Physiology Block 3 Week 17 20 Physiology of Aging Flashcards
Are chronology and biology the same?
No
Young Old = 65-75
Aging
Aging is NOT a disease
occurs at different rate among and within individuals
increases susceptibility to many conditions
does not generally cause symptoms
Arteriosclerosis vs Atherosclerosis
Atherosclerosis–plaque in endothelium
Arteriosclerosis–aging in the blood vessels
Changes in connective tissue
Proteostasis changes, breakdown of elastin–stiff blood vessel
Arteriosclerosis + Aoortic stenosis looks normal in pulse contour
Pseudohypertension
Get artificially high BP reading with arteriosclerosis
–Vessel is so stiff, BP cuff can’t constrict it properly
Osler’s maneuver – pump up cuff above systolic
- -should lose pulse
- -If you can still feel vessel – pseudohypertension
Low responsiveness to catecholamines
o 220 – age is maximum heart rate
o beta receptors are blunted as function of age
Adrenal
- norepinephrine increases
- epinephrine unchanged
- aldosterone decreased
- cortisol unchanged but harder to suppress
Determinants of BP and Changes with Aging:
Peripheral vascular resistance Plasma catecholamines Alpha receptor response Betra receptor response Baroreceptor response Plasma renin Sodium retention/excretion
Peripheral vascular resistance--inc Plasma catecholamines--no change/inc Alpha receptor response--no change Betra receptor response--dec Baroreceptor response--dec Plasma renin--dec Sodium retention/excretion--dec
Altered Baroreceptors
Change with age because arteriosclerosis prevents sensing
Exponential decline in baroreceptor sensitivity
For Angina -> may not compensate as well if you give them nitroglycerin
Review of Systems
Aging and Blood Pressure Blood Vessel Changes Low Renin Activity Low Responsiveness to Catecholamines Altered Baroreceptors Declining Cardiac Output
Hypertension
140/80 is extremely common
between 60-80% of populace over 80 yoa
morbidity greatly increases with high blood pressure more so with older people
Heart and Cardiac Output
Gets bigger with age
LV thickens–due to increased peripheral resistance
CO declines with age - FALSE
–Study included people that have subclinical heart disease
Ejection fraction at rest does not change with age
CO maintained even with exercise and age
Heart rate at rest = no change with age
HR with exercise = dec
–how do they maintain CO = HR x SV
–increased end diastolic volume to maintain CO from atrial contraction
With exercise, maximum CI decreases
Respiratory
TLC does not change with age
Residual volume increases (less recoil)– elastin changes
Vital capacity decreases with age
100 - .3 * age = normal PO2
net PO2 declines with age
VO2 max (max oxygen consumption with exercise) declines due to:
• Loss of lean muscle mass
• Loss of maximum heart rate
• Deconditioning
Aging and Brain
- Might see some slowness in thinking with aging
* Other problems with thinking or judgment are indicative of dementia
Dementia
- Decline in memory
- Decline in other cognitive functions
- Resulting functional loss
• Types o Alzheimer’s o Vascular o Lewy Body o Parkinson’s o Frontotemporal o Alcoholic
• 5.2 million people have dementia
o rising prevalence due to aging population
o greatest cause of loss of independence
Alzheimer’s
Don’t diagnose by imaging, but by history
–Help determine if something else is causing it like tumor or bleed
Amyloid plaques
Neurofibrillary tangles
Amyloid production and accumulation
–oxidation and destruction of neurons leading to cognitive and behavioral changes
Body codes proteases that clips amyloid protein
- -mutations lead to incorrect clipping = insoluble
- -accumulates as plaque, causing inflammation and cell death
ACh made in presynaptic neuron and glial cell
ACh esterase recycles ACh
Alzheimer’s kills pre or postsynaptic cell so ACh doesn’t have anywhere to go
Tx: Drugs that block ACh esterase or enhance BuChE to make more ACh so stays in synaptic cleft longer
PET scan for research, not Dx
Who is at risk for dementia?
o Age o Female gender o Head trauma o Family Hx o Apoliprotein E4 o Down syndrome o Mut. On chrom. 1, 14, 21
Early onset Alzheimer’s disease
o <60 years old
o familial Autosomal dominant pattern w/ high penetrance
o chromosome: 1, 14, 21–incorrect protease cleaving
Last Onset Alzheimer’s Disease
o Chromosome 19
• Apoliproprotein E gene
2 alleles
• APOE 2 – protective against dementia
• APOE 4 – increases risk by 30%
• APOE 3 unknown
What happens to weight and height as get older?
Decreases
IV discs become desiccated (lose water) and compaction of collagen
Potassium is a gamma emitter – can determine total body potassium = lean body mass
–men losing lean mass at more accelerated rate
Decrease in lean mass and cell mass
Increase in body fat
Specific gravity:
- Younger bodies are more dense
- Older ppl have more fat, less body water
Can have same weight, but body is put together differently
Increase lean mass–resistance exercise
Decrease fat–aerobic exercise
Renal
Glomerular count goes down
- -Cortical: Afferent and Efferent Vessels shrivel
- -Juxtomedullary: shunts
Less flow/renal mass
–Hard time vasodilating
Creatinine clearance steadily declines with age
- -creatinine decrease is not clinically significant because creatinine production is also decreasing
- -due to less lean body mass
Cockgroft Gault Equation for Creatinine Clearance:
[(140 – age) x wt (kg)]/ (72 x creatinine (mg/dl) )
–for women multiply by 0.85
Cockgroft Gault Equation for Creatinine Clearance
[(140 – age) x wt (kg)]/ (72 x creatinine (mg/dl) )
–for women multiply by 0.85
Thyroid
Fibrosis of the gland
Cellular infiltration
Follicular atrophy
Basometabolic rate declines as function of age
–Thyroid hormone is driver of basal metabolism
Decline in metabolic rate is an indirect proxy for loss of lean body mass for aging
Thyroid hormone levels do not change with age
Ovarian Changes
Follicular loss
Vessel obliteration
Parenchymal fibrosis with atrophy of corpora lutea and albicania
With menopause lose, estrogen = gonadotropins peak and then start to decline
• Symptoms: o Vulvar atrophy o Atrophy of uterus and vagina o Vasomotor instability o Cessation of menses o Accelerated bone loss
Male Gonad Changes
• Prostate enlargement
• Patchy degeneration of Leydig cells
• Testosterone SECRETION rates peak at 20s and then start to decline
–plasma levels decline in later life
Hypogonadism in 80s (50-90% of men)
Glucose
Fasting glucose does not change with age
Insulin levels don’t change with function of age
However…
Body can’t handle glucose challenge
–hyperglycemia
- Insulin production and excretion is adequate
- Insulin receptors are fine, bind glucose fine
- Something beyond receptor (i.e. glucose transporters) is causing glucose intolerance
• Criteria for diabetes are not age modified
Growth Hormone
Declines as function of age
Can give growth hormone to reverse some anatomy, but doesn’t appear will function any better for geriatric patients
–side effects > reward
