2. OBJECTIVES
• Define aging
• Enlist theories of ageing
• Describe physiological changes in different body system related to aging.
• Explain various disease related to aging.
• Discuss prevention and management of health related issues in elderly.
3. INTRODUCTION
• Aging, the normal process of time-related change, begins with
birth & continues throughout life.
• Ageing in humans refers to a multidimensional process
of physical, psychological, and social change.
• Some dimensions of ageing grow and expand over time, while
others decline.
4. INTRODUCTION
Ageing is the progressive and generalized impairment of functions resulting in
the loss of adaptive response to stress and in increasing the risk of age related
disease.
The older adult period is divided into
• Young old – 64 to 74 years
• Middle old – 75 to 84 years
• Old old _ 85 and above
5. THEORIES OF AGEING
• Activity theory (Havighurst)
• Disengagement theory (Elaine Cumming and William Henry)
• Continuity theory (Neugarten)
• Course of human life theory (Charloutte Buhler)
6. THEORIES OF AGEING
• Error theory (Orgel)
• Wear and tear theory (August Weismann)
• Free radical theory of ageing (Dr Denham Harman)
• Molecular cross linkage theory (Johan Bjorksten)
8. • Decrease in lung compliance and chest wall thickness.
• The number of glandular epithelial cells decline
• Reduced production of protective mucous
• Loss of supportive elastin and collagen
• Decrease in the cough reflex
• Frequent bacterial colonization.
• Declined respiratory muscle strength
• Lung volumes and capacities fall.
RESPIRATORY SYSTEM
9. RESPIRATORY SYSTEM
• Change shape of ribcage
• Muscle that supports breathing, the diaphragm, becomes
weakened
• Airways close easily.
• Air sacs to lose their shape and become baggy
• Nerves in your airways that trigger coughing become less
sensitive
• Immune system can get weaker and body is less able to fight lung
infections and other diseases.
10.
11.
12. • Pneumonia
• Tuberculosis
• Bronchial asthma
• Chronic obstructive pulmonary disease
• Lung cancer
MANAGEMENT
• Avoid smoking and do physical excercise
• Administration of oxygen and nebulized drugs
• Instruct a person to use 'pursed lip breathing’
COMMON RESPIRATORY
PROBLEMS
13. • Progressive degeneration of the cardiac structures takes place
• Pumping capacity of the heart is reduced
• Loss of elasticity, fibrotic changes in the valves of the heart, and
infiltration with amyloid.
• Increase in heart mass with aging
• Increase in valvular circumference
• Calcific deposits in the valves leads to aortic valvular stenosis and
mitral valvular insufficiency
CARDIOVASCULAR SYSTEM
14.
15. ELECTRICAL CONDUCTION
SYSTEM OF THE HEART
• Decrease in the number of pacemaker cells in the sinoatrial node with
age.
• Increase in elastic and collagenous tissue in all parts of the conduction
system.
• Fat accumulates around the sinoatrial node
• The conduction time from the bundle of His to the ventricle is not altered.
• Leftward shift of the QRS axis takes place.
• S-T segment becomes flattened, and the amplitude of the T wave
diminishes.
• Maximum cardiac output and aerobic capacity are reduced with age
16. ELECTRICAL CONDUCTION
SYSTEM OF THE HEART
• Decline in maximal heart rate
220 - age = max heart rate
• Max. HR and aerobic capacity are reduced with age due to
changes in the autonomic nervous system, along with age-related
decrease in the number of cells in the sinoatrial node.
• Sarcopenia present a major challenge
• Age-dependent defects of adrenergic signaling
and calcium handling takes place.
17. • Plasma levels of norepinephrine significantly increase with age,
as the result of reduced plasma clearance and increased spillover
from the tissues .
• Reduction of the catecholamine reuptake transporter
• Elevated catecholamine concentrations with aging
• Impair adrenergic responsiveness, resulting in β-
adrenergic desensitization cause chronotropic incompetence
• Reuptake by the myocardial sarcoplasmic reticulum calcium
adenosine triphosphatase (SERCA2a) is another key feature
of cardiomyocyte aging. AF
18. MYOCARDIAL SUBCELLULAR
CHANGES
• Nucleus, containing DNA, becomes larger
• Mitochondria show alteration
• The cytoplasm is marked by fatty infiltration or
degeneration, vacuole formation, and a progressive
accumulation of pigments such as lipofuscin.
19. VASCULAR MODIFICATIONS
• 2 main features:
Generalized endothelial dysfunction
Central arterial stiffness.
• Reduced NO bioavailability
• eNOS uncoupling takes place
• Increased production of the highly pro-oxidant superoxide anion (O2
−) .
20. FACTORS PLAY ROLE IN AGING
• Mitochondrial overproduction of ROS likely contributes to cellular
senescence
• Mitochondrial adaptor p66Shc
• JunD
• Nicotinamide adenine dinucleotide-dependent proteins
termed sirtuins have an established role in human aging
• Age-related loss of SIRT1 correlated with functional deficits,
diminished stress response, reduced capacity for
migration/proliferation, and increased senescence
21. FACTORS PLAY ROLE IN AGING
• SIRT1 blockade also impairs eNOS functionality
• MicroRNA-217, an endogenous SIRT1 inhibitor
• Klotho protein is a key molecules preserving longevity
• Genomic instability takes place with aging
• Chromatin modifications include DNA methylation and post-
translational histone modifications.
22. IMPAIRMENT OF ANGIOGENESIS
• Reduced capillary density, which is associated with microvascular disease,
defective eNOS functionality, and impaired insulin sensitivity
• Senescent endothelial cells have lower proliferative capacity,
decreased telomerase activity, and reduced production of angiogenic growth
factors
• Reduced hypoxia-inducible factor 1α (HIF1α) activity
• The activity of PGC-1α, an emerging transcriptional coactivator that plays an
essential role in hypoxia-driven angiogenesis, also declines with age.
• Dysregulation of angiogenic pathways is associated with an age-dependent
reduction in the number and functionality of stem and progenitor cells (i.e.,
circulating angiogenic cells [CACs] and bone marrow [BM]-derived cells).
23.
24.
25. • Blood vessels become rigid due to decreased elastin and narrowed with
atherosclerosis resulting in increased peripheral vascular resistance.
• Dilation and tortuosity of veins results in decreased venous return.
• The baroreceptors become less sensitive with aging resulting in
orthostatic hypotension.
• Increases in BP with age is a result of changes in total peripheral
resistance.
VASCULAR AGING
26. VASCULAR AGING
• Increases in vessel diameter and vessel wall rigidity
• Factor (TGF)-β activity favors the accumulation of collagen in the aortic wall.
• Peripheral vessels throughout the body become thicker
• Valves also tend to become stiff and incompetent.
• Increased stiffness raises reflected waves and elevates systolic pressure.
Yet diastolic pressure tends to decline with age.
• Diastolic pressure increase.
27. VASCULAR AGING
• Increased systolic pressure with age
• TGF-β, angiotensin II, and the mineralocorticoid aldosterone,
contribute mechanistically to hypertrophy and fibrosis in the
pressure-overloaded LV
• Coronary atherosclerosis also advances with age,
• Remodeling of the myocardial microvasculature.
• Thickening of the tunica media of myocardial arterioles can
further impede LV perfusion and impair vasomotion.
32. • Nerve cell degeneration & atrophy
• Neuronal loss occurs
• Decrease in rate of nerve cell conduction impulses
• Reduced cerebral blood flow
• Decreased sense of balance or uncoordinated
motor response
NERVOUS SYSTEM
33. NERVOUS SYSTEM
• With aging increased activation in some areas and decreased
activation in others
• More brain activity is needed to maintain cognitive performance.
• The neuronal plasma membrane contains redox enzymes that
provide electrons for energy metabolism and recycling of
antioxidants such as coenzyme Q and α-tocopherol.
34. NERVOUS SYSTEM
• The reactive oxygen species (ROS) produced during mitochondrial
oxidative phosphorylation are associated with damage to DNA,
lipids, and proteins.
• The programmed cell death(PCD ) pathways may also be activated
by various insults.
• Loss of astroglial function and astroglial reactivity with age and
contributes to the aging of the brain as well as neurodegenerative
diseases.
35. MORPHOLOGICAL ALTERATIONS IN
AGING BRAIN
• Cerebral volume loss and ventriculomegaly
• Cellular and sub-cellular alterations
• The white matter loss
• Age-related changes in neurons
• Loss of neural circuits and brain plasticity
• Neurofibrillary tangles
36. ETIOGENESIS OF CHANGES OF THE
AGING BRAIN
• Brain is more sensitive to oxidative damage and the increased
oxidative stress has been linked with cognitive impairment
• Oxidative stress can damage DNA replication and inhibit repair through
various complex processes, including telomere shortening
• As the telomere length is partly inheritable.
• The DNA damage increasingly accumulates with age in the brain,
DNA-protein cross links and malondialdehyde (MDA) adducts. MDA is
a highly reactive compound and a marker for oxidative stress and a
measure of free radical activity.
37. ETIOGENESIS OF CHANGES OF THE
AGING BRAIN
• DNA damage may reduce the expression of selectively vulnerable
genes involved in learning, memory and neuronal survival,
initiating a pattern of brain aging that starts early in life
• number of neurotransmitters, as well as their receptors which
exhibit alterations in various regions of the brain with the aging
process
• The failing sex hormones in men with andropause and in women
at menopause, affect cognitive function with aging
38.
39. SUBCLINICAL AND CLINICAL
MANIFESTATIONS OF AGING BRAIN
• Neuropsychological changes
• Changes in orientation
• Changes in attention:
• Changes in memory
• Changes in language
• Cholesteryl ester transfer protein (CETP):
42. THE PROTECTIVE FACTORS AND
MEASURES
• High level of education, staying intellectually engaged in mental
activities and maintaining social and friendship networks, and
underline the importance of regular intellectual exercise.
• Non-specific and delay the aging process in general, like maintaining
a healthy diet, including omega-3 fatty acids, and protective
antioxidants.
• Calorie restriction and CRAN
The concept of calorie restriction with adequate nutrition (CRAN)
protects the brain against aging and neurodegeneration
43. GASTROINTESTINAL SYSTEM
• Oral mucous membrane atrophies takes place.
• Muscles of mastication became weak
• Tooth enamel thins.
• Periodontal disease rate increases.
• Taste buds decrease in number, and saliva production diminishes.
• Effectiveness of the gag reflex lessens, resulting in increased risk
of choking.
• The number of fibres in the olfactory bulb and olfactory receptors
decrease noticeably with age reducing the sense of smell
44.
45. GASTROINTESTINAL SYSTEM
Esophagus
• Presbyesophagus takes place, but the movement of food is not impaired by
these changes.
Stomach
• With age, the stomach lining's capacity to resist damage decreases, which in
turn may increase the risk of peptic ulcer disease.
• The stomach cannot accommodate as much food
• Rate at which the stomach empties food into the small intestine decreases
• Lactase levels decrease which leads to develop lactose intolerance
• Bacterial overgrowth syndrome takes place
46. Pancreas, and gallbladder
• With age, the pancreas decreases in overall weight, and some
tissue is replaced by scarring (fibrosis)
Large intestine and rectum:
• The large intestine does not undergo much change with age.
• The rectum does enlarge somewhat.
GASTROINTESTINAL SYSTEM
47. • Liver volume & weight decreases
• Liver blood flow decreases by 30-40%
• Drugs are no longer inactivated quickly
• The production and flow of bile (involved in fat emulsification)
decreases with ageing. In addition, bile becomes thicker with higher
cholesterol content.
• Gallstones are therefore more likely to form.
HEPATOBILIARY SYSTEM
48. • Hiatus hernia
• Gastro oesophageal reflux
• Peptic ulcer
• Polyps
• Cancers of the GI tract
• Constipation
• Diverticulitis
• Dysphagia
COMMON GI DISORDERS
49. MANAGEMENT
• A diet of small frequent feedings of
bland but nutritious food
• Stay hydrated by drinking a lot of water.
• Judiciously use of medications
• Increase activity
• Lifestyle modification
50. RENAL SYSTEM CHANGES
• Nephrons in the kidneys decrease in number and function.
• Glomerular filtration decreases.
• Blood urea nitrogen increases.
• Sodium-conserving ability diminishes
• .Bladder capacity decreases
• Renal function increases when the older client lies down.
• Bladder and perineal muscles weaken
• Incidence of stress incontinence increases in older females.
• Prostate may enlarge in older males, causing urinary frequency
and dribbling.
51. • Decreased GFR impairing the filtering process
• The nervous system takes longer to respond to sensory stimuli
resulting in decreased sensation to void.
• The capacity of the bladder is decreased to about 250 ml. The
bladder does not empty completely resulting in urinary
retention.
• Blood flow to the kidneys is also reduced as a result of sclerosis
of renal vasculature
RENAL SYSTEM CHANGES
52. FACTORS AFFECTING KIDNEY
• Systemic hypertension
• Lead exposure
• Smoking
• Dyslipidemia
• Atherosclerotic disease
• Presence of inflammatory markers
• Increased levels of advanced glycosylation end products
• Obesity and male gender.
• Recently, a history of one or more episodes of acute kidney injury
53. FACTORS AFFECTING KIDNEY
• The age-related reduction in creatinine clearance (CrCl) is
accompanied by a reduction in the daily urinary creatinine excretion
due to reduced muscle mass
• Increase in glomerular basement membrane (GBM) permeability.
• The incidence of both microalbuminuria and overt proteinuria
increase with advancing age, even in the absence of diabetes,
hypertension or CKD.
54. FACTORS AFFECTING KIDNEY
• The GBM undergoes progressive folding and then thickening.
Eventually, the folded and thickened GBM condenses into hyaline
material with glomerular tuft collapse.
• Degeneration of cortical glomeruli results in atrophy of both afferent and
efferent arterioles, with global sclerosis
• Both diminished glomerular lobulation and sclerosis of glomeruli tend to
reduce the surface area available for filtration, and therefore contribute
to the observed age-related decline in Kf and GFR.
• Reduced cardiac output and systemic hypertension leads to progressive
reduction in renal perfusion and filtration.
• Tubulo-interstitial fibrosis contributes as well.
55. MEDIATORS OF AGE-RELATED
PHYSIOLOGIC CHANGES
• RAS blockade has been shown to slow the progression of age-
related CKD. Total body renin and aldosterone levels fall during
aging, due to decreased renin production and release.
• Prolonged low levels of renin and aldosterone may result in an
exaggerated renal response to these components of the RAS
when present.
• Impaired ability to autoregulate vasoconstrictor vs. Vasodilatory
can lead to a fall in GFR even when the magnitude of the
acquired renal insult is modest
56. MEDIATORS OF AGE-RELATED
PHYSIOLOGIC CHANGES
• Metalloproteases break down matrix, which may help prevent
matrix expansion
• Gender affects the age-related changes in the RAS and NO
systems, as well as metalloprotease activity.
• Estrogen therapy and androgen deprivation are protective against
progression of CKD.
• Increases in cellular oxidative stress that accompany aging result
in endothelial cell dysfunction and changes in vasoactive
mediators resulting in increased atherosclerosis, hypertension
and glomerulosclerosis
57.
58.
59. • Urinary tract infection
• Benign prostatic hypertrophy
• Malignancy of prostate
• Urinary incontinence / retention/ urgency
MANAGEMENT
• Exercises to improve the strength of pelvic musculature
• Bladder retraining
• Increase the fluid intake
COMMON RENAL DISORDERS
60. MUSCULOSKELETAL SYSTEM
• Changes in the muscles, joints, and bones affect the posture and
walk, and lead to weakness and slowed movement.
• Decrease in BMD and sarcopenia takes place
• Vertebrae also lose some of their mineral content, making each bone
thinner.
• The spinal column becomes curved and compressed (packed
together).
• Bone spurs caused by aging and overall use of the spine may also
form on the vertebrae.
• The foot arches become less pronounced, contributing to a slight
loss of height.
61. MUSCULOSKELETAL SYSTEM
• The long bones of the arms and legs are more brittle, but they do
not change length. This makes the arms and legs look longer when
compared with the shortened trunk.
• The joints become stiffer and less flexible.
• Fluid in the joints may decrease.
• The cartilage may begin to rub together and wear away
• Calcification takes place
• Hip and knee joints and finger joints lose cartilage and the bones
thicken slightly
62. • Cartilage becomes thinner.
• May lead to osteoarthritis.
• Additionally, tendons and ligaments become more rigid and brittle
which makes joints more stiffer and limits the range of motion of
joints.
• Lean body mass decreases
• caused by a loss of muscle tissue (atrophy).
MUSCULOSKELETAL SYSTEM
63. MUSCULOSKELETAL SYSTEM
• Lipofuscin (an age-related pigment) and fat are deposited in
muscle tissue.
• The muscle fibers shrink.
• Muscle tissue is replaced more slowly.
• Lost muscle tissue may be replaced with a tough fibrous tissue.
This is most noticeable in the hands, which may look thin and
bony.
• Muscles are less toned and less able to contract
64.
65. • Osteoarthritis
• Rheumatoid arthritis
• Osteoporosis
• Increased susceptibility to fractures
• Gait changes, instability, and loss of balance may lead to falls.
• Some older people have reduced reflexes.
• Fasciculations
• People who are unable to move, may get muscle contractures
• Paresthesias
MUSKULOSKELETAL DISORDERS
66. MANAGEMENT
• Regular exercise program.
• Well balanced, calcium and vitamin D rich diet.
• Identify and correct safety hazards.
• Assist in correct use of assistive devices
67. • Menopause is a normal part of a woman's ageing process. Prior to
menopause, menstrual cycles often become irregular.
• The level of reproductive hormones will eventually decrease.
• The vaginal walls become less elastic, thinner, and less rigid.
REPRODUCTIVE SYSTEM
68.
69. • Uterine prolapse
• Hormonal changes
• Stress incontinence
• Hot flushes
• Atrophic vaginitis
REPRODUCTIVE PROBLEMS IN
FEMALES
70. REPRODUCTIVE PROBLEMS IN
FEMALES
• Dysparenuia
• Decrease breast tissue
• Vaginal yeast infections
• Mood disturbances, headaches, and sleep disturbances are also
common symptoms that occur during menopause.
71. • Men do not experience a major, rapid change in fertility as they age . Instead,
changes occur gradually during a process called andropause.
• Testicular tissue mass decreases and the level of the male sex
hormone testosterone stays the same or decreases very slightly.
• There may be problems with erectile function..
• The testes continue to produce sperm, but the rate of sperm cell production
slows.
MALES
72.
73. • Erectile dysfunction
• BPH
• Prostatitis
• Prostate cancer
• Testicular cancers
• Bladder cancer
REPRODUCTIVE PROBLEMS IN
MALES
74. SKIN
• Wrinkling
• Due to less production of natural oils the skin tends to bruise easily and age spots
occur.
• Reduced ability to regulate body temperature by losing or retaining heat.
• Subcutaneous tissue and elastin fibers diminish, causing skin to become thinner
and less elastic.
• Hyperpigmentation or liver spots.
• Diminished secretions and moisturization.
• Body temperature regulation diminishes.
INTEGUMENTARY SYSTEM
75. INTEGUMENTARY SYSTEM
• Capillary blood flow decreases, resulting in slower wound healing.
• Blood flow decreases, especially to lower extremities.
• Vascular fragility causes senile purpura.
• Cutaneous sensitivity to pressure and temperature diminishes.
• Melanin production decreases, causing gray-white hair.
• Scalp, pubic, and axillary hair thin, and women display increased facial
hair.Nail growth slows, nails become more brittle, and longitudinal nail ridges
form.
76.
77. • Reduced lacrimal gland secretion
• Dry eyes
• Rigid lens and loss of accommodation
• Denaturation of lens proteins leading to cataract
• Retinal degeneration
• Defective accommodation
• Extra sensitivity to glare
• Defective colour vision
EYES
78. EYES
• The lens becomes less pliable and less able to increase its curvature in
order to focus on near objects.
• Accommodation of pupil size decreases, resulting in both decreased
adjustment to changes in lighting and decreased ability to tolerate
glare.Vitreous humor changes in consistency, causing blurred vision.
• Lacrimal glands secrete less fluids, causing dryness and itching.
• Lens yellows, causing distorted color perception.
79.
80. • Cataract
• Glaucoma
• Macular degeneration
• Diabetic retinopathy
MANAGEMENT
• Encourage the use of good lighting in patient rooms.
• Avoid glare whenever possible.
• Encourage annual eye exams
COMMON EYE DISORDERS
81. EARS
• Thickening of tympanic membrane
• Sclerosis of inner ear
• Ear wax build up
• Decreased blood supply to cochlea
• Decline in the number of sensory nerve fibres from the sense organ
• Presbycusis is common
82. • Assess for cerumen impactions.
• Hearing aid is helpful
• Speak clearly & face to face with patient
• Do not shout at people with hearing impairments, but rather use lower tones
of your voice
• Provide written instructions
• Notify the primary care provider of any sudden change in hearing.
• Avoid loud noise in the environment
MANAGEMENT
83. HEALTH RISKS IN OLDER
ADULTS
Sleep
disturbances
Falls
Accidents
84. • Teaching about the adverse effects of medication if they are taking any
• Advising to take precautions like changing position slowly
• Rearranging furniture for a clear pathway
• Providing night light in the bathroom
• Safe use of assistive devices like canes, walkers and wheel chairs
• Regular exercise: Keeping as active as
possible can make falls less likely.
NURSING INTERVENTIONS
85. STRESSORS OF OLD AGE
• Widowhood and death of other significant relatives
• Care giver stress
• Fear of death
• Retirement
• Financial difficulties
• Loss of independence
MENTAL HEALTH
86. • Old age diseases
• Changes in living arrangements
• Social isolation
• Emotional responses to these problems include grief, guilt, loneliness, loss of
meaning in life, lack of motivation, anger, anxiety, feelings of powerlessness,
and depression
MENTAL HEALTH
87. • Depression and suicidal tendencies
• Anxiety disorders
• Post traumatic stress disorder
• Somatoform disorder
• Late life delusional disorders
• Obsessive compulsive disorders
• Personality disorders
• Self neglect
• Alcoholism
• Drug abuse
PSYCHIATRIC DISEASES OF OLD
AGE
88. • Identify the problems as early as possible
• Prompt treatment for the problem
• Never underestimate the problem
• Avoid blaming the victim for the situation
• Psychological support
• Take the help of protective services or legal authorities if needed.
• Involve the family members in care & discuss with them
MANAGEMENT
89. • Assessment of older person’s physical and mental capacity
• Assessment of general quality of care
• Assessment of relationship with the abuser at home or institution
• Assessment of abusers for his or her problems
• Counselling of the abuser
MANAGEMENT
90. • Documentation, liaison and interaction with other
professionals
• Involvement of family members, relatives and
community leaders.
• Institutionalization in old age home or nursing
home if abuse cannot be prevented with the
above means.
MANAGEMENT
95. PAIN ASSESSMENT IN ELDERLY
ICU PATIENTS
For communicable patients:
• Use Patient’s self-reporting of pain using a 1-10 numerical rating scale (NRS) =
Gold standard
For unable to communicate patients:
Use observable behavioral and physiological indicators
Most valid and reliable behavioral pain scales for ICU patients = Behavioral Pain
Scale (BPS) and the Critical‐Care Pain Observation Tool (CPOT)
BPS monitors 3 behavioral domains (facial expression, upper limbs, and
compliance with mechanical ventilation)
CPOT, the most commonly used, is feasible, easy to complete, and simple to
understand and includes evaluation of 4 behaviors (facial expressions, body
movements, muscle tension, and compliance with the ventilator for mechanically
ventilated patients or vocalization for nonintubated patients)
96. PAIN TREATMENT IN ELDERLY ICU
PATIENTS
• Pain medications should be routinely administered in the presence of
significant pain:
NRS > 4
BPS > 5
CPOT > 3
Prior to performing painful invasive procedures
97.
98. AWAKENING TRIAL IN OLDER ADULTS
2013 ICU PAD GUIDELINES
• Minimizing sedative use and maintaining a light level of sedation
• Use either a daily sedative interruption strategy (i.e., SAT), or by
continuously titrating sedatives to maintain a light level of sedation (i.e.,
targeted sedation strategy)
• Goal-directed delivery of psychoactive medications to avoid oversedation, to
promote earlier extubation, and to help the medical team agree on a target
sedation level by using sedation scales i.e., RASS and the Riker sedation-
agitation scale (SAS)
• Daily SATs are the stopping of narcotics (as long as pain is controlled) and
sedatives every day and, if needed, restarting either narcotics or sedatives at
50% of the previous dose and titrating as need
99.
100.
101. CHOICE OF SEDATION IN OLDER
ADULTS
Choice of sedation is crucial to patients’ clinical outcomes
Psychoactive medication administration should be goaldirected
to ensure adequate pain control, anxiolysis, and prevention and
treatment of delirium
Always consider type of drug, dose, titration, and prompt
discontinuation of these medications
102. DELIRIUM IN OLDER ADULTS
Delirium diagnosis identifies the constellation of altered brain
function signs but does not identify the etiology
Delirium diagnosis should prompt further investigation into
potential patient vulnerability factors and precipitating factors
associated with the current illness or hospital course
105. EFFECTS OF DRUG
Absorption
• Elderly patients have been shown to have decreased gastric acid
secretion and splanchnic blood flow which can lead to decreased
absorption of various drugs
• Water-soluble drugs tend to have a smaller distribution volume in
the elderly. This leads to increased concentrations of water
soluble drugs that can lead to toxicity
• In addition, lower serum protein levels in this population lead to
increased free (non-protein bound) concentrations of drugs that
accentuates drug toxicity for a given dose.
106. EFFECTS OF DRUG
Metabolism
Age-related hepatic dysfunction is extremely challenging and
requires careful dose titration and monitoring for adverse effects
to minimize side effects.
Excretion
Renal excretion is decreased (up to 50%) in about two thirds of
elderly subjects, secondary to age-related decline in glomerular
function and the effect of other comorbidities such as
hypertension.
107.
108.
109.
110. • Definition of aging
• Theories of ageing
• Physiological changes in different body system related to aging.
• Various disease related to aging.
• Prevention and management of health related issues in elderly.
SUMMARY
111. • Gerontologic nursing, Annette G Lueckenotte, Mosby publications
• Medial surgical nursing, Phipps.W.J, Monahan.F.D,7th edition, Mosby publications
• CRIME AGAINST ELDERLY:A CRITICAL ANALYSIS BY Shri PARANTAP. K. DAS
,Lok Nayak Jayaprakash Narayan National Institute of Criminology and Forensic
ScienceMinistry of Home Affairs,Government of IndiaNew Delhi
• Demographics of Population Ageing in India, Lekha Subaiya, Dhananjay W. Institute
for Social and Economic Change, Bangalore, United Nations Population Fund, New
Delhi, Institute of Economic Growth, Delhi, December 2011
• health.bih.nic.in/Docs/Guidelines-NPHCE.pdf
• Situational analysis of elderly in India, june 2011
• www.agewellfoundation.org
• www.helpageindia.org
• www.oldagesolutions.org
REFERENCES
Therefore whereas a young adult of 20 can be expected to have a maximal heart rate of 200 bpm (beats per minute), in a 70 year old this will be only 150 bpm, in an 80 year old 140bpm and in a 90 year old 130 bpm
The stiffer the artery, the greater the exposure of the endothelium to hemodynamic load, promoting endothelial activation, inflammation, and damage. Age-related reductions in NO bioavailability described earlier may contribute to impaired arterial distensibility via changes in smooth muscle tone
Endothelial dysfunction includes reduced vasodilatory and antithrombotic properties, with an increase in oxidative stress and inflammatory cytokines favoring atherogenesis and thrombosis, and predisposing to CVD.
Central Illustration. Molecular Hallmarks of CV Aging (Cellular Senescence, Genomic Instability, Chromatin Remodeling, and Mitochondrial Oxidative Stress)
These molecular events are strongly interconnected and contribute to vascular and cardiac dysfunction in elderly patients. A thorough understanding of these complex processes may offer pharmaceutical targets to improve human health during aging. CV = cardiovascular; CVD = cardiovascular disease; eNOS = endothelial nitric oxide synthase; NADPH = nicotinamide adenine dinucleotide phosphate; SIRT1 = sirtuin 1; VSMC = vascular smooth muscle cell
decrease of elasticity of the arterial vessels
increases in vessel diameter and vessel wall rigidity
factor (TGF)-β activity favors the accumulation of collagen in the aortic wall.
activity of various elastases
contribute to depletion of elastin.
Factors that contribute to the increased wall thickening and stiffening in aging include increased collagen, reduced elastin, and calcification.
peripheral vessels throughout the body become thicker
because of an increase in connective tissue and calcium deposits.
valves also tend to become stiff and incompetent. Varicose veins develop
Increased systolic pressure with age increases left ventricular (LV) afterload, a major determinant of myocardial oxygen requirements.
TGF-β, angiotensin II, and the mineralocorticoid aldosterone, contribute mechanistically to hypertrophy and fibrosis in the pressure-overloaded LV
coronary atherosclerosis also advances with age,
remodeling of the myocardial microvasculature.
Thickening of the tunica media of myocardial arterioles can further impede LV perfusion and impair vasomotion.
Figure 3. Features of Age-Related Stem Cell Dysfunction and Approaches to Boost Their Therapeutic Potential in Elderly Patients With CVD
Future strategies to ameliorate the efficiency of autologous transplantation may include ex vivo reprogramming of maladaptive pathways, in situ reprogramming by stimulating cardiomyocyte dedifferentiation, or in situ stimulation of endogenous cardiac stem cells. BM = bone marrow; CSC = cardiac stem cell; CVD = cardiovascular disease; HF = heart failure; MI = myocardial infarction.
The reactive oxygen species (ROS) produced during mitochondrial oxidative phosphorylation are associated with damage to DNA, lipids, and proteins.
The programmed cell death(PCD ) pathways may also be activated by various insults, such as misfolded proteins, reactive oxygen and nitrogen species, mitochondrial-complex inhibition, calcium entry, excitotoxicity, trophic-factor withdrawal, and death receptor activation.
Loss of astroglial function and astroglial reactivity with age and contributes to the aging of the brain as well as neurodegenerative diseases.
the stomach cannot accommodate as much food (because of decreased elasticity)
bacterial overgrowth syndromelead to pain, bloating, and weight loss.
decreased absorption of certain nutrients, such as vitamin B12, iron, and calcium
Impaired ability to autoregulate vasoconstrictor vs. Vasodilatory can lead to a fall in GFR even when the magnitude of the acquired renal insult is modest
Gender affects the age-related changes in the RAS and NO systems, as well as metalloprotease activity. The impact of gender on the renin angiotensin system relates to the interaction between 17β-estradiol (E2) and Ang II. E2 decreases tissue levels and activity of both Ang II and angiotensin II and angiotensin converting enzyme (ACE). Conversely, testosterone tends to increase RAS activity.
estrogen therapy (56) and androgen deprivation are protective against progression of CKD.
androgens may stimulate the renin-angiotensin system and thereby increase sodium retention, resulting in worsening hypertension which may adversely impact CKD progression.
Androgens may increase fibrosis and mesangial matrix production
Muscle tremors and fine movements called fasciculations
Potential mechanisms and therapies for intensive care unit (ICU) delirium. Hypothesized mechanisms for ICU delirium include systemic inflammation, endothelial dysfunction, increased blood–brain barrier (BBB) permeability, and reduced cholinergic control of the inflammatory response that, along with baseline patient vulnerability factors, predispose patients to neuroinflammation and subsequent neuronal injury. Primed and overactivated microglia from these processes may also exacerbate the pathophysiologic changes. Therapeutic agents studied for the prevention or treatment of ICU delirium have targeted these pathways.