Changes with Aging

Characteristic Change Other

CV
TPR ↑ Normal ↑ d/t arteriosclerosis
Dz ↑ d/t atherosclerosis
Blood Vessels ↑calcification PseudoHTN
Pulse can feel “normal” d/t offsetting effects of
arteriosclerosis and Ao stenosis
Renin-Angiotensin System ↓ - ∴ ↓ aldosterone ↓ Na+ retention/excretion
Catecholamines ↓ responsiveness Reason why max HR ↓ w/ age
α receptor response ↔ Plasma Norepi ↑, Epi ↔, Cortisol ↔
β receptor response ↓
Baroreceptors ↓ sensitivity
CO ↓
BP ↑ HTN >140/80 common
Heart ↑ weight, ↑ LV thickness, ↑
Dz (vascular, valvular,
myocardial)
Cardiac Index ↓
Rest Exercise
EF ↔ ↓
CO ↔ ↔
HR ↔ ↓
EDV ↔ ↑
Respiration
TLC ↔
VC ↓(?) ↓ w/
FRC ↔
RV ↑ d/t ↓ eleasticity
Areterial PO2 ↓
VO2 Max ↓ Progressively d/t ↓ lean m. mass, ↓ max HR, deconditioning
Body Composition
Weight ↑, then plateau, then ↓
Height ↓ d/t intervertebral disc ∆’s (dessication, etc)
Pathological height loss d/t osteoporosis (usually)
Lean Body Mass (fat-free mass) ↓ ∆ in body composition affects pharmacokinetics
% Body Fat ↑
Renal
Glomeruli ↓ d/t sclerosis, ↑ Basement membrane
Flow ↓ ↓ 10%/decade
Creatinine clearance ↓ 133-(0.64 x age)
Serum Creatinine ↔ Less produced d/t ↓ lean body mass – loss of mass
offsets ↓ clearance
Na+ Retention/Excretion
Vascular Responsiveness (ACh) ↓ Maximally dilated?
Endocrine ↓ Renin-Angiotensin, ↓ Vit.
D, ↔/↓ EPO, more sensitive
to AVP/ADH (hyperresponse
to osmotic stimulus)
 Characteristic Change Other
Thyroid
Anatomical ↑ fibrosis, cellular infiltration,
follicular atrophy
BMR ↓ Linked w/ ↓ lean body mass
Basal O2 Consumption (Whole ↓
Body)
Non-Muscle O2 Consumption ↔
Hormones (tT4, fT4, rT3) Minimal if any ∆
Female Gonads
Anatomical Loss of follicles, Vessel
obliteration, parenchymal
fibrosis, atrophy of corpus
lutea and alicania
Total Gonadotropic Hormones in Slow rise until menopause,
Urine then rapid rise, then decline
Estrogen Cycle throughout life, then
decline post-menopause
Clinical Effects Uterine, vaginal, vulvar d/t ovarian, estrogen loss
atrophy; vasomotor
instability; menopause; ↑
bone loss
Male Gonads
Prostate ↑ size
Leydig Cells, Seminiferous Patchy degeneration
tubules
Testosterone ↑ until post-puberty, then
plateau, slow decline after 35
Glucose
Blood Glucose ↔
Glucose Tolerance ↓ Higher blood glucose 2hr post-meal – some insulin
resistance (post receptor defect)
Andrenal
Cortisol ↔ ↓ Suppression w/ dexamethasone
↑ Response w/ stimulation
DHEA ↓↓
GH ↓