32. 32 M ANIFESTATIONS OF C ELLULAR I NJURY ( CONT ’ D )

33. 33 E CCHYMOTIC PROGRESSION

34. 34 C ELLULAR D EATH Necrosis Sum of cellular changes after local cell death and the process of cellular autodigestion Apoptosis Regulated or programmed cellular death

35. 35 C OAGULATIVE N ECROSIS Coagulative necrosis Kidneys, heart, and adrenal glands Protein denaturation

36. 36 C OAGULATIVE N ECROSIS ( CONT ’ D )

37. 37 L IQUEFACTIVE N ECROSIS Liquefactive necrosis Neurons and glial cells of the brain Hydrolytic enzymes Bacterial infection Staphylococci, streptococci, and Escherichia coli

38. 38 L IQUEFACTIVE N ECROSIS ( CONT ’ D )

39. 39 C ASEOUS N ECROSIS Caseous necrosis Tuberculous pulmonary infection Combination of coagulative and liquefactive necrosis

40. 40 C ASEOUS N ECROSIS ( CONT ’ D )

41. 41 F AT N ECROSIS Fat necrosis Breast, pancreas, and other abdominal organs Action of lipases

42. 42 G ANGRENOUS N ECROSIS 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. 43 G ANGRENOUS N ECROSIS ( CONT ’ D ) Gas gangrene Clostridium

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

45. 45 A POPTOSIS VS. N ECROSIS

46. 46 A POPTOSIS VS. N ECROSIS VIDEO https://www.youtube.com/watch?v=7WRkY8q_F3k

47. 47 A GING VS. D ISEASE

48. 48 L IFE SPAN AND EXPECTANCY Span: 80-100 years old Not much variation among populations Expectancy: average number of years of life remaining at a given age.

49. 49 D EGENERATIVE 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. 50 F REE R ADICALS

51. 51 A GING Cellular aging 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. 52 F RAILTY

53. 53 S OMATIC D EATH 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. 54 T EST Y OURSELF ! 1.Which of the following is the most common cause of cellular injury? A.Hypoxia B.Chemical injury from drugs C.Free radical-induced injury D.Chemical injury from pollutants

55. 55 T EST Y OURSELF ! 2.Which type of necrosis best describes death of a cell from hypoxia, generally as a result of ischemia in the lower extremities? A.Fat B.Coagulative C.Liquefactive D.Gangrenous

56. 56 T EST Y OURSELF ! 3.Which statement is TRUE with regard to cellular change due to aging? A.The cellular changes are reversible. B.DNA becomes less susceptible to injurious stimuli. C.The cellular changes proceed slowly and in small increments. D.Lipid, calcium, and plasma proteins are less likely to be deposited in vessel walls.