Physiology Block 3 Week 17 20 Physiology of Aging Flashcards Preview

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Flashcards in Physiology Block 3 Week 17 20 Physiology of Aging Deck (26)

Are chronology and biology the same?


Young Old = 65-75



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



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



• 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



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



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



• 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



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?


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



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



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)



Fasting glucose does not change with age
Insulin levels don't change with function of age

Body can’t handle glucose challenge

• 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