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Geriatric Bioscience: Physical Perspectives of Aging

Geriatric Bioscience: Physical Perspectives of Aging. Andrew Neal Dentino, M.D., F.A.C.P., A.G.S.F., F.A.P.A., F.A.A.H.P.M. Professor and Vice Chairman The Donald W. Reynolds Department of Geriatric Medicine U niversity of Oklahoma Health Sciences Center College of Medicine. WHY GERIATRICS?.

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Geriatric Bioscience: Physical Perspectives of Aging

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  1. Geriatric Bioscience:Physical Perspectives of Aging Andrew Neal Dentino, M.D., F.A.C.P., A.G.S.F., F.A.P.A., F.A.A.H.P.M. Professor and Vice Chairman The Donald W. Reynolds Department of Geriatric Medicine University of Oklahoma Health Sciences Center College of Medicine

  2. WHY GERIATRICS? • 1. The Science • 2. The Sites • 3. The Team • 4. The Fulfillment

  3. WHY GERIATRICS? • “Gerontology” – the study of aging • “Geriatrics” – a medical subspecialty caring for older adults • “Palliative Medicine” – a medical specialty caring for persons near to the end of life

  4. WHY GERIATRICS? • “Hospice and Palliative Medicine” (HPM) – the OUHSC HPM fellowship to begin in 2014 • Open to graduates of residencies in: • anesthesiology, emergency medicine, family medicine, internal medicine, neurology OB/GYN, pediatrics, physical medicine and rehabilitation (PM&R), psychiatry, radiology or surgery

  5. WHY GERIATRICS? • “GeriPal” (ger-i-pal): noun; the care of older persons who inevitably will one day die, and the most comfortable, fulfilling trajectory towards that fruition in the lives of us all - - a “good death”

  6. WHY GERIATRICS? • “GeriPal” • There are five board certified faculty in the OUHSC Reynolds Department of Geriatric Medicine board-certified in both geriatric medicine and hospice and palliative medicine (HPM) to serve as guides, technical experts, helpers and fellow journeyers on this shared journey for our patients and their families

  7. WHY GERIATRICS? • Gerontologic Science • Geriatric Art • Biopsychosocialspiritual

  8. I. Introduction: the “Oldest Old” “ Man’s days shall be a hundred and twenty years.” (Western Asia, author unk.; +/- 2000 B.C.E.) “Oldest Old” Oldest person known reached age 122 - Jeanne Louise Calment (FR)

  9. Maria capovilla (ecuador) – age 116

  10. oldest person alive (115) - JiroemonKimura (Japan)

  11. “Oldest Old” (cont.) • Oldest 5 recorded persons all women; 91 of 100 all-time oldest were women • Male death rates exceed female across life spectrum, in all parts of world • Male stillbirth rates greater than in females

  12. II. Organ System Aging • Rule of thumb: “potential for organ system senescence of 10% per decade after age 30”– Dentino / others • (“1% per year”) • Decreasing degrees of stresses required to cause death in a 100 y/o vs a 50 y/o • ‘Practically any stress’ can kill someone over 100 • Actuarial tables for life expectancies after 85-90 • ?maybe some plateau/protective effect for some (especially women) who’ve survived to 80-85 (for next 10-15 years)

  13. Organ System Aging:General (cont.) • “so little reserves left by age 120, nobody can make it past that” • “(Successful) Aging is coping with fewer and fewer resources, with good will and cheer, until there are no more physical personal reserves (and death ensues)” – Dentino • Barry Reisberg’s longitudinal study of Alzheimer’s patients (“retrogression”)

  14. III: Specific Organ System Changes with Age • 1. Skin 7. Genitourinary • 2. Special Senses 8. Hematopoietic • 3. Cardiac 9. Endocrine • 4. Pulmonary 10. Musculoskeletal • 5. Gastrointestinal 11. Nervous system • 6. Renal

  15. III: Specific Organ System Changes with Age: SKIN

  16. III: Specific Organ System Changes with Age: 1. Skin • A. Epidermis • (Basement membrane) • B. Dermis • C. Subcutis • D. Appendages

  17. 1. Skin Changes with Age: Epidermis • Keratinocytes: • Decreased proliferative potential • decreased wound healing, decreased barrier • Decreased response to environment • Decreased cytokine, Glomerular Filtration and Vit. D production • Melanocytes • Decrease 1-20% per decade • Decreased photoprotection, white hair • Langerhans cells • Decreased up to 40% • Decreased delayed hypersensitivity reactions

  18. 1. Skin Changes with Age: Basement Membrane • Decreased surface area • Decreased epidermal-dermal adhesion, increased blistering

  19. 1. Skin Changes with Age: Dermis • Fibroblasts - decreased collagen and elastin • Decreased tensile strength and elasticity • Blood vessels decrease • Decreases thermoregulation • Decreases response to injury • Mast cells decrease • Decreased immediate hypersensitivity response • Neural elements decrease by 1/3 • Decreased sensation • Increased pain threshold

  20. 1. Skin Changes with Age: Subcutis and Appendages • Subcutaneous fat decreases • Decreases mechanical protection and insulation • Eccrine and Apocrine glands decrease in number and output • Decreases thermoregulation • Sebaceous glands decrease in output • Hair: decreased number and growth rate • Results: infections, rad. damage, CA’s

  21. Special Sense Changes with Age: • Taste: • diminished taste • Smell • food enjoyment • salivary output • dental quality • chewing efficiency • MANY illnesses associated with such changes • Laryngopharyngeal coordination lessens (great increase in swallowing disorders in the elderly)

  22. Special Sense Changes with Age: THE EYE

  23. Special Sense Changes with Age: • Eye: lids thin; intraocular pressure increases; tearing decreases; conjunctiva thins; cornea thickens; lens changes properties • anterior chamber shallows • accommodation lost (age 45) “1st sign of aging”; • pupillary narrowing and retinal cell loss (central rods more than foveal cones) lessens dim light acuity • Vitreous gel liquefies (‘floaters’)

  24. 2. Special Sense Changes with Age: Auditory • Anatomically: • External ear: • Skin and cerumen gland changes • Doesn’t make more wax with age, ear just dryer due to lessened glandular function (hence more accumulation and impaction) • Middle ear: • Otosclerosis (“arthritis of the ear bones”)

  25. 2. Auditory Changes with Age (cont.): Inner ear High frequency loss first (males worse) – sensory presbycusis “Central” (neural) presbycusis, or ‘Central auditory processing disorder’: • “hear ok, just can’t understand speech” • Worse with rapid speech, higher pitch/frequencies, ‘poor phone connections’ (or with increased background noise, as in groups) • Vestibular decline with age (dizziness): • CN VIII (dysequilibrium vs. vertigo)

  26. Body Composition: • Total body mass does not change with age • Skeletal muscle mass declines • Body fat increases

  27. 3. Cardiac Changes with Age: At Rest • Cardiac Output (Cardiac Index): • CI = HR x SV • HR: decreases (10%) • Stroke volume: increases (10%)

  28. 3. Cardiac Changes with Age: At Rest

  29. 3. Cardiac Changes with Age: At Rest • Preload: • EDV:may not change overall as early filling decreases however late filling increases • Afterload: compliance decreases; Reflected waves increase • LV mass increases (compensation) • Ejection fraction unchanged

  30. 3. Cardiac Responses to Stress with Age: • Tonic noradrenergic state increases with age • Myocardial/vascular responses to B-stimulation decreases with age • Decreased heart rate variability with orthostatic testing • Peripheral vascular resistance increases with age (and decreases less with exercise)

  31. 3. Cardiac Responses to Stress with Age: • Treadmill VO2max(weight-adjusted) and peak O2 consumption decrease with age • In exercise, early filling slower (longer diastole), greater EDV, slower HR; afterload increases • But, LV ESV does not greatly increase with exercise, hence CO, EF do not rise (worse with disease)

  32. Lipid changes with age: • Total cholesterol, LDL, and tg’s incr. w/age • LDL in rises in women later in life • See more ‘small, dense apo-B’ LDL with age • ?ApoE relationship • Lp(a) link not as substantiated yet in elders as is in middle-aged CHD • HDL: • Falls in men at puberty • (?increase In late life – survivorship effect) • Doesn’t fall in women until menopause • See more small HDL forms (less atheroprotective) with age too

  33. 4. The Aging Lung

  34. 4. The Aging Lung Spirometry changes with age: Static: • No overall change in TLC with normal aging • RV increases (resp. mm. shorter, less efficient) • MIP decreases: • elastic recoil decreases (MEF decreases; so, should make lungs easier to expand), but, chest wall stiffens with age also • thus, Increased MIP can’t increase TLC in healthy aged • VC decreases (as is diff. between TLC and RV) • FRC slightly increases (due to increased RV) • In smokers though, TLC greatly increases (hyperinflation)

  35. Aging Lung (cont.): Spirometry: Dynamic: • FEV1 decreases (due to decreased mean diameter of small airways with age) about 300 mL/decade • FVC declines (due to increased RV), but less than FEV1 • Therefore FEV1/FVC ratio decreases • Diaphragm strength decreases 25% • If expiratory muscles of abdominal and thoracic walls cannot empty the lungs below the FRC, will reduce VC further • Load on these muscles increases with age because chest wall compliance decreases more than lung tissue compliance does

  36. 4. Aging Lung (cont.): • pO2 decreases on from middle adulthood (increasing RV) • May plateau in 80’s (?survivor effect) • DLCO declines +/- 5% per decade after age 40 • “Asthma vs COPD” • Age is not a predictor of bronchodilator (B-agonist) response in healthy persons • Bronchial hyperreactivity does increase with age though (methacholine challenge)

  37. 5. GI System Aging Changes: • Oropharynx:impaired neuromuscular coordination • dysphagia, choking, aspiration • Esophagus:Altered motility (“presbyesophagus”); proximal (Zenker’s) diverticulae • Stomach:Decreased cytoprotection • Liver:Altered drug metab., Incr. risks of drug interactions • Gall bladder/biliary tree:Increased cholelithiasis • Pancreas:Decreased exocrine secretion • Small bowel:Alt. drug metab., Decr. mucosal immunity • Colon:Delayed transit, Incr. mucosal proliferation • Anus: Incr. connective tissue, Decr. sphincter pressure

  38. 6. Renal System: Age Changes • Anatomic: • Decreased renal size and volume • Increased number of sclerotic glomeruli • Decreased tubular mass • Increased tubular diverticula • Sclerosis or pre- and postglomerular arterioles • Renal Function: • Progressive decrease in GFR • Progressive decrease in RBF • Sluggish response to sodium deprivation • Decreased rate of response to acid load

  39. 6. Renal System: Age Changes • Creatinine clearance = (140 – age) x wt (kg) _________________ (x 0.85 if female) 72 x serum creatinine

  40. 6. Renal System: Age Changes • Creatinine clearance for a perfectly healthy 80 year-old woman who weighs 70 kg and whose serum creatinine is perfectly normal at 1.0 (140 – 80) x 70 kg _________________(x 0.85) 72 x 1.0 = 49.6 ml/ min (Stage 3 CKD)

  41. 6. Renal System: Age Changes • (90 year-old woman = 41 cc/min) • Creatinine clearance for a perfectly healthy 100 year-old woman who weighs 70 kg and whose serum creatinine is perfectly normal at 1.0 (140 – 100) x 70 kg _________________(x 0.85) 72 x 1.0 = 31 ml/ min (Stage 4 CKD, approaching ESRD/dialysis)

  42. 6. Renal System Aging (cont.): Salt Homeostasis • Sodium: • Decreased basal and upright renin and aldosterone concentrations • Delay in reducing urinary sodium excretion in response to decreased salt intake • Increased basal and stimulated ANP levels • Decreased renal response to ANP • Potassium: • Decreased total body potassium content • Decreased mass of tubular cells, limiting the rate of potassium excretion • Increased frequency of clinical condition of hyporeninemic hypoaldosteronism

  43. 6. Renal System Aging (cont.): Water Homeostasis • Increased basal and stimulated vasopressin levels • Decreased renal response to vasopressin • Decreased maximal urinary osmolality • Decreased thirst response to hyperosmolality • Sluggish renal excretion of free water loads

  44. 7. Genitourinary System Changes with Aging: Females: Timing of average age of menopause (as opposed to menarche) remarkably stable last several centuries (50-51 yr.); Smoking only factor seen to hasten it • Age-related losses of number of ova and follicles • Perimenopausal ovarian resistance to FSH, and reductions in levels of 17-B-estradiol (so FSH and LH levels rise) • Shortening of ovulatory cycles around age 45 (follicular phase shortens, not luteal phase), then near menopause menstrual intervals lengthen and anovulatory cycles ensue (before final cessation of menses) • Postmenopausally, major form of estrogen is estrone (especially from adipose) Males: ? climacteric also

  45. 8. Hematopoietic System Aging:

  46. 8. Hematopoietic System Aging: • CFU-S: the totipotent stem cell • Older cells have decreasing self-renewal capacities and increasing differentiation potential • Maintenance of hematopoiesis in long-term bone marrow culture varies inversely with donor age • CFU-S from younger donors better able to repopulate marrow of irradiated mice than old donors • Conversely, young cells will age quicker (when transplanted into) older recipients

  47. 8. Hematopoietic System Aging (cont.): • “Committed” progenitor Stem Cells • BFU-E, CFU-E (erythroid) and GM-CFC (myeloid/macrophage) cell lines: • no age-related reductions in normal animals • Mature erythroid cell lines: • Unchanged with aging: • RBC survival, RBC mass, plasma and RBC iron turnover • What does change is ability to make new cells as quickly as when young • after phlebotomy, after high-altitude stress • after erythropoietin injection

  48. 8. Hematopoietic System Aging (cont.): • PMN’s: • Respiratory burst (maximal stimulation) decreased • Lysozyme secretion during degranulation decreased • Responses to stress and to cytokines decreased • Monocytes(may actually increase with age) • Macrophages:may lessen efficiency with processing/presenting antigens

  49. 8. Hematopoietic System Aging (cont.): • T-cells: • Most of thymus has involuted by time of puberty (both genders) • Reduced T-cell function in elderly • Decr. synthesis of IL-2 receptors and of IL-2 production • Decreased ligand binding (T-cell surface) • Protein kinase C-dependent function changes (2nd messengers)

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