Geriatric

Physiology
Leandro D. Vila, MD, MSc, FPSA

Edmee Martinez, MD
 Aging Population
65
years old increasing (more from developing countries)

Philippines 1969 to 1990 Increase of 146% of 65

Females
higher life expectancy

Factors
that resulted in Aging Population
Increase life expectancy
Declines in Fertility (Last 3 decades of 20th century)

Increases
Life Expectancy
Improved Health Care Services
Better Nutrition
More Effective Therapeutic and Preventive Interventions
Aging Population. . .
E
pidemiologic Shift
From acute illnesses and infectious diseases
CHRONIC AND DEGENERATIVE diseases

2001 leading cause of death in developed

countries
Cardiovascular diseases and Cancer (ranked 1st)
Cerebrovascular and Chronic Obstructive Lung Diseases (2 nd)
Diabetes Mellitus (7th)
Alzheimers Disease (14th)
Aging Population. . .

P
hilippines Statistics (1997)
Cardiovascular disease (1st)
Cerebrovascular disease (2nd)
DM (9th)

Challenge to Health Care:
Provision of Medical and Social
Services
AGING
SENESENCE P
rogressive increase throughout life or after a
given stadium in the likelihood that a given
individual will die during the next succeeding
unit of time. (Comforts The Biology of Senescence)

A
ccumulation of changes responsible for
sequential alterations that accompany
advancing age and the associated progressive
increases in the chance of diseases and death.
(Hartman)
AGING
SENESENCE D
eteriorative changes with time during post-
maturational life that underlie an increasing
vulnerability to challenges thereby decreasing
the ability of the organisms to survive.
(GERONTOLOGISTS)

P
rogressive loss of physiologic processes
I
ncrease probability of death
2 General Characteristics of
the Aging Process

Age - associated disease process
Occur only at an advance age
More prevalent among the aged
e.g. CVA, Parkinsons Disease

A
ge - associated physiologic process
Occur normally in the absence of a disease
 US)
(Stochastic Theories)

Program Theories
Genetic Control Theories
Aging is due to something inside an organisms
control mechanisms that triggers ageing
process

Error Theories
due to non-adaptive homeostatic failures
resulting from random assaults from both
external and internal environment
Theories of Aging. . .
G
enetic Theories
Species Theory of Weisman
Biologic Clock or Pacemaker Theory
Immune Theory of Ageing
E
rror Theories
Somatic Mutation Theory
Free-radical Theory
Rate of Living Theory
Error Catastrophe Theory
Antagonistic Pleitropy Theory
Theories of Aging. . .

G
enetic Theory
1. Species Theory of Weisman (August Weisman
19th C)
Aging is an adaptive characteristic that contributes to
the fitness of human species by removing
reproductively inactive individuals from the population

Genetic control is carried out by limiting the

proliferative capacity of somatic cells

Specific death mechanism designed by natural selection

to eliminate the old to clean the living space and to
free resources for younger generations
Theories of Aging. . .
G
enetic Theory
Species Theory of Weisman (August Weisman
19th C)
Abandoned
Life span NOT individually inherited
If inherited then should be constant for
generations
Some species lives only for specified life span
( NO fruitfly has lived more than 12 months nor a
Lab mouse living more than 2 to 3 years)
Embryo cells divide the most but cells from older
people divide just 4 times
Limited cell division Gerontogenes
Theories of Aging. . .

enetic Theory
2. Biologic Clock / Pacemaker Theory
Best example controlled by small number of
genes

Semiparous organism rapid aging follows

reproduction (eg. Pacific Salmon)

Humans best defined clock female

menstrual cycle (Menarche and Menopause)
Theories of Aging. . .

enetic Theory
3. Immune Theory of Aging
Involution of immune system
Decreases in competency after 20 y/o
Thymus involutes
Leads to critical age-related infections
Theories of Aging. . .
G
enetic Theories
Species Theory of Weisman
Biologic Clock or Pacemaker Theory
Immune Theory of Ageing
E
rror Theories / Stochastic Mechanisms
Somatic Mutation Theory
Free-radical Theory
Rate of Living Theory
Error Catastrophe Theory
Antagonistic Pleitropy Theory
Theories of Aging. . .

rror Theories (Wear and Tear Theories)

Homeostatic Failure Theories
Loss of highly regulated functioning with increasing
age as a result of random effects of environment
Gross deterioration (e.g. erosion of teeth)
Chromosomal abnormalities and structural
abnormalities increase with age
Theories of Aging. . .
E
rror Theories
1. Somatic Mutation Theory
Proposed by Szilard
Aging is due to random hits that inactivate large
chromosomal regions lesser ability to faithfully
replicate genetic material
Differences in DNA repair capacity and in susceptibility
to mutagenesis also influences a species life span
Ionizing radiation accelerates aging (Lindop and Rotblat)
Telomeres shorten / lost with age
Hutchinson-Gilford Syndrome (Childhood Progeria)
Theories of Aging. . .

rror Theories
2. Free Radical Theory
First proposed by Denham Harman (1954)
Agents damage biological molecules with time
Damages provide substrates for aging
physiologic deficits
Splitting of covalent bond Highly reactive
Irreversible damage
In the body from fuel radicals
Exogenous UV light, gamma-rays and metal
ions, etc.
Theories of Aging. . .

rror Theories
Free Radical Theory
Superoxide from O2 most common free radical
Lipids and CHON of cell membranes most vulnerable
Aging production of control to production of free
radicals
catalase, glutathione peroxidase and superoxide dismutase
Vitamins C and E good anti-oxidant agents
Theories of Aging. . .

rror Theories
3. Rate of Living Theory
Metabolic Theory
Life span is related to metabolic rate
Finite amount of metabolic lifetime
Higher metabolic rate Shorter life span
1928 Rate of Energy Expenditure (EE) negative
correlation with life span (Pearl)
EE ROS Prolonged Life Span
1935 Energy Restriction Intake - life span (Clive
Mcay)
Theories of Aging. . .

rror Theories Oxidative Stress

Free Radical Theory of Aging

Rate of Living Theory

Theories of Aging. . .

rror Theories
4. Error CatastropheTheory
Leslie Orgel (1963)
Errors occur during transcription or translation
Error in information transfer at sites other than DNA
Error in synthesis of CHON Error-containing CHON
produced Further errors Defective CHONS
Aging
Theories of Aging. . .

rror Theories
5. Antagonistic Pleitropy Theory
George Williams (1957)
Evolutionary Theory Selection and Mutation
2 Assumptions:
1. A particular gene may affect several traits (pleitropy)
2. Pleitropic effects is opposite or antagonistic at different
ages

Pleitropic effects favorable at young age but

deleterious at old age
Species with younger ages of sexual maturity and more
vigorous reproductive lives tend to have shorter life span.
AGING and . . .
Nervous System
Cardiovascular
System
Gastrointestinal
Tract
Endocrine
System
Urinary System
Respiratory
System
 Aging and
The Nervous
System
Nervous
System Benign Senescent
Forgetfulness

Memory Age associated Memory

and Impairment

Higher
Difficulty of remembering
Cortical names and misplacing of
common objects
Function
s tandard Intelligence
Preserved until 80s
Nervous WAIS vocabulary subtest
System (Semantic knowledge or crystallized
knowledge)

Memory Semantic memory is stable or

improves in time
and
Higher rocedural memory unaffected
Cortical
Function pisodic memory most
sensitive to aging (Tulving)
s
(declines after 70 y/o)
Nervous
Decline in;
System Ability to learn new information
Reaction time

Memory
and Decline in efficiency to
Higher perform complex tasks

Cortical
Function Decline in timed tasks
Declines steadily throughout life
s (after 70 y/o)
Slowing down of speech in time
difficult to understand
Nervous
System anagement:
Memory
Education
and
Higher Exercise
Cortical
General Cognitive
Function abilities
s
Nervous
System

ptical Component
Thickening of Cornea
Visual Less corneal curvature
System Less elastic lens
Presbyopia starts at 15 y/o
and clinically significant at
40 y/o
Increase opacity of lens
(cataract)
Nervous
eceptive Component
System Visual acuity poor esp. in low
contrast and low luminance
Photoreceptors begin to
deteriorate at 20 y/o
Difficulty in contrasting green

Visual from blue but easy to

differentiate red from yellow

System Impairment of pupilloconstriction

Has miotic, poorly reactive pupils
rhodopsin
tear production
visual field
Floaters Vitreous changes
Nervous
Hearing Acuity
System Higher frequency
(Presbycusis)
Starts at 50 y/o
Loss of hair cells for high
Auditory- frequencies
ability to discriminate and
Vestibular understand speech

System
estibular Dysfunction
Unsteadiness,
disequilibrium, vertigo
Somatosensory function
(demyelination)
Nervous 0 60 y/o 50% taste buds
System lost

hreshold to taste substances

Gustatio elevated
Quality-specific (sucrose stable; salt
n and increases)

Olfaction etronasal route influence on

taste decreases compared to
orthonasal route

lfactory threshold

erceived odor intensity

dor naming impaired

Nervous Physical performance
System Functional and structural decline

ait impairment and

Posture deformities
Shuffling with short strides
Motor Altered NM control, impaired
muscle power and degenerative

System joint disease

Females > Males

ecline begins at 50 59 y/o

Denervation > Re-innervation
Atrophy of Type II Muscles
CHON metabolism and blood
flow
Nervous
System
Motor
Expression of DHPR
System
Conduction velocity

Distal motor latency

Ankle jerk (most

common)
Nervous
System
Vibratory sense
Somatic Most commonly affected
sensation
Sensory Vibratory threshold
Vibratory sensitivity
System Mostly on distal LE
Decline starts in the 4th decade

Threshold to other
modalities of sensations
Nervous
System Sleep quality
Developed before 65 y/o
Sleep maintenance
Sleep onset

Sleep
Early morning awakening

Pattern Slow wave sleep

(progressive)

isappearance of Stage 4
sleep

REM and non-REM

Nervous
System

CBF by 24% (8th decade)

Cerebral More on Temporal and Frontal
lobes
Blood Cognitive functioning
Memory processing
Flow
 Aging and
The
Cardiovascular
System
CVS
tructural

Heart iochemical

unctional
 Structural
CVS 1 gm / year male
1.5 gm / year
female
0.55% BW 30 y/o

Heart 0.9% BW 100 y/o

SBP Compensatory
hypertrophy

5 10% diastolic
lumen at rest and
myocardial mass
(eccentric
hypertrophy)
CVS ES afterload due to

in aortic stiffness

Heart
in heart volume in relation
to body SA (30 70 y/o) (cell mass
)

dilated and thickened heart

more oxygen needs
 Biochemical
CVS
heart mass -
collagen

Heart fat cel

infiltration

actin activation
 Lumen of Blood Vessel Blood Vessel
Resistance Wall Thickness Wall Compliance
Vessels

Resting Peripheral
Vascular Resistance

Total Blood
Volume
MAP

Flow to Dependent Circulations

Cerebral Blood Coronary Blood

Renal Blood
Flow Flow
Flow

FUNCTION
 Resting heart rate
CVS
Decrease;
- HR (exercise)
- pacemaker cells
Heart - myocardial
compliance
- systolic function
- diastolic
function
- left ventricular
filling period
 Increase;
CVS - depolarization
phase
- repolarization
phase
Heart - refractory period
- duration of
contraction
- isovolumic
relaxation period
SV
CO
 Aging and
The Gastro-
intestinal System
 MOUTH
COMPONE CHANGE COMPONE CHANG
NT NT E
TEETH DUCTS

MUSCLE BULK INFLAMMATORY

CELLS

TASTE BUDS FIBROFATTY

TISSUES

SCENT BASAL
RECEPTORS SECRETION

SALIVARY STIMULATED
GLANDS SECRETON
ACINI

CONTENT
 ESOPHAG
US COMPONE
COMPONEN CHANG CHANG
T E NT E
STRUCTUR RELAXATION
LATENCY
AL
COMPLIANCE THRESHOLD
MYENTERIC PERISTALSIS
NEURONS PRESSURE
THICKNESS WAVE
VELOCITY
FUNCTION LES BASAL
PRESSURE
AL
UES BASAL
PRESSURE
 ESOPHAG
US COMPONE
COMPONEN CHANG CHANG
T E NT E
STRUCTUR RELAXATION
LATENCY
AL
COMPLIANCE THRESHOLD
MYENTERIC PERISTALSIS
NEURONS PRESSURE
THICKNESS WAVE
VELOCITY
FUNCTION LES BASAL
PRESSURE
AL
UES BASAL
PRESSURE
 STOMACH
COMPONENT CHANGE COMPONENT CHANGE
STRUCTURAL PG Synthesis
Mucosal Cell Basal HCO3
Number Production
Response Injury Stimulated HCO3
Production
Blood Flow Basal
Glycoprotein
Synthesis
FUNCTIONAL Stimulated
Glycoprotein
Synthesis
Basal Acid Intrinsic Factor
Secretion
Stimulated Acid Liquid Emptying
Secretion Time
Pepsin secretion
Solid Emptying
Time
Gastrin levels Electrical
 SMALL
COMPONENT INTESTINES
CHANGE COMPONENT CHANGE

STRUCTURAL Zinc Excretion

Mucosal Cell Calcium Absorption

Number

FUNCTIONAL Iron Absorption

Carbohydrate Vit. B 12 Absorption

Absorption

Liquid Absorption GI Immunity

Protein Absorption Intestinal Transit

Time

Zinc Absorption
 PANCREAS
COMPONENT CHANGE COMPONENT CHANGE

STRUCTURAL FUNCTIONAL

Alveolar Nuclear Amylase

Size Secretion
Alveolar Lipase secretion
Nucleolar
Substance
Acinar Size HCO3 Secretion

Ductal Size Pancreatic Flow

Insulin Levels

Insulin Sensitivity
 LIVER
COMPONENT CHANGES COMPONENT CHANGES

STRUCTURAL FUNCTIONAL

Liver Mass Drug Metabolism

Hepatic Blood Flow Cholesterol Secretion

Size of Hepatocytes Bile Acid Secretion

Number of Binucleate Liver Function Test

Cells
 GALL BLADDER AND BILIARY
TRACT
COMPONE CHANGE COMPONE CHANGE
NT NT

Gall Bladder
Emptying Biliary Duct Size

Sensitivity to Sphincter of Odi

CCK

CCK Production

 COLON

COMPONE CHANGES COMPONE CHANGES

NTS NTS

Mucosal Cell Connective

Number Tissue

Muscle Layer Colonic Transit

Thickness Time N/A

Elastin Content

 RECTU
M
COMPONENT CHANGE COMPONENT CHANGE

STRUCTURAL FUNCTIONAL

Wall Elasticity Urgency Threshold

Internal Sphincter Maximum Anal
Thickness Resting Pressure
Maximum Rectal
Squeeze Pressure
 Aging and
The Endocrine
System
PITUITARY GLAND
rowth Hormone

Somatopause ( GHRH GH IGF
Size Axis)
Decline begins at 30 y/o in men

Patchy Fibrosis

Focal Necrosis rolactin
Quantitative change not biologically

significant
Iron Depositions

Micro-adenoma Formation
CTH
Unchanged Basal Plasma Levels
Peak Cortisol Response Greater and
Sustained

TSH No Change
THYROID GLAND

Fibrosis
Insignificant
Thyroid
Follicular Cellularity and Size can sufficiently
maintain Euthyroid

Microscopic Nodularities state

T4
Metabolic Disposal by 50%

Peripheral Conversion of T4

Incidence of Hyperthyroidism
ADRENAL GLAND
CORTEX
Gross Weight
Cortical Nodule Formation
Fibrosis
Pigment Deposition
Unchanged Plasma Steroids (Diurnal
Secretion is Unchanged)
DHEAS
Adrenopause
activity of 17, 20 Desmolase
Aldosterone Renin System response to
salt restriction
ADRENAL GLAND

MEDULLA
Urinary NE
NE Nocturnal secretion

Plasma Epi Unchanged

Tissue responsiveness (alpha receptors)

Alterations in structure and function of receptors
GLUCOSE
Glucose
Intolerance
Insulin
is Normal or Slightly Increased
Glucose
Absorption is slowed
Hepatic
glucose production is delayed
Insulin
Resistance
Post Receptor Events
Decline in lean body mass
Increase in body fat
Drugs exacerbate resistance
CALCIUM

PTH
GIT absorption
Vitamin D availability

Calcitonin
REPRODUCTIVE
Male Female
Menopause
Reproductive Function
Endocrine Symptoms (Bleeding
Rate of Conception irregularities)
Sexual Interest, Nervous System disturbances
(HA, Mood, Insomnia etc.)
Activity, Capacity
Metabolic Changes
(Impotence, Libido and (Osteoporosis)
Ejaculation) Estrogen and Progesterone
Testosterone FSH (15 X)
basal LH LH (13 X)
basal FSH (greater Uterine Size and Weight
than LH due to inhibin) Vaginal Mucosa shrinks and
opening is narrowed
Aging and
The Urinary
System
 STRUCTURAL FUNCTIONAL

Renal Mass (10 Cortical) RBF

GFR (starts after 30 40 y/o)

A
therosclerotic Vessels

Na+ Reabsorption C
ortex Atrophy of afferent and
efferent vessels K+ Secretion

J
uxtamedullary continuity of asal pH, pCO2 and HCO3 Unaffected
afferent and efferent arterioles

Concentrating ability V
asa Recta unaffected
Total Body Water ( F > M)

hirst Mechanisms Blunted
PCT Number and Length
 Aging and
The Respiratory
System
RESPIRATO ore Pliant

RY SYSTEM oss of Elastic Recoil

LUNGS ncrease in Lung Compliance

Mean Bronchiolar

Diameter
RESPIRATOR
Y MUSCLES Maximal Inspiratory and

Expiratory Pressures
and
Muscle Strength (Atrophy
CHEST
of muscles)
WALL
iaphragm Thickness

unchanged
RESPIRATO TLC a little
RY SYSTEM
RV (Early airway closure Air trapping)

LUNGS RV / TLC
FUNCTION
VC (Muscle weakness and chest wall

stiffness)

FEV1, FVC and FEF 25%-75%

Lung function similar to young heavy smokers.

RESPIRATO
O2 Uptake
RY SYSTEM V/Q Mismatch
Gas Exchange Due to Intra-pleural Pressure collapsing
the base of the lung

Breathing Response to Hypercapnia

and Hypoxemia

Lung Defense
Laryngeal and Cough Reflex

Mucociliary Transport
THANK YOU