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By Dr. Doha Rasheedy
Associate Professor of Geriatric Medicine
Basic Geriatrics and internal medicine for physiotherapist
Content
Title Page No.
Chapter 1
 Ageing .....................................................................................………..2
 Age related physiological changes........................................………..5
Chapter 2
 Disease presentations in Elderly…………...........................………..12
 Comprehensive Geriatric Assessment………… .................………..14
 Delirium, Dementia, Depression…………...........................………..17
 Health promotion in elderly…………..................................………..28
 Geriatric pharmacology…………........................................………..29
 Sarcopenia………… ..............................................................………..33
 Frailty………… .....................................................................………..37
 Osteoporosis………… ...........................................................………..42
 Sleep disorders………… .......................................................………..48
Chapter 3
 Chronic respiratory diseases………… ................................………..52
 Hypertension………… ..........................................................………..56
 Orthostatic hypotension…………........................................………..59
 Congestive heart failure…………........................................………..61
 Metabolic syndrome………… ..............................................………..64
 Obesity………… ....................................................................………..67
 Dyslipidemia…………...........................................................………..70
 Diabetes Mellitus…………....................................................………..72
 Constipation………… ...........................................................………..76
 Arthritis………… ..................................................................………..78
 Anemia…………....................................................................………..82
 Chronic liver disease………… .............................................………..84
 Chronic Kidney Disease………… ........................................………..87
Chapter 4
 Immobilization………….......................................................………..94
 Falls………….........................................................................………..102
 Dizziness…………..................................................................………..108
 Fatigue………… ....................................................................………..123
CHAPTER (1): AGEING PROCESS
Definition of Ageing
Types of Ageing
Theories of Ageing
Ageing of different Body systems
1
Ageing Process
Definition of ageing:
 Physiological ageing (normal ageing): is a complex process of progressive reduction in the
function of all body organs. This process may be summarized in the expression
“homeostenosis”. It reflects alteration of organ structure and function with time alone and
in the absence of supervening disease processes.
 Physiological ageing is an inevitable changes can be explained from both biologic and
psychosocial perspectives.
 Processes influencing ageing include gene variations and differences in expression and
environmental factors.
 Age and disease are closely associated phenomena. Secondary ageing then refers to those
aspects of the aged state that are attributable to disease.
Characters of the ageing process:
Aging is characterized by being Universal, Cumulative, Unidirectional, Heterogeneity, Intrinsic,
and Deleterious.
Characters of ageing process
Universal All humans age
Cumulative the effects of aging are irreversible and accumulate over time
Unidirectional For example, a postmenopausal woman cannot become ovulatory again.
Heterogeneity occurs at different rates among individuals and within individuals
Intrinsic Because even under the best environmental conditions an individual ages,
aging is intrinsic to the organism.
Deleterious aging is harmful, resulting in decreased vitality and an increased vulnerability
to disease and environmental stresses
Ageing is different from Cellular senescence is the process by which a cell loses its ability to
divide, grow, and function, ultimately leading to cell death.
Fig 1: Predictors of the Ageing process
2
Theories of ageing (biological)
Fig 2: examples of biological theories of ageing
Cellular senescence/ telomere theory:
 Replicative senescence is a specific type of cellular senescence that ultimately results from
loss of telomeres (specialized structures composed of a repeating DNA sequence and
located at the ends of each linear chromosome).With each cell division, a small amount of
DNA is lost at each chromosome end, resulting in shorter telomeres, altered telomere
structure, and eventual replicative senescence.
 Activation of the telomerase enzyme will regenerate telomeres, prevent replicative
senescence, and immortalize human primary cell cultures
Free Radical theory:
 Free radicals are reactive oxygen species (ROS) are highly reactive molecules that can
damage all sorts of cellular components.
 ROS can originate from exogenous sources such as ultraviolet (UV) and ionizing radiations
or from several intracellular sources: (phagocytosis, fatty acid degradation, drug
detoxification by liver, ATP utilization).
 Toxic accumulation of ROS interfere with cell communication, disturb DNA, RNA and
protein synthesis, lower energy levels and generally impede vital chemical processes.
 To protect against oxidation there are many different types of antioxidants, from vitamins
C and E selenium, CoQ10 and lipoic acid to enzymes such as superoxide dismutase (SOD),
catalase, and glutathione peroxidase. Briefly, antioxidant enzymes are capable of degrading
ROS into inert compounds through a series of chemical reactions.
3
The Neuro-endocrine Theory
 Hypothalamo-pituitary-adrenal (HPA) axis is the master regulator that control the onset
and termination of each life stage. It is also responsible for the maintenance of the internal
“homeostasis” (steady state) despite the continuing changes in the environment.
 During life span, chronic exposure to severe stress from a multitude of physical, biological,
or emotional stimuli may exhaust or weaken the capacity to adapt and lead to the so-called
“diseases of adaptation” and death . Aging would then result from “a decreasing ability to
survive stress.
 Evidence to this theory: the cortisol hormone which is considered to be responsible for
stress is one of the few hormones that increases with age.
The immunosenescence theory:
 The immune system must control and eliminate foreign organisms and substances in the
host body while at the same time recognizing and therefore sparing from destruction the
molecules (cells and tissues) from oneself. In most elderly humans, immunosenescence is
characterized by a decreased resistance to infectious diseases, a decreased protection
against cancer, and an increased failure to recognize self (hence, autoimmune pathology.
The disposable soma
 The somatic cells are only preserved to maintain reproductive functions. After reproduction
somatic cells become disposable.
Antagonistic pleiotropy
 The theory of antagonistic pleiotropy is based on two assumptions. First, it is assumed that
a particular gene may have an effect not on one trait only but on several traits of an
organism (pleiotropy). The second assumption is that these pleiotropic effects may affect
individual fitness in opposite (antagonistic) ways.
 Such genes will be maintained in the population due to their positive effect on reproduction
at young ages despite their negative effects at old age (their negative effects in later life
will look exactly like the aging process)
Error catastrophe
 Gene expression accuracy diminishes with age. This culminates in a higher proportion of
abnormal proteins.
 There is a certain rate of error tolerance of a cell, exceeding which the cell fails in its ability
to sustain and function normally.
 Thus, accumulation of errors in the genomic replication machinery beyond a certain
threshold might lead to erroneous dysregulation of the protein synthesis, folding and
expression mechanisms which ultimately might bring about deterioration in the
functionality of the cell.
4
Types of Ageing:
Chronological The number of years a person has lived since birth.
Biological age changes in physical structures and functions that affect either ability to
survive or appearance
Social How a person perceives the aging process and how it relates to the society
in which they live
Psychological age changes in mental processes and behavior
The elderly are special population with special needs:
 Physiological Changes in the Elderly (Normal Aging is not a disease)
 Multiple comorbidities and multiple medications: The incidence of chronic diseases
increases with ageing e.g. dementia, Parkinsonism, stroke, heart diseases leading to
polypharmacy.
 Overlapping Variables (physiological, social, psychological, environmental variables)
&multiple diseases): heterogeneous Population: Need for Individualized Treatment:
 Atypical presentations of diseases
 They need different assessment approach (see comprehensive geriatric assessment)
through Multidimensional, Interdisciplinary, Geriatric team
 The goal of elderly care is maintaining function &quality of life:" To add life to years
NOT only years to life
Age related physiological changes:
 Aging and disease are not synonymous. Although the aging process makes individuals
more vulnerable to illness and disease, pathology is not inevitable with age. Aging alone
generally does not cause symptoms.
 The major age-related biologic change is a diminished reserve capacity and the inability to
maintain homeostasis in the face of stressors such as a disease or adverse environmental
factors such as excessive heat.
Body system Physiological change Clinical implications
General body
composition
The percent of body water (TBW)
decreases with aging
↑risk of dehydration
Pharmacokinetic effect
Lean body mass decreases because of
muscle loss
Slower gait speed, weaker hand grip
Pharmacokinetic effect
Increased percent of body fat (until
around 70, then decreases)
Pharmacokinetic effect
Decreased bone mass
Changes in
Resting Energy
Rate
Decreased Basal Metabolic Rate
Vision loss of rods and cones ↓ light sensitivity, color perception,
dark adaptation, night vision (stressor)
5
The lens becomes denser, thicker, and
less elastic.
↑ risk of cataract
Hearing loss of hair cells in the organ or Corti
and loss of cochlear nerve cells
Difficulty in speech discrimination esp.
in noisy environments (stressor).
↑ difficulty to determine the source of
sound
Smell and taste ↓the number of taste buds and
olfactory receptors.
Smell is more affected than taste with
age and declines rapidly after age 50
↑ risk of malnutrition
↓ quality of life
Difficult compliance on therapeutic diets
Immunity Thymic involution and attenuated T-
cell-mediated
Immunity, ↓T cells
lead to reactivation of quiescent
infections, such as TB and varicella.
decline in delayed-type skin-
hypersensitivity reactions to injected
antigens (anergy) in many frail aged
subjects
↓production of antibody by B cells ↑ risk of infection.
↓efficacy of vaccination
Autoantibodies occur more frequently
(e.g. antiphospholipid
antibodies) and are associated
with vascular disease
Their significance in older people is
uncertain.
Cardiovascular
system
Loss of cardiac myocytes secondary to
apoptosis, with compensatory
hypertrophy of remaining cells.
Changes in stroke volume and diastolic
function
Accumulation of intracellular lipofuscin
and extracellular amyloid.
Increased intercellular collagen.
leading to reduced LV diastolic
compliance
Loss of pacemaker cells Increase risk of sick sinus syndrome
Patchy fibrosis of the conduction
system
Increase risk of heart block
Reduced baroreceptor sensitivity Increased risk of orthostatic hypotension.
↓ β-adrenergic receptors number &
sensitivity
Lead to altered response to beta blockers
Beta-adrenergic-mediated vasodilatation
decreased while Alpha-adrenergic-
mediated vasoconstriction unchanged
leading to hypertension
Increased vascular stiffness Increases risk of systemic hypertension
Respiratory
system
Calcification of the intercostal
cartilages; arthritis of the costo-
vertebral joints
Rigidity and stiffness of the wall increases
and chest wall compliance
decreases
Gradual atrophy of intercostal
muscles (loss of muscle mass)
Greater contribution from
diaphragmatic and abdominal muscles
and may lead to diaphragmatic fatigue
The cilia beat decreases with
age and there is a reduction in
number of cilia
Reduces clearance of debris and
pathogens
Increases chance of infection
6
Thickening of the alveolar
basement membrane
Decrease gas-diffusing capabilities,
increase in ventilation/perfusion
heterogeneity. Arterial oxygenation
declines.
Ventilation control Diminishes Diminishes response to hypercapnia and
hypoxia
Endocrine
system
Marked decrease in
dehydroepiandrosterone (DHEA)
Decreased free and bioavailable
testosterone
Decreased production of vitamin D by
skin and activation in kidney
Decreased GH, IGF1
Increased cortisol level
Increased risk of frailty, sarcopenia, and
osteoporosis.
↓ Aldosterone secretion Increased risk of Orthostatic hypotension
Musclo-skeletal
system
Muscle
Marked decrease in muscle mass (sarcopenia) due to loss of muscle fibers
Decreased myosin heavy chain synthesis
Decreased innervation, increased number of myofibrils per motor unit
Infiltration of fat into muscle bundles
Bone
Slower healing of fractures
Decreasing bone mass in men and women, both trabecular and cortical bone
Decreased osteoblast bone formation
Joints
Disordered cartilage matrix
Modified proteoglycans and glycosaminoglycans
Gastrointestinal ↓ Saliva production ↑ Oral infections, ↑ Gum disease
Decreased liver size and blood flow
Hepatocytes accumulate secondary
lysosomes, residual bodies, and
lipofuscin
Impaired clearance by liver of drugs that
require extensive phase I metabolism
Reduced inducibility of liver mixed-
function oxidase enzymes Mild decrease
in bilirubin
Mild decrease in stomach acid
production, probably due to
nonautoimmune loss of parietal cells
Impaired response to gastric mucosal
injury
Decreased mucus secreting cells
Slowed gastric emptying Prolonged gastric distention,↑
Postprandial satiety
Decreased pancreatic mass and
enzymatic reserves
Insulin resistance
Decrease in effective colonic
contractions
Increased risk of constipation
7
↓ Calcium absorption ↑ Bone loss
Skin Epidermal turnover rates decrease by
30% to 50% by the age of 70
Rougher skin with decreased barrier
function, delayed wound healing.
The dermal- epidermal junction fattens Resulting in decreased contact between
the two layers. As a result the two layers
may easily separate, making older skin
more likely to tear and blister.
Basal and peak levels of cutaneous
blood flow are reduced by about 60%
compromised vascular responsiveness
during injury or infection
Collagen synthesis decreases and
degradation increases
Loss of the connective tissue matrix and
impaired wound healing.
Elastic fibers decrease in number and
size
decreased skin elasticity
Subcutaneous fat decreases with age Decreasing its ability to protect deeper
structures from injury.
Decreased Langerhans cells Increased risk of infections
Hematologic Bone marrow reserves decreased Failure to response to high demand e.g
infections , hemorrhage, hemolysis
Kidney ↓ Kidney size, mass, and number of
functional glomeruli
Decreased creatinine clearance and GFR
10 ml/decade affecting drug excretion
↓ Number/length of functional
renal tubules
↓ Concentrating/diluting capacity, ↑
Fluid and electrolyte abnormalities
↓ Renal blood vessel elasticity ↓ Renal blood flow
↓ Vitamin D activation Vitamin D deficiency
Decreased serum renin and
aldosterone
Increased risk of Volume depletion and
hypokalemia
Peripheral
nervous system
Loss of spinal motor neurons
Decreased size of large myelinated
fibers
Increased heterogeneity of axon
myelin sheaths
Decreased vibratory sensation, especially
in feet
Decreased thermal sensitivity (warm–
cool)
Decreased sensory nerve action potential
amplitude
Central nervous
system
1. Small decrease in brain mass, Nonrandom
loss of neurons to modest extents
2. Decreased brain blood flow and impaired
autoregulation of perfusion
3. Decreased density of dendritic
connections, synapses.
4. Increased numbers of scattered
neurofibrillary tangles and senile plaques
5. Decreased myelin and total brain lipid
6. Altered neurotransmitters, including
dopamine and serotonin
Decline in fluid intelligence
Slowed central processing
and reaction time
Affected working memory,
divided attention
8
9
QUIZ 1:
1. Age-related changes in the cardiovascular system among older adults include:
A. Adrenergic receptors number-Decreased βA.
B. Decreased systolic blood pressure
C. Increased maximal heart rate during exercise
D. Increased β-adrenergic receptors sensitivity
E. Increased cardiac output under stress
2. Age related changes in vision include
A. Increase color Sensitivity
B. Decrease dark Adaptation
C. Decrease intraocular pressure
D. Increase risk of iridocyclitis
E. Decreased risk of cataract
3. The following can cause decrease appetite among elderly
A. Decrease taste sensation
B. Decrease intestinal motility
C. Loss of teeth
D. Cognitive impairment
4. Elderly are more prone to develop infections because
A. Decrease T cell immunity
B. Increased environmental factors
C. Cognitive impairment
D. Iron deficiency Anemia
5. Elderly develop sarcopenia due to all of the following except
A. Decreased myosin heavy chain synthesis
B. Decreased innervation, increased number of myofibrils per motor unit
C. Infiltration of fat into muscle bundles
D. Excess mitochondrial ATP production
10
CHAPTER (2): GERIATRIC MEDICINE
Disease presentations in Elderly
Comprehensive Geriatric Assessment
Delirium, Dementia, Depression
Health promotion in elderly
Geriatric pharmacology
Sarcopenia
Frailty
Osteoporosis
Sleep disorders
11
The definition of an atypical presentation of illness is: when an older adult presents with a disease
state that is missing some of the traditional core features of the illness usually seen in younger
patients.
1. Examples for altered presentations of diseases
 Dwindles (Functional decline)
 Weakness
 Falls
 Immobility
 Incontinence
 Cognitive Change
 Mood Change
2. Examples for non-specific presentations of diseases: e.g. Fatigue which can be a
presentation of any of the following:
Organic conditions
Cardiopulmonary (heart failure, COPD, IPF)
Neurological (MS, Parkinsonism)
metabolic/ (DM, hypothyroidism
toxic (chronic lead exposure)
infections (HCV, HBV, HIV)
Deficiency states (Vitamin D deficiency)
neoplasm
Psychogenic: depression
Drugs: beta-blockers, diuretics, chemotherapy
3. Examples for silent presentations of diseases:
During preoperative assessment, the presence of ECG changes suggestive of previous
myocardial infarction in elderly patient without history suggesting coronary ischemia.
Osteoporosis is usually silent until fracture occurs.
Prevalence of atypical presentations in elderly:
Atypical presentations were found in approximately 20% of elderly patients in the
Emergency Department (ED), with (35%) of older adults with infectious diseases presented
atypically.
12
Silent MI in elderly, detected incidentally on electrocardiogram (ECG) is high, ranging
between 38% and 60%.
Consequences of atypical presentations in elderly:
Delayed diagnosis, misdiagnosis, and mismanagement with increased morbidity.
Presentations of ischemic heart disease in elderly:
Typical Pain is usually substernal chest pain/discomfort with exercise, relief by
nitroglycerin or rest
Non specific Fatigue , Shortness of breath
silent Minimal or no chest pain, no shortness of breath or acute confusion, silent ECG
or Echo findings
Altered Acute confusion
Syncope
Acute functional decline
Attack of Epigastric pain
Attacks of back pain
Attacks of jaw pain
Attacks of neck pain
Presentation of Pneumonia
Typical Productive cough of purulent sputum
The temperature may rise to 38.9°–39.4°C
Non specific Minimal cough, no sputum production, no fever
No leucocytosis
May appear tired or confused
Altered Dwindles, delirium
Causes of atypical presentations in elderly:
• The aging process: fever is usually absent in elderly due to lower basal body temperature,
thermoregulatory center aging, lower skeletal muscle mass
• Multiple Co-morbidities: presence of severe osteoarthritis of the knee with reduced physical
performance may delay the presentations of heart failure and peripheral arterial disease until
symptoms are present during minimal activity or even at rest.
• Poly-pharmacy: (use of beta blockers mask tachycardia in anemia or infections)
Remember: New onset functional decline is a manifestation of an acute illness
in elderly.
13
Comprehensive Geriatric Assessment
Comprehensive geriatric assessment (CGA) is a multidimensional, interdisciplinary diagnostic
process to determine the medical, psychological, and functional capabilities of a frail elderly
person in order to develop a coordinated and integrated plan for treatment and long-term follow
up.
Interdisciplinary Team - Team Members Overview
 Nurse
 Physician trained in Geriatrics
 Dietitian
 Physical Therapist
 Social Worker
 Patient, Family members, caregiver
 Psychologist
 Speech-Language specialist
 Audiologist
 Occupational Therapist
Assessment Domains
Medical (Medical illnesses, surgical history, medications, nutrition, dentition, Vision, Hearing, Pain,
impotence, Sleep, health promotion, Geriatric giants: Urinary incontinence,, Frailty)
Psychiatric (Cognitive status, Emotional status)
Functional status (Activities of daily living ADLs, Instrumental activities of daily living IADLs)
Physical (Balance and gait, Falls)
Environmental (Social, financial status, Environmental hazards).
Geriatric depression scale – 15items
1
-
.‫دلوقتى‬ ‫حياتك‬ ‫عن‬ ‫راضى‬ ‫انت‬
2
-
.‫واهتماماتك‬ ‫نشاطاتك‬ ‫من‬ ‫كثير‬ ‫قللت‬ ‫انت‬
3
-
.‫فاضية‬ ‫حياتك‬ ‫ان‬ ‫حاسس‬ ‫انت‬
4
-
.‫وزهقان‬ ‫متضايق‬ ‫انك‬ ‫بتحس‬ ‫الغالب‬ ‫فى‬
5
-
‫الغالب‬ ‫فى‬
.‫عالية‬ ‫بتكون‬ ‫معنوياتك‬
6
-
.‫تحصلك‬ ‫ها‬ ‫وحشة‬ ‫حاجة‬ ‫ان‬ ‫خايف‬ ‫انت‬
7
-
.‫مبسوط‬ ‫انك‬ ‫بتحس‬ ‫الغالب‬ ‫فى‬
8
-
.‫الحيلة‬ ‫قليل‬ ‫انك‬ ‫بتحس‬ ‫الغالب‬ ‫فى‬
9
-
.‫جديدة‬ ‫حاجات‬ ‫تعمل‬ ‫تخرج‬ ‫انك‬ ‫عن‬ ‫البيت‬ ‫فى‬ ‫تقعد‬ ‫بتحب‬
10
-
.‫االخرين‬ ‫من‬ ‫اكثر‬ ‫الذاكرة‬ ‫فى‬ ‫مشاكل‬ ‫عندك‬ ‫انك‬ ‫بتحس‬ ‫انت‬
11
-
.‫عايش‬ ‫لسة‬ ‫انك‬ ‫حلوة‬ ‫حاجة‬ ‫دى‬ ‫ان‬ ‫بتعتقد‬ ‫انت‬
12
-
.‫ليك‬ ‫مناسبة‬ ‫مش‬ ‫بطريقة‬ ‫الحياة‬ ‫عايش‬ ‫انك‬ ‫شايف‬ ‫انت‬
13
-
.‫ونشاط‬ ‫حيوية‬ ‫عندك‬ ‫ان‬ ‫حاسس‬ ‫انت‬
14
-
.‫منها‬ ‫ميئوس‬ ‫دى‬ ‫حالتك‬ ‫ان‬ ‫حاسس‬ ‫انت‬
15
-
‫اغلب‬ ‫ان‬ ‫حاسس‬ ‫انت‬
‫منك‬ ‫احسن‬ ‫حواليك‬ ‫اللى‬ ‫الناس‬
14
Mental State Examination (MMSE)
-
Mini
‫المختصر‬ ‫العقلية‬ ‫الحالة‬ ‫فحص‬
1
-
( )‫(االهتداء‬ ‫التوجه‬
10
)
‫إيه؟‬ ‫فصل‬ ‫فى‬ ‫احنا‬ ‫لى‬ ‫تقولى‬ ‫تقدر‬ ‫؟‬ ‫كام‬ ‫سنة‬ ‫احنا‬ ‫لى‬ ‫تقول‬ ‫تقدر‬
‫إيه؟‬ ‫شهر‬ ‫فى‬ ‫احنا‬ ‫لى‬ ‫تقول‬ ‫تقدر‬
‫إيه؟‬ ‫النهاردة‬ ‫لى‬ ‫تقول‬ ‫تقدر‬
‫؟‬ ‫النهاردة‬ ‫تاريخ‬ ‫لى‬ ‫تقول‬ ‫تقدر‬
‫؟‬ ‫دلوقت‬ ‫فين‬ ‫احنا‬
‫؟‬ ‫الكام‬ ‫الدور‬ ‫فى‬ ‫احنا‬
‫؟‬ ‫إيه‬ ‫حى‬ ‫تتبع‬ ‫أنت‬
‫؟‬ ‫إيه‬ ‫محافظة‬ ‫تتبع‬ ‫أنت‬
‫فى‬ ‫احنا‬
‫؟‬ ‫إيه‬ ‫جمهورية‬
2
-
( : ‫المعلومات‬ ‫تسجيل‬
3
)
‫قولك‬ ‫ها‬
3
‫واحفظهم‬ ‫ورائى‬ ‫وكررهم‬ ‫كلمات‬
‫كورة‬
-
‫شجرة‬
-
‫كرسى‬
3
-
( : ‫والحساب‬ ‫االنتباه‬
5
)
‫من‬ ‫أكثر‬
5
: ‫دراسة‬ ‫سنوات‬
‫اطرح‬
7
‫من‬
100
‫منه‬ ‫اطرح‬ ‫والباقى‬
7
‫بعد‬ ‫وتوقف‬ ‫نازل‬ ‫وأنت‬
5
( ‫مرات‬
93
-
86
-
79
-
72
-
65
)
‫من‬ ‫أقل‬
5
‫د‬ ‫سنوات‬
: ‫راسة‬
‫اطرح‬
3
‫من‬
20
‫منه‬ ‫اطرح‬ ‫والباقى‬
3
‫بعد‬ ‫وتوقف‬
5
‫مرات‬
: ‫قادر‬ ‫غير‬ ‫كان‬ ‫إذا‬
‫بالعكس‬ ‫األسبوع‬ ‫أيام‬ ‫قول‬
4
-
( : ‫الذاكرة‬ ‫استرجاع‬
3
)
‫الـ‬ ‫لى‬ ‫قول‬
3
‫كده‬ ‫قبل‬ ‫قولناهم‬ ‫اللى‬ ‫كلمات‬
‫كورة‬
-
‫شجرة‬
-
‫كرسى‬
5
-
: ‫اللغـة‬
)‫األشياء‬ ‫هذه‬ ‫عن‬ ‫واسأل‬ ‫والساعة‬ ‫القلم‬ ‫على‬ ‫(شاور‬ ‫ده‬ ‫إيه‬
(
2
)
( ‫عاجبانى‬ ‫حاجة‬ ‫وال‬ ‫والمانى‬ ‫والكانى‬ ‫ورائى‬ ‫كرر‬
1
)
‫من‬ ‫مكون‬ ‫ألمر‬ ‫المريض‬ ‫استجابة‬
3
( ‫حركات‬
3
)
.‫األرض‬ ‫على‬ ‫وحطها‬ ‫االثنين‬ ‫بإيديك‬ ‫اثنين‬ ‫وطبقها‬ ‫اليمين‬ ‫بإيدك‬ ‫دى‬ ‫الورقة‬ ‫امسك‬
‫نقو‬ ‫أو‬ ‫ونفذه‬ ‫المكتوب‬ ‫اقرأ‬
( )‫عينك‬ ‫(غمض‬ ‫له‬ ‫ل‬
1
)
( .‫مفيدة‬ ‫جملة‬ ‫قل‬ ‫أو‬ ‫معنى‬ ‫لها‬ ‫مفيدة‬ ‫جملة‬ ‫اكتب‬
1
)
( : ‫الشكل‬ ‫هذا‬ ‫ارسم‬
1
)
15
‫اليومية‬ ‫األنشطة‬ ‫تأدية‬ ‫على‬ ‫القدرة‬ ‫قياس‬
ADL
‫بمفرده‬
‫بمساعدة‬
‫كاملة‬ ‫بمساعدة‬
:‫االستحمام‬ ‫تستطيع‬ ‫هل‬
:‫وخلعها‬ ‫مالبسك‬ ‫ارتداء‬ ‫تستطيع‬ ‫هل‬
‫التبول‬ ‫تستطيع‬ ‫هل‬
:‫والتبرز‬
‫االنتق‬ ‫تستطيع‬ ‫هل‬
:‫الكرســـى‬ ‫او‬ ‫السرير‬ ‫والى‬ ‫من‬ ‫ال‬
:‫والتبرز‬ ‫التبول‬ ‫فى‬ ‫التحكم‬ ‫تستطيع‬ ‫هل‬
:‫والشراب‬ ‫الطعام‬ ‫تناول‬ ‫تستطيع‬ ‫هل‬
IADL
‫بمفرده‬
‫بمساعدة‬
‫كاملة‬ ‫بمساعدة‬
1
-
‫التليفون؟‬ ‫استعمال‬ ‫تستطيع‬ ‫هل‬
2
-
‫طعامك؟‬ ‫تجهيز‬ ‫تستطيع‬ ‫هل‬
3
-
‫هل‬
‫لها؟‬ ‫تمشى‬ ‫أن‬ ‫من‬ ‫أبعد‬ ‫ألماكن‬ ‫الذهاب‬ ‫تستطيع‬
4
-
‫المنزل؟‬ ‫بأعمال‬ ‫القيام‬ ‫تستطيع‬ ‫هل‬
5
-
‫المالبس؟‬ ‫أو‬ ‫البقالة‬ ‫شراء‬ ‫تستطيع‬ ‫هل‬
6
-
‫بك؟‬ ‫الخاصة‬ ‫األدوية‬ ‫تناول‬ ‫تستطيع‬ ‫هل‬
7
-
‫بالمال؟‬ ‫التعامل‬ ‫تستطيع‬ ‫هل‬
‫بنفسك‬ ‫مالبسك‬ ‫غسيل‬ ‫تستطيع‬ ‫هل‬-8
16
Delirium (Acute Confusional State)
Delirium is a serious disturbance in mental abilities that results in confused thinking and reduced
awareness of the environment (inattention), and altered level of consciousness.. The start of
delirium is usually rapid — within hours or a few days.
Causes
 Drugs: sedatives, anticholinergic drugs, drug withdrawal
 Infection (eg: chest infection, urinary tract infection)
 Urine retention– Fecal impaction
 Metabolic: hypoglycemia-hyperglycemia, end organ disease (uremia, hepatic
encephalopathy, respiratory failure)
 Electrolytes disturbance: ↓ Na, Ca
 Myocardial infarction(MI)
 Pain
Clinical picture: ACUTE ONSET, FLUCTUATING COURSE, SECONDARY TO MEDICAL
condition, INATTENTION, DISORGANIZED THINKING (The Confusion Assessment
Method CAM)
1. Inattention:
 inability to stay focused on a topic or to switch topics
 inability to stay focused on a topic or to switch topics
2. Altered consciousness:
 Increased; irritability and excitability
 Decreased; apathy, decreased consciousness and decreased response to stimuli
3. Cognitive impairment
 Poor memory, particularly of recent events
 Disorientation — for example, not knowing where he is
 Rambling or nonsense speech
 Trouble understanding speech
4. Neuropsychiatric findings;
 Hallucinations
 Illusions
 Delusions
 Emotional distress
 sleep disturbances
Types: hyperactive, hypoactive, mixed
 Hyperactive delirium. Probably the most easily recognized type, this may include
restlessness (for example, pacing), agitation, rapid mood changes or hallucinations, and
refusal to cooperate with care.
17
 Hypoactive delirium. This may include inactivity or reduced motor activity, sluggishness,
abnormal drowsiness, or seeming to be in a daze.
 Mixed delirium. This includes both hyperactive and hypoactive signs and symptoms. The
person may quickly switch back and forth from hyperactive to hypoactive states.
Complications delirium:
1. Iatrogenic complications (eg: antipsychotic use, mechanical constraints)
2. Incontinence
3. Complications of bed ridden (eg: deconditioning, pressure ulcers, aspiration)
4. Malnutrition
5. Hospitalization
6. Long-term care admission
7. Falls
8. Functional decline
Management of delirium:
1. Identify and remove or treat underlying cause (may be life threatening MI,
hyponatremia)
2. Provide general supportive measures:
 Keep patient in quiet, well-lit room (eg, night lights)
 Ensure safe environment and strict supervision
 Avoid excessive noise, stimulation
 Reorientation:
o Encourage familiar faces (family members) at bedside for reassurance
o Provide orientation (eg, calendar, clock)
o Correct sensory impairment (eg, vision, hearing)
 Nutrition and good hydration
 Enhance mobility and range of motion
 Care of bowel and bladder
3. Control of disruptive behavior
 Use physical restraints only as last resort to maintain patient safety (eg, prevent patient
from pulling out tubes, catheters)
 For acute agitation or aggression: use a high-potency antipsychotic such as haloperidol
(Haldol) 0.5-2mg po or IM.
Role of physical therapy in prevention and management of delirium:
 Early mobilization and walking following surgeries
 Minimizing use of immobilizing equipment
 Individual active mobilization strongly encouraged, Progress through range-of-motion,
sitting, standing, walking, ADLs
 Assisted walking for frail patients routinely performed by PT
18
Delirium and dementia
Dementia and delirium may be particularly difficult to distinguish, and a person may have both.
In fact, delirium frequently occurs in people with dementia. But having episodes of delirium does
not always mean a person has dementia. So a dementia assessment should not be done during a
delirium episode because the results could be misleading.
Dementia is the progressive decline of memory and other thinking skills due to the gradual
dysfunction and loss of brain cells. The most common cause of dementia is Alzheimer's disease.
Some differences between the symptoms of delirium and dementia include:
Onset. The onset of delirium occurs within a short time, while dementia usually begins with
relatively minor symptoms that gradually worsen over time.
Attention. The ability to stay focused or maintain attention is significantly impaired with delirium.
A person in the early stages of dementia remains generally alert.
Fluctuation. The appearance of delirium symptoms can fluctuate significantly and frequently
throughout the day. While people with dementia have better and worse times of day, their memory
and thinking skills stay at a fairly constant level during the course of a day.
Because symptoms of delirium and dementia can be similar, input from a family member or
caregiver may be important for a doctor to make an accurate diagnosis.
19
Dementia
Dementia is a syndrome of acquired (not learning difficulties), chronic (lasts months to years),
global (not just memory or just language problems), progressive impairment of higher brain
function, in an alert patient (not drowsy), which interferes with social and functional abilities.
What are the higher brain functions?
 Learning and Memory (e.g. free recall, cued recall)
 Aphasia (e.g. word-finding difficulty)
 Apraxia (inability to perform motor tasks, such as cutting a loaf of bread, despite intact
motor function)
 Agnosia (inability to recognize objects despite intact sensory function)
 Impaired executive function (poor abstraction, mental flexibility, planning, and judgment).
Different causes of dementia
Reversible causes of dementia Irreversible causes of dementia
 Thyroid disease
 Vitamin B 12 deficiency
 Depression
 Tumors
 Hypercalcemia
 Subdural heamatoma
 Normal pressure hydrocephalus
 Syphilis- HIV
 Drugs(anticholinergic)
Degenerative disorders:
 Alzheimer disease
 Lewy body dementia
 Frontotemporal dementia
Vascular dementia
Mixed dementia
Infections:
 AIDS-related dementia
 Creutzfeldt–Jakob (C-J) disease
Toxins:
 Chronic alcholism
Pathology of Alzheimer disease
Differential Diagnosis
1. Amyloid plaques
2. Neurofibrillary tangles
3. Loss of synapses and dendrites
4. Cerebral atrophy eventually occurs;
however, atrophy is not strongly
correlated with clinical severity.
Acetylcholine is the main neurotransmitter
that is deficient
20
Delirium
Depression
Age related memory loss:
• Much milder symptoms
• Not substantially progressive
• Does not impair function
Mild cognitive impairment
• May represent a transitional state between normalcy and dementia but some cases may
not progress to Dementia
• Either amnestic or non-amnestic MCI
• No functional impairment
21
Alarming signs:
1. People with dementia often forget things and never remember them.
2. Asking the same question over and over
3. Difficulty in performing familiar tasks.
4. Problems with language.
5. Time and place disorientation.
6. Misplacing things.
7. Poor judgment
Consequences of dementia
Malnutrition, safety issues, fall risk, functional decline, incontinence, Delirium,
depression, sleep disorders, aspiration, immobility, Caregiver stress.
Means of Confirmation or Diagnosis
Definitive diagnosis is made upon autopsy.
Exclude reversible causes
Laboratory Tests
Cerebrospinal fluid (CSF) for protein analysis
Neuropsychological testing
Mini mental state examination
Imaging
Computed tomography (CT) of the brain
Magnetic resonance imaging (MRI) of the brain
Single-photon emission computed tomography (SPECT) for hypoperfusion in the parietal
and temporal regions
Positron emission tomography (PET) scan for abnormal brain proteins
Treatment
Memory issues: not curative may delay progression
Cholinesterase inhibitors: donepezil
Memantine: Namenda
Behavioural and psychological symptoms BPSD:
 Behavioural symptoms that may occur in dementia include wandering, aggression
and agitation. Psychological symptoms include anxiety, depression and
hallucinations. The mainstay of treatment for BPSD is non-pharmacological and
approaches include orientation, reassurance, and complementary therapies.
 Antipsychotic drugs may have a role but should only be prescribed by specialists.
 Acetylcholinesterase inhibitors are increasingly used for their effect on BPSD.
22
Depression
Depression is not a normal response to the aging process (It is a disease). It is very common
problem in elderly with 25% of patients at primary care report depressive symptoms.
Effects of depression
 Depression is associated with poorer self-care and slower recovery after acute medical
illnesses.
 It can accelerate cognitive and physical decline and leads to an increased use and cost of
health care services.
 Less effective rehabilitation
 Lower quality of life, higher level of chronic pain, and increased disability (is the fourth
leading cause of disability in the United States).
 The mortality rate coincided with the level of depression even when controlling for other
factors.
Types of depression
 Primary depression is not triggered by any other psychological or medical cause. Rather,
this type of depression is triggered by psychological instability, genetic predisposition.
 Secondary depression is caused by one or more negative life events such as illness, this
kind of depression is triggered by a medical condition as thyroid gland disorder and by a
psychiatric illness as schizophrenia.
Symptoms of depression and how old age can modify its presentation?
1. Depressed mood and/or lack of interest or pleasure in usual activities
 The older adults may be more likely to express a loss of pleasure than to
specifically complain of depression
2. Feelings of worthlessness or inappropriate guilt
 Less common in older adults than in younger adults
3. Diminished ability to concentrate or make decisions
 Often manifested as a complaint of memory problems—adults of all ages with
moderate-to-severe depression complain of problems with concentration and
memory, but depressed elders, in contrast to younger adults, exhibit impairment on
psychological testing even when they do not have a comorbid dementing disorder
4. Fatigue Common regardless of age
5. Psychomotor agitation or retardation
 Older persons may exhibit either of these symptoms
6. Insomnia or hypersomnia
 Older persons rarely, if ever, exhibit hypersomnia—a symptom that is much more
common in adolescence and young adults
7. Significant decrease or increase in weight or appetite
23
 Older adults rarely gain weight or experience an increase in appetite during a
depressive episode
8. Recurrent thoughts of death or suicidal ideation
 Although thoughts of death are not uncommon in older adults, suicidal ideation
among depressed elders is less frequent than among the depressed who are
younger but more risky.
9. More likely to express somatic complaints
 65% have hypochondriacal symptoms
Medical Conditions and medications Causing Depression
Medical disorders
• Autoimmune (SLE, RA)
• Cerebrovascular (CVS)
• Chronic pain
• Degenerative Disease PK, Alzheimer
• Endocrine DM, hypothyroidism
• Metabolic cirrhosis, uremia
• Neoplasms
• Infections chronic: TB, HCV, HIV
Drugs
▫ Non steroidal anti-
inflammatory
▫ Propranolol
▫ Cimetidine
▫ Clonidine
▫ Benzodiazepines
▫ Steroids
▫ Tamoxifen
▫ Chemotherapy
Screening for depression is performed as a part of comprehensive geriatric assessment by many
tools:
1. Geriatric Depression Scale - 15
2. Zung Self-Rated Depression Scale
3. Patient Health Questionnaire-2
INTERVENTIONS
• Seek out medical illness, Recognize medical side effects
• Rehab services to maximize remaining function and retrain impaired ADL’s
• Involve family and caretakers
• Psychotherapy
• Medications: Best to use Selective Serotonin Reuptake Inhibitor Citalopram (Celexa) and
Escitalopram (Cipralex) least side effects and drug interactions but may cause
hypernatremia and sexual dysfunction.
• Electro-convulsive therapy
24
Exercise has been shown to benefit patients with mild to moderate mood
disorders, especially anxiety and depression.
1. Aerobic and resistive exercises release endorphins from the pituitary gland which are
responsible for
 Relieving pain
 Improving mood.
 Lower cortisol levels which have been shown to be elevated in patients with
depression.
2. Additionally, exercise increases the sensitivity of serotonin in the same way
antidepressants work, allowing more serotonin to remain in the nerve synapse.
3. Depression symptoms can be decreased significantly after just one session but the effects
are temporary. An exercise program must be continued on a daily basis to see continued
effects.
4. As a person continues to exercise they may experiences changes in their body type which
can help to improve self-esteem and body image issues they may have been having.
5. Regular exercise program can enhance social integration
6. Some other benefits of regular physical exercise include: (general benefits apply to
all patients)
a. Reduces/prevents functional declines associated with ageing
b. Maintains/improves cardiovascular function
c. Aids in weight loss and weight control
d. Improves function of hormonal, metabolic, neurologic, respiratory, and
hemodynamic systems
e. Alteration of carbohydrate/lipid metabolism results in favourable increase in high-
density lipoproteins
f. Strength training helps to maintain muscle mass and strength
g. Reduces age-related bone loss; reduction in risk for osteoporosis
h. Improves flexibility, postural stability, and balance; reduction in risk of falling and
associated injuries
i. Psychological benefits (preserves cognitive function, alleviates symptoms/behaviours
of depression, improves self awareness, promotes sense of well-being)
j. Improves immune function
k. Reduces age-related insulin resistance
l. Improves sleep pattern
25
WHAT IS YOUR DIFFERENTIAL DIAGNOSIS?
5. Delirium
6. Depression
7. Dementia
Why delirium most likely??
1. Acute onset
2. Confusion
But other criteria needs to be confirmed and further
history and examination needed
75 years old female underwent coronary artery bypass graft surgery 3 days ago.
She lays in bed most of the day and is not interacting with staff, which is impairing her recovery.
She is confused, and appears sad and unmotivated. Is she depressed???.”
WHAT OTHER INFORMATION WOULD YOU LIKE TO
KNOW ABOUT MRS. x ?
1. Past psychiatric history
2. Past medical history
3. Current medications
4. Pre-morbid cognitive status
Now that you have collateral information,
you summarize the case:
– 76 year old female post-CABG
– Decreased level of consciousness
– Confused and disoriented
– Amotivated and apathetic
– Fluctuation of symptoms
– No prior history of depression
– No prior history of dementia
– What is the diagnosis?
– What is the subtype?
Hypoactive delirium
– WHAT SHOULD YOUR NEXT STEP BE?
Search for the cause, exclude life threatening condition
first
 You now attempt to see Mrs. X to obtain her history and observe her current mental status.
 She is dressed in a hospital gown lying in bed, looking older than her stated age. Her eyes are closed, and you have
a difficult time rousing her.
 Her words are slurred and difficult to understand.
 She is unable to respond appropriately to your questions.
 She appears to be picking at things in the air.
 You are unable to assess her mood, but her affect is restricted. She is confused, and when asked where she is
mumbles something about “being in Newfoundland”.
 You attempt to perform an MMSE, but Mrs. X is unable to pay attention long enough to complete the test
As you are unable to obtain much information from Mrs.x, what should you do now?
OBTAIN COLLATERAL
You review the medical chart and speak with Mrs. x’s daughter to obtain collateral information. You find out the following
information.
No prior psychiatric problems
– No history of depression
Past medical history:
Angina, Hypertension, Dyslipidemia, Hearing impairment (Uses hearing aid), Hysterectomy (1985),
Smoker (30 pack years)
Medications
Atenolol 25 mg BID. Atorvastatin 20 mg OD, Aspocid 81 mg OD, Multivitamin ī tab OD, Amitriptyline 10 mg HS, Ramipril 5
mg OD*, Ranitidine 150 mg OD*, Hydromorphone 2-4 mg on demand Receiving approx. 6 mg/day
Pre-morbid cognitive functioning
– Mrs. x has occasionally been forgetting names of friends/family over the past year, but there are no other
memory deficits.
– She is independent for all IADL’s/ADL’s
– She scored 30/30 on a recent MMSE done at her GP’s office
– Her family now find her drowsy and confused, which gets worse later in the day
Real case scenario
26
Possible causes to investigate:
 Drugs: sedatives, anticholinergic drugs, drug
withdrawal
 Infection (eg: chest infection, urinary tract
infection)
 Urine retention– Fecal impaction
 Metabolic: hypoglycemia-hyperglycemia, end
organ disease (uremia, hepatic encephalopathy,
respiratory failure)
 Electrolytes disturbance: ↓ Na, Ca
 Myocardial infarction(MI)
 Pain
Role of rehabilitation in a case of delirium:
Care of immobile patient:
• Pressure ulcer prevention:
– Proper positioning, change positions at least every two hours
– Air mattress, keep skin dry and clean
• For contracture prevention
– Do stretching and range-of-motion exercises to each of the joints every day, and several times a day (active better
than passive).
– Maintain proper body alignment, therapeutic splints.
– Pain control, treatment of spasticity.
• For muscle weakness, atrophy prevention
– Muscle strength can be maintained without loss or gain with daily muscle contractions of 20% or more of maximal
tension for several seconds each day.
– Functional electrical stimulation and biofeedback training can increase or maintain muscular strength in those
muscles with less than antigravity strength.
• For cardiac deconditioning prevention:
– Isotonic exercise prevent fluid shift
– Tilt table therapy
– Elastic leg wrapping
– Fludrocortisone therapy
• Thrombo-embolisation prevetion:
– Anticoagulation, elastic stocking, intermittent pneumatic compression.
• Airway Secretions Elimination
– Oral, nasal, or transtracheal suctioning
– Chest percussion and postural drainage
– Flutter mucus clearance devices
– Mechanical vibration devices to the chest wall
– Regular deep breathing, coughing
• Maintain an adequate fluid intake to prevent: thick secretion ,constipation, UTI, renal stones, dehydration, clotting
• Laxative use
• Nutritional support
• OCCUPATIONAL THERAPY IN THE MANAGEMNET OF IMMORBILE OLDER PATIENTS
– Assessment of mobility(Bed mobility, Transfers, Wheelchair propulsion)
– Assessment of other ADL using actual or simulated environments
– Visit home for enviornmental assessment and recommentations for adaptation
– Recommend and teach use of assisitive devices (cane, crutches)
– Recommend and teach use of safety devices (e.g., grab bars and railing, raised toilet seats, shower chairs)
Support delirious patient:
– orienting environment :easy-to-read calendars and clocks
– Presence of family members can be helpful , frequent interaction , Frequent verbal orientation
– Support for confusion or hallucinations , encouraged to express fears and discomforts
– Adequate lighting and reasonable noise level
– Devices available - eye glasses and hearing aids, Avoid sensory deprivation and overload
– Manage pain, Support normal sleep pattern
You perform an appropriate work-up and
order investigations. You obtain the
following ABNORMAL results:
Na 152
BUN 25
All other results are normal
This suggests dehydration and hyponatremia
that was corrected by fluid therapy
27
Health promotion in elderly
Disease prevention
The goal of preventive medicine in older people should be not only reduction of morbidity and
mortality but also preservation of function and quality of life.
Attempts to prevent diseases of old age should start in youth. Even in the very elderly, preventive
interventions can limit disease and disability. However, selecting appropriate interventions
requires consideration of:
1. Life expectancy
2. Patient’s preferences
3. Direct and indirect harm of the intervention
4. Goals of care
Levels of prevention
Primary Prevention of disease by targeting cause and risk factors
1. Life style modifications:(Diet- Physical activity- Safety and injury
prevention- Smoking cessation
2. Immunizations influenza vaccine
3. Chemoprophylaxis aspocid, omega 3 for cardiovascular risk reduction,
vitamin D and calcium for osteoporosis prevention
Secondary the early detection of disease before it becomes symptomatic
1. Screen for malignancy: mammography to detect early breast cancer,
colonoscopy to screen for cancer colon)
2. Screen for medical conditions: DM, obesity, malnutrition
3. Screen for geriatric giants: incontinence, sleep problem, dementia,
depression
Tertiary Managing established diseases (e.g. tight control of DM) to prevent
complications e.g. MI, diabetic foot
PREVENTING DISABILITY: While there may be little that can be done to
prevent the occurrence of a disease in an elderly person, much can be done to
minimize the impact of that disease (Proper treatment, Rehabilitation,
occupational therapy).
28
Pharmacotherapy in elderly
Many older patients are prescribed multiple drugs, take over-the-counter drugs, and are then
prescribed additional drugs to treat the side effects of medications they are already taking resulting
in polypharmacy (usually defined as consuming ≥ 5 medications). The elderly are the biggest
consumer of the drug industry, Elderly account for 1/3 of prescription drug use, while only 13%
of the population.
The Effects of Aging on pharmacokinetics:
Several age-related biological and physiological changes are relevant to pharmacology. Except for
changes in renal function, however, the effects of these age-related changes on dosages of specific
drugs for individual patients are variable and difficult to predict
Parameter
Absorption Decreases in absorptive surface
Decreased splanchnic blood flow
Increased gastric pH
Altered gastrointestinal motility
not clinically significant as they do not affect the absorption of most
drugs
Distribution  body water  Vd for hydrophilic drugs e.g. ethanol, lithium
 lean body mass  Vd for drugs that bind to muscle e.g. digoxin
 fat stores  Vd for lipophilic drugs e.g. diazepam
 plasma protein (albumin)  % of unbound or free drug (active) e.g. , phenytoin, warfarin
Metabolism Decreases in liver blood flow,
Decreases in enzyme activity,
Decreases in enzyme inducibility
Reduced liver volume and enzyme activity means that hepatic
metabolism of many drugs decreases.
To prevent toxic accumulation doses should be reduced or the dosing
interval increased
Excretion Decreases in renal blood flow,
Decreases in glomerular filtration
rate
Decreases in tubular secretory
function
Serum creatinine alone not accurate in the elderly to reflect GFR
 lean body mass  lower creatinine production
Cockroft-Gault formula formula for estimating creatinine clearance
Cr clearance=(140-age)(IBW)/creatinine(72) (multiply by 0.85 for
women)
The Effects of Aging on pharmacodynamics:
1. Generally, lower drug doses are required to achieve the same effect with advancing age.
2. Change in receptor numbers, affinity can increase or decrease drug sensitivity: HR response
to beta-blockers
3. Changes in homeostatic mechanisms can increase or decrease drug sensitivity.  sensitivity to
warfarin due to a greater decrease in clotting factor synthesis
Other factors affecting drug prescription in elderly:
1. Multiple morbidities: e.g. NSAIDs may cause acute decompensation in patients with chronic
heart failure.(drug- disease interaction)
2. Multiple medications leading to drug-drug interactions: ACEIs and aldactone causes
hyperkalemia
3. Psychological factors: depressed patients may have their stable conditions exacerbated due to
non-adherence to treatment
4. Social factors: economic problems and Problems with transportation may interfere with
obtaining the medications.
29
5. Diminished hearing, impaired vision, poor literacy, and poor short-term memory can
interfere with patient education and adherence to treatment regimens.
POTENTIALLY INAPPROPRIATE MEDICATIONS FOR OLDER PERSONS:
Multiple tools are available to clinicians that can assist in making information readily available to
avoid adverse drug reactions and interactions.
1. The Beers Criteria: developed to assist healthcare providers in improving medication safety
in older adults. The criteria were originally published in the Archives of Internal Medicine
in 1991 and were updated in 1997 and again in 2003,2012,2015. Last edition on 2019
https://onlinelibrary.wiley.com/doi/full/10.1111/jgs.15767
2. STOPP criteria (Screening Tool of Older Persons’ Potentially Inappropriate Prescriptions)
Principles of Prescribing in the Elderly:
 Consider non-pharmacologic agents
 Start with a low dose and titrate slowly
 Avoid starting 2 agents at the same time
 Reach therapeutic dose before switching or adding agents
 Review meds regularly (at least q3 months)
 Avoid prescribing to treat side effect of another drug
 Use 1 medication to treat 2 conditions, Use simplest regimen possible
 Adjust doses for renal and hepatic impairment
 Use least expensive alternative.
 Monitor for adverse drug reactions, drug-disease, drug-drug, and nutrients-drug
interaction.
 Avoid inappropriate drug prescription for old age using The Beers Criteria or similar tools.
NB: example of nutrients drug interactions:
1. Tyramine, a component of cheese and a potent vasoconstrictor, can cause hypertensive
crisis in some patients who take monoamine oxidase inhibitors and eat cheese.
2. Foods with vitamin K (arugula, avocado, green beans, Cucumber), produce blood-clotting
substances that reduce the effectiveness of oral anticoagulants (Warfarin).
30
Safe analgesic prescription in elderly:
World Health Organization (WHO) analgesic “pain ladder” is a good model to follow for the
treatment of acute pain in older adults:
1. Mild pain should be treated with non-opiates (e.g., acetaminophen).
2. Moderate pain (pain score 4–7) should be treated with an oral opioid (e.g., oxycodone).
3. Severe pain (pain score 8–10) should be treated with an opioid (preferably parenteral) that
can be easily titrated.
Acetaminophen:
 It is the safest analgesic when it is used with the recommended dosage.
 Most mild or moderate pain in the elderly is of musculoskeletal origin and responds well to
acetaminophen given around-the-clock.
 This agent is well tolerated in older patients provided that both renal and hepatic functions are
normal. The daily dose of acetaminophen should not exceed 2 gm.
 Risks of hepatic toxicity with acetaminophen are minimal and have primarily been observed with long-
term use.
 Nonetheless, acetaminophen should be avoided in patients with liver disease or a history of heavy
alcohol use.
 Unfortunately, it is not as effective for inflammatory pain,
Nonsteroidal anti-inflammatory drugs (NSAIDs):
 All commonly used NSAIDs are on the Beers list of inappropriate medications for older adults. Even
short-term use of NSAIDs should be considered unacceptable in older adults with diabetes, impaired
kidney function, or taking medications that may impair kidney function (diuretics, ACE inhibitors) or
metformin.
 Both renal and gastrointestinal toxicity from NSAIDs are dose- and time-dependent. The patient’s risk
factors for side effects and recent history of NSAID exposure should be reviewed prior to
administering or prescribing NSAIDs.
 Gastric acid suppression with a proton pump inhibitor should also be considered.
 Because of their association with a lower incidence of gastrointestinal bleeding, selective
cyclooxygenase-2 (COX-2) inhibitors (coxibs) have been viewed as a safer alternative to the other
NSAIDs; however, concern about their association with heart disease and stroke has dampened their
acceptance and resulted in the withdrawal of rofecoxib (Vioxx) from the market.
 Prolonged use of NSAIDs in the elderly should be avoided whenever possible.
Opioid analgesics:
 Administration of opioid analgesics to manage chronic non-cancer pain in the elderly has become
acceptable; these agents are effective in treating patients with moderate to severe nociceptive pain.
 True addiction in the elderly is uncommon, and the possibility of addiction should not be used as
justification for undertreatment of the elderly for pain.
 Morphine sulfate and oxycodone hydrochloride, now available in both short-acting and sustained-
release preparations, are commonly used. Short-acting opioids can be used in treatment of patients
with intermittent pain, whereas sustained-release opioids should be given for continuous pain (with
short-acting preparations available for breakthrough pain). The dosage of sustained-release opioids
can be titrated based on the frequency of use of the short-acting preparation.
31
 For patients who may not be able to take oral preparations periodically, opioids are available as
parenteral, sublingual, suppository (oxymorphone hydrochloride), and transdermal (eg, fentanyl
patch) products.
 Physicians should anticipate, prevent, and manage side effects.
o They should initiate prevention of constipation through the use of stool softeners and other
prophylactic bowel regimens whenever opioid therapy is used in the elderly.
o When opioid therapy is initiated, sedation and delirium are commonplace until tolerance
develops.
o Although respiratory depression occurs uncommonly, tolerance develops rapidly. If needed,
naloxone hydrochloride could be used for profound respiratory depression and sedation; care
must be taken when reversing this adverse effect since an antagonist action that is too
powerful could propel the patient on long-term opioid therapy into withdrawal. It is advisable
that patients take a maintenance dose for several days before they resume driving.
o Antiemetics such as prochlorperazine or metoclopramide may be needed early on with the
initiation of opioid therapy.
o Falls, dizziness, and gait disturbances are not uncommon; therefore, preventive precautions
are often recommended, such as the use of an assistive device.
o Eventually, for most patients, the analgesic effect of opioids is preserved while tolerance
develops to most side effects (eg, respiratory depression, sedation, nausea, and vomiting).
However, because tolerance does not develop to gastric hypomotility, patients need to take
stool softeners for as long as they are on opioid therapy. Chewing or crushing sustained-
release opioids must be avoided as doing so can cause rapid absorption of the entire dose
resulting in overdosing.
o Certain opioids should be avoided in elderly patients when possible. Propoxyphene is thought
to be no more effective than aspirin or acetaminophen, but it is associated with ataxia,
dizziness, and neuroexcitatory effects due to drug accumulation.22 Meperidine
hydrochloride should not be used because of the accumulation of a nephrotoxic metabolite.
Methadone hydrochloride should also be avoided in the elderly because it has a long and
variable half-life, which makes titration difficult. In addition, the analgesic action is shorter
than that of respiratory depression1 so patients whose methadone dosage is too low may
increase their daily amount, which increases the risk of death from respiratory depression.
 Transdermal fentanyl, contraindicated in opioid-naïve patients, should also be used with extreme
caution in the elderly. It has a variable absorption rate in older adults and a long residual effect even
when the patch is removed.
 Tramadol hydrochloride, an analgesic that has some opioid properties and is used for mild to
moderate pain, should be used with caution in the elderly because it may cause dizziness and reduce
the seizure threshold.
Adjuvant Medications
 Anticonvulsants, steroids, topical local anesthetics, and antidepressants are such agents that may be
used alone or in combination with nonopioid or opioid analgesics.
 Adjuvant medications are particularly useful in managing neuropathic pain.
1. Tricyclic antidepressants such as amitriptyline hydrochloride (cardiotoxic)
2. Anticonvulsants such as gabapentin and carbamazepine are thought to be more effective and safe,
anticonvulsant pregabalin is effective and easier to tolerate than gabapentin.
3. Serotonin norepinephrine-reuptake inhibitor (SNRI) in duloxetine, has been shown to be effective for
the treatment of patients with neuropathic pain and seems to be well tolerated in the elderly.
32
Sarcopenia
Definition: a progressive and generalized loss of skeletal muscle mass and strength with a risk of
adverse outcomes such as physical disability, poor quality of life, and death. Both low muscle
mass and function are fundamental criteria for sarcopenia diagnosis.
Prevalence:
– The prevalence in 60–70-year-olds is reported as 5–13%.
– The prevalence ranges from 11 to 50% in people >80 years.
– Highly related to frailty and osteoporosis.
Although it is primarily a disease of the elderly, its development may be associated with conditions
that are not exclusively seen in older persons. It can be divided in primary (or age related) and
secondary sarcopenia.
Sarcopenia can occur secondary to
• A systemic disease, especially one that may invoke inflammatory processes, e.g.
malignancy or organ failure.
• Physical inactivity also contributes to development of sarcopenia, whether due to a
sedentary lifestyle or to disease-related immobility or disability.
• Inadequate intake of energy or protein, which may be due to anorexia, malabsorption,
limited access to healthy foods or limited ability to eat.
•
Stages pre-sarcopenia, sarcopenia, and severe sarcopenia
Operational definition of sarcopenia by The European Working Group on Sarcopenia in Older
People (EWGSOP) in 2019
• Low muscle strength (Criterion 1)
• Low muscle quantity or quality (Criterion 2)
• Low physical performance (Criterion 3)
1. Probable sarcopenia is identified by Criterion 1.
2. Diagnosis is confirmed by additional documentation of Criterion 2.
3. If Criteria 1, 2 and 3 are all met, sarcopenia is considered severe.
4. The ‘presarcopenia’ stage is characterized by low muscle mass without
impact on muscle strength or physical performance
33
Acute and chronic sarcopenia
Acute sarcopenia is that lasted less than 6 months, while sarcopenia lasting ≥6 months is
considered a chronic condition. Acute sarcopenia is usually related to an acute illness or injury,
while chronic sarcopenia is likely to be associated with chronic and progressive conditions and
increases the risk of mortality. Differentiation is done by periodic clinical assessment.
Mechanisms underlying sarcopenia
1. Loss of both slow and fast motor units, with an accelerated loss of fast motor units.
2. Myosteatosis
3. Age-related muscle denervation
4. Increased protein degradation/decreased protein synthesis
5. Increased inflammatory cytokine expression (IL-6 and TNF-alpha)
6. Decreased GH and IGF-I production
7. Increased oxidative damage
8. Insulin resistance, which occurs with aging and obesity, plays an important role in
decreasing available glucose and protein for muscle anabolism.
34
Sarcopenia diagnosis stepped approach:
Screening: with SARC-F if score > 4
suggest sarcopenia
Muscle mass measurement: Computed
tomography (CT) and magnetic resonance
imaging (MRI), Dual energy X-ray
absorptiometry (DXA), Bioimpedance
analysis (BIA).
Muscle strength assessment: Grip
strength, chair stance test
Assessment of physical performance:
Timed up and Go test, Short physical
performance battery (SPPB).
35
Management:
1. Physical activity is the primary treatment of sarcopenia (also prevention).
– Resistance exercise improves skeletal muscle strength and mass
– Aerobic exercise may also show some benefit
2. Nutritional interventions combined with exercise:
• adequate intake of protein
• vitamin D,
• antioxidant nutrients
• long-chain polyunsaturated fatty acids
3. No specific drugs have been approved for the treatment of sarcopenia, however; many
drugs were considered for potential benefits without enough clinical evidence: vitamin D
(only if <50 nmole) , dehydroepiandrosterone, growth hormone, growth hormone-releasing
hormone, combined testosterone-growth hormone, insulin- like growth factor-1,
testosterone (in hypogonadism), and angiotensin-converting enzyme inhibitors.
36
Frailty in Older Persons
Frailty can be defined as an age-associated declines in physiologic reserve and function across
multi-organ systems, leading to increased vulnerability for adverse health outcomes.
Clinical implications of frailty:
• It is a warning sign for high risk of adverse health outcomes.
• The explanation for downward spiral in many elderly patients after acute illness.
• Frailty has been widely utilized as a mortality risk assessment tool. Reflects biological age
that predicts mortality better than chronological age.
• Frailty is often described as a transitional phase between successful ageing and disability.
• Frail elderly need specific management: Regardless of age, a frail person may be unable
to withstand aggressive medical treatment that could benefit a nonfrail person.
Epidemiology:
• Although exact definitions and screening methods vary, approximately 15 % of the US
population over age 65 and living in the community are considered frail.
• In 15 studies that included 44,894 participants identified a prevalence of frailty of 9.9 %;
when psychosocial aspects were included in the definition, prevalence was 13.6 % among
eight studies that included 24,072 participants.
• Prefrail individuals, generally identified with a physical frailty type tool , are more common
in these population studies, with prevalence ranging from 28 to 44 %.
• Of those individuals who were prefrail, over 10 % went on to become frail over the next 3
years.
The biology of frailty is explained by two models:
37
1. Phenotypic frailty
• A cycle of physiological decline was hypothesized that included interrelated and
reinforcing declines in metabolism, nutrition utilization, and skeletal muscle that in sum
drove worsening vulnerability.
• Triggers of this cycle of decline included acute illnesses, some medications, and aging
related biological changes in genetic predisposed elderly.
• These physiological impairments result in the five clinical characteristics of frailty:
weakness, low energy, slow walking speed, low physical activity and weight loss.(Fried
criteria for frailty diagnosis)
• The presence of any three of these phenotypes indicates that a person is ‘frail’; one or two
phenotypes indicate that the person is ‘prefrail’ and absence of these characteristics
indicates the person is ‘robust’.
2. Deficit-driven frailty
• Frailty as an aggregate of illnesses, disability measures, cognitive and functional declines
that has been termed deficit-driven frailty. According to this model, the more deficits or
conditions that an individual has, the more frail the individual is.
• In this diagnostic approach, almost any conditions or deficits are interchangeable in index
tools.
• This conceptual basis has also been widely utilized to develop risk assessment tools that
tally a broad range of comorbid illnesses, mobility and cognitive measures, and
environmental factors to capture frailty.
Initiators (triggers) of frailty:
Aging Genetics
Environmental factors (UVR, Pollution),
Drugs
Internal stressors (inflammatory, malignancy,
malnutrition)
38
The mechanisms of frailty
Chronic inflammatory pathway activation Decline in skeletal muscle function and
mass(Sarcopenia)
Endocrinal changes contribute to frailty
1. Serum levels of the proinflammatory
cytokine IL-6 and C-reactive protein (CRP),
as well as white blood cell and monocyte
counts, are elevated in frail older adults.
2. IL-6 acts as a transcription factor and signal
transducer that adversely impacts skeletal
muscle, appetite, adaptive immune system
function, and cognition and contributes to
anemia.
3. Immune system activation may trigger the
clotting cascade, with a demonstrated
association between frailty and clotting
markers (factor VIII, fibrinogen, and D-dimer).
4. there is evidence linking a senescent
immune system to chronic CMV infection
and frailty.
1. chronic inflammation
2. age-related changes in α-motor
neurons,
3. poor nutrition
4. ↓growth hormone (GH) production,
sex-steroid levels, and physical
activity.
5. Age-related insulin resistance
causes an increase of fat infiltration
into muscle and a decline in muscle
strength.
6. Mitochondrial dysfunction in aging
skeletal muscle causes oxidative
damage and the decline of energy
generation to maintain function
properly
1. Decreased growth hormone and insulin-like
growth factor-1 levels in later life (IGF-1)
2. Decreased levels of the adrenal androgen
dehydroepiandrosterone sulfate (DHEA-S).
3. Chronically increased cortisol levels,
blunted diurnal variation of cortisol.
4. Evidence is mixed that lower levels of the
reproductive hormones estrogen and
testosterone contribute to frailty.
5. there is stronger evidence that links
decreased 25(OH) vitamin D levels to f
6. railty
Management
• Once a frail or prefrail patient is identified there are no succinct guidelines on how to best
mange them.
• Diagnosis, differential diagnosis (rule out underlying medical or psychological issues that
may be driving signs and symptoms of frailty)
Diagnosing frailty:
39
40
• Laboratory Testing (in order to rule out treatable conditions, A suggested initial screen,
based on the differential diagnosis, might include: Complete blood count, basic metabolic
panel, liver biochemical tests, including albumin, vitamin B12, vitamin D, and TSH).
Exercise
• Exercise is believed to be the most effective intervention in older adults to improve quality
of life and functionality. However, data on specific exercise interventions designed to
improve outcomes in patients with frailty are limited.
• The demonstrated benefits of exercise in older adults include increased mobility, enhanced
performance of activities of daily living (ADL), improved gait, decreased falls, improved
bone mineral density, and increased general well-being.
Nutritional Supplementation
• In treatment of weight loss, oral nutritional supplements between meals (low-volume, high
caloric drinks or puddings) may be helpful in adding protein and calories.
• Vitamin D supplementation for those with low serum vitamin D levels (< 20 ng/ml)is
effective for fall prevention, improving balance, and preserving muscle strength.
• those taking leucine-enriched whey protein plus vitamin D had significant improvement in
physical frailty related measurements
• Whey protein, omega 3 fatty acids rich items, amino acid glutamine, carnitine have been
suggested for their useful role.
Pharmacotherapy
• Not adequately evaluated.
• Such hormonal therapy as testosterone, while it improves muscle strength, has significant
systemic side effects. Estrogen-replacement therapy in postmenopausal women also has an
unfavorable safety profile.
• Even growth hormone, DHEA, testosterone when deficient, may be considered
• Friedlander et al reported that IGF-1 therapy had a beneficial impact on bone density,
muscle strength, or physical function in elderly women with no clinical IGF-1 deficiency.
• Currently available anti-inflammatory agents, while not formally evaluated in clinical trials
in treating the frailty syndrome, also have significant adverse effects, particularly in the
elderly. Statin has no effect in management of frailty.
• While vitamin D and angiotensin-converting enzyme inhibitors have favorable
pharmacological and safety profiles, their clinical utility in the prevention and treatment of
frailty has yet to be investigated
41
Osteoporosis
• Osteoporosis is: ‘progressive loss of bone mass associated with change in bone micro-
architecture, leading to enhanced bone fragility and a consequent increase in fracture risk’.
Epidemiology:
• It is estimated that 1 in 3 women and 1 in 12 men over the age of 50 years worldwide suffer
from osteoporosis. Above age of 60, one in two women and one in three men will have a
minimal trauma fracture because of osteoporosis.
• Associated with excess morbidity and mortality – 33% of people die and 35% require help
to walk one year after a hip fracture.
Pathophysiology
• The risk of osteoporosis depends on the peak bone mass attained in young adult life and the
rate of bone loss in later years.
• The peak bone mass, excessive bone resorption and inadequate formation of new bone
remodeling are the three main mechanisms by which osteoporosis develops.
• Achieving peak bone mass depends on adequate nutrition, appropriate intake of
calcium and vitamin D, exercise and regular menstrual cycles.
• Remodeling is: A normal process continually taking place within bone to repair micro
damage through continuous bone formation and resorption.
• Stages of bone remodeling are:
1. Activation of osteoclasts from circulating precursor cells, mediated by receptor binding of NF-
κB (RANK) ligand.
2. Aggregation and adherence of osteoclasts to regions of active bone resorption on the trabecular
plate.
3. Osteoclastic breakdown of bone matrix, releasing calcium, minerals and active growth factors.
4. Simultaneous osteoblastic deposition of osteoid with subsequent mineralization as calcium and
phosphate (hydroxyapatite) is deposited.
• In postmenopausal women, there is a shift towards bone resorption, leading to net bone loss.
Osteoclasts function in a less regulated manner, perforating through the trabecular plate.
There is then no framework for osteoblast activity and structural integrity is lost. This loss
of connectivity between the trabecular plates is typical of the microstructural changes
associated with osteoporosis.
42
Risk Factors for primary
osteoporosis
Causes of secondary osteoporosis
 female gender
 current smoker
 alcohol intake >3 units/day
 low calcium and vitamin D
deficiency
 Low body mass index (<19 kg/m2).
Endocrinal: hyperthyroidism/ hyperparathyroidism/
Cushing
rheumatoid arthritis
chronic malabsorption or malnutrition (e.g. coeliac)
Chronic liver disease.
Renal failure
Hematological diseases: multiple myeloma, Leukemia
Drugs: heparin, phenytoin, steroids
• In men the major causes of secondary osteoporosis are hypogonadism and corticosteroid
therapy.
Possible symptoms:
• Osteoporosis remains asymptomatic till fracture occurs.
• Back pain, caused by a fractured or collapsed vertebra
• Loss of height over time
• A stooped posture (kyphosis)
• Fragility fractures
• The fracture sites in osteoporosis, the wrist, the hip and the vertebra, have relatively high
trabecular bone to cortical bone ratio
Risk stratification tools
• The FRAX tool (http://www.shef.ac.uk/FRAX/) was developed by the World Health
Organization as a free-online resource to calculate 10-year fracture risk. These calculations
help to inform decisions about treatment alongside investigations.
Investigations
• Blood tests – FBC, UE, LFT, TFT, Ca, PO4, vitamin D, PTH, coeliac serology, myeloma
screen.
• Dual-energy X-ray absorptiometry (DEXA) scanning is: The gold-standard
investigation used to establish a formal diagnosis of osteoporosis by measuring bone
mineral density (BMD).
• Reported as a T score, corresponding to the number of standard deviations (SDs)
above or below the bone mineral density for an average 25-year-old. A T-score of
2.5 SDs below normal represents osteoporosis.
• Z score, corresponding to the number of SDs above or below the bone mineral
density in age-matched controls.
43
• A whole-spine X-ray may be helpful to establish the presence of asymptomatic fractures.
Up to one-third of vertebral fractures fall into this group.
• Bone turnover markers such as serum C-terminal telopeptide (CTX) levels are used in
specialist clinics to establish compliance and effectiveness of treatment.
Management
• Diet rich in calcium and vitamin D
• Exercise
• Stopping smoking
• Reducing alcohol
Pharmacological
• All patients with osteoporotic fractures, or at risk of sustaining them, should be commenced
on vitamin D supplementation. Co-administration of calcium will depend on baseline serum
calcium levels and dietary intake.
• Bisphosphonates are the mainstay of treatment. These inhibit osteoclastic bone resorption.
Because the processes are linked, impaired bone resorption results in reduced bone
formation and turnover as a whole is reduced. Usually patients receive bisphosphonates for
3–5 years. Beyond this, benefits of therapy must be balanced against risk of atypical
subtrochanteric fracture and osteonecrosis of the jaw. Continuation after 3 years depends on
a reassessment of fracture risk and up-to-date
• Teriparatide, denosumab and raloxifene are reserved for specific indications
44
Recommendations for Prescribing Exercise to Patients with Osteoporosis:
Weight-bearing aerobic exercises and muscle-strengthening exercises have been shown to be an integral
part of osteoporosis prevention, as well as a part of the treatment process.
All three components of an exercise program are needed for strong bone health: weight-bearing aerobic
exercise such as jogging, brisk walking, stair climbing; muscle strengthening exercise with weights; and
balance training such as Tai Chi.
Any form of resistance training should be site specific i.e. targeting areas such as the muscle groups around
the hip, the quadriceps, dorsi/plantar flexors, rhomboids, wrist extensors and back extensors.
Precautions:
1. As many patients may present with comorbidities, it may be necessary to tailor the exercise
prescription accordingly.
2. There are currently no established guidelines regarding contraindications for exercise for people
with osteoporosis. The general recommendation is to prescribe moderate intensity exercise that
does not cause or exacerbate pain.
3. Exercises that cause twisting (e.g. golf swing), bending or compression of the spine (e.g. rowing or
other dynamic abdominal exercises including sit-ups) should also be avoided.
4. Exercises that involve high-impact loading should be avoided. Low impact weight-bearing activity
is characterized by always having one foot on the floor. Jumping (both feet off floor) is termed high
impact training.
45
QUIZ:
Kindly comment on the following DXA reports
46
47
Sleep problems
Normal age related changes in sleep:
 Decreased sleep efficiency (time asleep divided by time in bed)
 Decreased total sleep time
 Stable or increased sleep latency (time to fall asleep)
 Earlier bedtime and earlier morning awakening
 More arousals during the night
 More daytime napping
 Decreases in deeper stages of sleep stage 3 and stage 4 sleep.
 Stages 1 and 2 (the lighter stages of sleep) increases.
Common sleep problems include:
1. Insomnia: difficulty initiation or maintaining sleep for at least 3 nights per week (primary or
secondary to psychiatric, medical problems, or medications.
2. Sleep disordered breathing: Obstructive sleep apnea, Central sleep apnea, mixed
3. REM behavioral disorder: enactment of dreams
4. Circadian rhythm related sleep disorder: jet lag, advance phase disorder
5. Restless leg syndrome, and periodic limb movements.
Consequences of sleep disorders: Depression, poor quality of life, day time fatigue and somnolence, falls,
irritability, and cognitive impairment. Resistant hypertension may occur in cases with chronic insomnia.
Sleep disordered breathing: is also an independent risk factor for hypertension and is associated with
obesity, pulmonary hypertension, and cardiac arrhythmias. The respiratory events may cause
oxyhemoglobin desaturation, which may cause morning headaches and decreased cognitive functioning.
Types:
1. Insomnia: acute<3months- chronic >3 months may be primary or secondary It occurs 2ry to
psychiatric disorders e.g. depression, generalized anxiety disorder or medical problems e.g. pain due to
arthritis and neuropathy, nocturnal dyspnea and cough in heart failure, nocturia, and GERD. Insomnia
can be secondary to medications use e.g alpha methyldopa, levodopa/carbidopa, diuretics, beta-
blockers, glucocorticoids, Decongestants, SSRI.
Main treatment is treating cause and behavioral therapy (sleep hygiene), short term
pharmacotherapy if other lines fail.
Short-acting agents (Eszopiclone, zaleplon) are recommended for problems with initiating sleep
• Lower associations with falls and hip fractures
• But produce the most pronounced rebound and withdrawal syndromes after discontinuation
Intermediate-acting agents (tenazepam)are recommended for problems with sleep maintenance
Other sedating drugs:
• Low doses of sedating antidepressants such as mirtazapine or trazodone at bedtime
• Sedating antihistamines (eg, diphenhydramine)
• Valerian is an herbal product with mild sedative action
• Melatonin receptor agonists
48
2. Obstructive apneas are caused by an anatomic obstruction of the airway during sleep. Patients
attempt to breathe and may appear to be choking or gasping for breath; Bed partner may report loud
snoring, cessation of breathing, and choking sounds during sleep. Main treatment = nasal CPAP =
continuous positive airway pressure and surgical correction of the obstruction. Weight loss in obese
patients with SDB can significantly reduce or eliminate the respiratory events. Oral appliances have
been developed for both obstructive sleep apnea and snoring.
3. Central apneas are caused by failure of the central nervous system respiratory centers. Central
apnea is common in patients with heart failure or stroke. Treatment is limited to treatment of heart
failure.
4. Periodic limb movement: Debilitating, repetitive, stereotypic leg movements that occur in non-
REM sleep. May present as difficulty maintaining sleep or excessive daytime sleepiness its
diagnosis requires polysomnography. Good response to dopamine agonist.
5. Restless legs syndrome: The diagnosis of restless legs syndrome is based on the patient’s
description of symptoms. The patient’s complaint is usually of nighttime leg discomfort or
difficulty in initiating sleep. There may be a family history of the condition and, in some cases, an
underlying medical disorder (eg, iron deficiency anemia, or renal or neurologic disease). Treatment
mainly by iron replacement and dopamine agonist.
Association between poor sleep quality and neurologic conditions, rehabilitation outcomes, and
mortality
• Emerging evidence suggests that poor sleep quality may also contribute to the development of
neurologic conditions e.g. Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative
diseases.
• Sleep disturbances are likely present in many individuals receiving PT services, which may exacerbate
their condition and slow recovery and impact their outcomes. Poor nighttime sleep quality) was
associated with less functional recovery.
• As sleep contributes to the modulation of pain, thus; addressing sleep disturbances may potentially
impact pain severity.
• Lower survival rates among the elderly during inpatient post-acute rehabilitation was associated with
self-reported poor sleep quality. Furthermore, healthy individuals (age range 30–70 years) who sleep
less than 6 hours or more than 8 hours each night had a higher risk for mortality compared with those
with adequate sleep (6–8 hours)
Role for Physical Therapist
1. Assess overall sleep health and screen for risk of sleep disorders.
2. Refer for additional assessment if individual is identified as at increased risk for a sleep disorder:
to sleep lab (polysomnography)
3. Provide sleep hygiene education.
4. Provide an appropriate exercise program.
5. Consider positioning to promote sleep quality.
6. Address bed mobility issues.
Screening for Common Sleep Disorders
Pittsburgh Sleep Quality Index (PSQI): https://www.med.upenn.edu/cbti/assets/user-
content/documents/Pittsburgh%20Sleep%20Quality%20Index%20(PSQI).pdf
Epworth Sleepiness Scale (ESS): http://www.sleepapnea.org/assets/files/pdf/ESS%20PDF%201990-
97.pdf
49
Sleep hygiene:
• Maintain a regular rising time
• Maintain a regular bedtime, unless not sleepy
• Decrease or eliminate naps, unless necessary
• Exercise daily, but not immediately before bedtime
• Do not use bed for reading or watching television
• Relax mentally before going to sleep
• If hungry, have a light snack (except with symptoms of gastroesophageal reflux or
medical contraindications), but avoid heavy meals at bedtime
• Limit or eliminate alcohol, caffeine, nicotine.
• Control the nighttime environment with comfortable cool temperature, quiet, and
darkness
• Try a fan or other “white noise” machine
• Wear comfortable bed clothing
• If unable to fall asleep within 30 minutes, get out of bed and perform soothing activity
(avoid bright light)
• Get adequate exposure to bright light during the day.
• Bathing before sleep has been demonstrated to enhance the quality of sleep in older
people, perhaps related to changes in body temperature with bathing.
Exercise
• Acute and chronic exercise has a moderate positive benefit on sleep characteristics by
increasing slow-wave sleep (deep stages) and total sleep time and decreasing sleep onset
latency.
• Moderate-intensity exercise has also been shown to improve sleep in healthy, sedentary
people aged 50 and older who reported moderate sleep complaints at baseline. However,
strenuous exercise should not be performed immediately before bedtime.
• Exercise should be conducted in the morning or early afternoon but not in the evening.
• Meditative movement, including tai chi, and yoga, also appears to improve sleep quality
• The exact mechanism of how exercise improves sleep characteristics remains unknown:
1. One theory is that exercise raises body temperature, which triggers heat-loss mechanisms and leads
to sleep onset.
2. Another theory suggests that exercise uses energy and produces “wear and tear” on the body, which
leads to sleep to recuperate and restore energy.
3. It is also possible that exposure to bright light while exercising outside and the production of
inflammatory cytokines in response to exercise may influence sleep characteristics and sleep
quality.
4. Changes in depressive symptoms, improvements in physical function, and weight loss have also
been associated with improvements in sleep due to exercise.
Positioning for Sleep and Addressing Bed Mobility to Facilitate Sleep Quality
• Education about positioning for sleep in a pain-free or pain-reduced position may limit
sleep disruption. For example, an individual with low back pain may benefit from
instruction to sleep side-lying with a pillow between his knees or to sleep supine with
pillows under his knees to reduce the lordosis of the back.
• The therapist should address the difficulty with transfers and bed mobility. Adequate bed
mobility is needed to change position while sleeping, and improved ease with changing
position with sleep may reduce sleep disruptions.
50
CHAPTER (3): APPROACH TO COMMON
MEDICAL PROBLEMS
Chronic respiratory diseases
Hypertension
Orthostatic hypotension
Congestive heart failure
Metabolic syndrome
Obesity
Dyslipidemia
Diabetes Mellitus
Constipation
Arthritis
Anemia
Chronic liver disease
Chronic kidney disease
51
Chronic respiratory diseases (CRDs)
Chronic respiratory diseases (CRDs) are diseases of the airways and other structures of the lung. Some of
the most common are asthma, chronic obstructive pulmonary disease (COPD), occupational lung diseases
and pulmonary hypertension.
Risk factors:
1. Smoking is the most common risk factor.
2. Genetics: cystic fibrosis, alpha 1 antitrypsin deficiency.
3. Other risk factors include: air pollution, occupational chemicals and dusts, and frequent lower
respiratory infections during childhood
4. Connective tissue diseases.
Airway diseases are classified into two groups
Obstructive disorders Restrictive disorders
Characterized by: reduction in airflow.
Shortness of breath in exhaling air.
Air will remain inside the lung after full
expiration
Characterized by reduction in lung volume
Difficulty in inhaling air
Due to stiffness of lung tissue or limited chest wall
expansion
COPD
Asthma
Bronchiectasis
Interstitial lung disease
Marked obesity
Scoliosis
Neuromuscular disorders
Clinical presentations can vary with each category:
 Chronic obstructive airway disease: includes both (emphysema and chronic bronchitis): chronic
productive cough, dyspnea, fatigue that may progress to respiratory failure and cyanosis. Peripheral
oedema, cor pulmonale, respiratory failure and polycythemia may develop in patients with COPD.
 Asthma: condition of airway hyper-responsiveness with reversible airflow obstruction that results
in intermittent symptoms of difficult breathing, wheezing, dyspnea, chest tightness, and non-
productive cough. Coughing often occurs at night or early in the morning. There are two forms of
bronchial asthma (allergic extrinsic and non-allergic intrinsic asthma). Early in the course of the
disease, the chest is usually free in between the attacks.
 Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD is a group
of respiratory diseases affecting the interstitium of the lungs. It may occur as an abnormal repair
process to a variety of injuries to the lungs leading to scarred and thickened alveoli. This makes it
more difficult for oxygen to pass into the bloodstream. The disease presents itself with the
following symptoms: shortness of breath, nonproductive coughing, fatigue, and weight loss, which
tend to develop slowly, over several months. Etiologies could be idiopathic, secondary to
connective tissue disease e.g. Sarcoidosis, SLE, Rh A, secondary to lung exposure to inorganic
inhalation: silicosis, asbestosis, or organic as Hypersensitivity pneumonitis (Extrinisic allergic
alveolitis).
 Pulmonary hypertension: Is abnormally elevated pressure in the pulmonary circulation.
Symptoms of pulmonary hypertension include: shortness of breath, tiredness, feeling faint or dizzy,
chest pain (angina), palpitations, edema, and ascites. The symptoms often get worse during
exercise. There are five classes.
52
o Class one pulmonary arterial HTN either
1. have no identifiable cause and is then referred to as idiopathic pulmonary
hypertension (formerly called primary pulmonary hypertension).
2. Or Drug- and toxin-induced (e.g., methamphetamine use)
3. Or associated with conditions: Connective tissue disease, HIV infection, Portal
hypertension, Congenital heart diseases, Schistosomiasis
o Class 2 – Pulmonary hypertension secondary to left heart disease
o Class III – Pulmonary hypertension due to lung disease, chronic hypoxia (COPD,
Obstructive sleep apnea, ILD).
o Class IV – chronic arterial obstruction: Chronic thromboembolic pulmonary
hypertension.
o class V :Pulmonary hypertension with unclear or multifactorial mechanisms:
Sarcoidosis, sickle anemia, glycogen storage disease
 Pulmonary hypertension is diagnosed by measuring the pulmonary pressures by
either echocardiogram or right heart catheterization.
Investigations to evaluate respiratory system:
Plain chest x-rays are most useful in identifying abnormalities in the heart, lung parenchyma, chest wall,
pleurae, diaphragm, mediastinum and hilum. Usually, a chest x-ray is the initial test performed to evaluate
the lungs.
Sputum microscopy and serology are useful for the diagnosis of infections of the lungs.
Flow rate and lung volume measurements are used to differentiate obstructive from restrictive
pulmonary disorders, to characterize disease severity and to measure responses to therapy. Obstructive
lung disorder is characterized by a decrease in the flow rate, whereas restrictive lung disorder is a
reduction in lung volume.
Arterial blood gas exchange analysis is useful in assessing accurate measures of PaO2, PaCO2 and
blood pH.
A Ventilation and perfusion scan, also called a v/q lung scan, is a type of medical imaging using
scintigraphy and medical isotopes to evaluate the circulation of air and blood within a patient's lungs in
order to determine the ventilation/perfusion ratio. The ventilation part of the test looks at the ability of air
to reach all parts of the lungs, while the perfusion part evaluates how well blood circulates within the lungs.
CT scan: CT scans of the chest define intrathoracic structures and abnormalities more clearly than do chest
x-rays. CT angiography using a bolus of intravenous contrast is employed to highlight pulmonary arteries,
useful in the diagnosis of pulmonary embolism.
Treatment:
Treatments for each chronic respiratory disease vary and the ideal solution is the reduction and avoidance
of risk factors. Neither asthma nor chronic obstructive pulmonary disease (COPD) can be cured but
treatments can reduce symptoms, prevent escalation and improve quality of life.
1. Smoking cessation
2. Supplemental oxygen should be prescribed for patients with PaO2 of 55 mmHg or less. Oxygen
should also be used in patients whose O2 saturation drops below 90% during exercise or sleep.
53
3. Asthma: based on avoidance of triggers, Bronchodilators (salbutamol inhalers and steroid
inhalers, such as beclometasone) using spacers or dry powder preparations, long acting β-agonist
(salmeterol) inhalers, and theophylline are effective.
4. COPD: use of bronchodilators, antibiotics, inhaled corticosteroids, mucolytics.
5. ILD is multiple conditions, hence treatment is different for each disease. If a specific occupational
exposure cause is found, the person should avoid that environment. If a drug cause is suspected,
that drug should be discontinued. Many cases due to unknown or connective tissue-based causes
are treated with corticosteroids, such as prednisolone. Some people respond to immunosuppressant
treatment.
6. Pulmonary hypertension: treat the cause, diuretics, anticoagulation, vasodilators (prostacyclin,
sildenafil, calcium channels blockers), Endothelium antagonists are the newest medications used
for this condition. These include bosentan and ambrisentan.
Role of physiotherapy:
1. Proper assessment and exclude acute on top of chronic conditions as infection, acute exacerbation
of COPD or acute asthma attack.
2. Screen for other comorbidities e.g. hypertension, IHD, or DM.
3. Stop smoking.
4. Nutritional counseling.
5. Vaccination pneumococcal, influenza.
6. Control environmental exposure to air pollution.
7. warm up and use of bronchodilators to avoid exercise- induced bronchospasm in asthma
8. Diaphragmatic breathing (to retrain the patient to use the diaphragm more than the chest
muscles).
9. Positioning changes can be used to address ventilation and perfusion mismatches and to help with
postural drainage.
10. Inspiratory muscle training is specifically directed at inspiratory muscles. It is usually performed
by breathing in against a measured resistance using a specific device. It is uncertain how much, or
if, inspiratory muscle training adds to a whole- body exercise programme, but it is known to be
effective alone and is potentially useful for individuals who are unable to cycle or walk.
54
11. More efficient coughing techniques can be taught to help expel secretions. This will help prevent
pooling of secretions, subsequent infections, or air trapping. Manual chest therapy, including
percussion or a vibrator, can help mobilize secretions.
12. A pulmonary rehabilitation program should include endurance and/or reconditioning exercises. For
these the therapist needs to monitor the patient’s heart rate and oxygen saturation. The heart rate
should be limited, generally as a percentage of an age-adjusted maximal heart rate (this is especially
important for patients with additional cardiac disease).
13. Oxygen saturation should be monitored as well as the patient’s perceived exertion. Exercise should
be discontinued for O2 saturation below 90%, significant increases in exertion or dyspnea, chest
pain, or tachycardia or irregular heart rate.
14. Therapy should be performed 3–5 days per week. Walking is a fundamental part of a pulmonary
rehabilitation, and patients should be encouraged to walk outside of therapy (with appropriate
precautions and oxygen supplementation if required).
15. An exercise bicycle may also be beneficial for home use. An important part of therapy is for patients
to learn their abilities and limitations so they can safely exercise at home. Physical or occupational
therapists should also help develop an upper body exercise program.
16. Occupational therapists may be helpful in assessing activity of daily living (ADL) impairments and
with prescribing assistive devices. Respiratory therapists can help instruct patients in the proper use
of medications and mobilization of secretions and teach them breathing techniques. In pulmonary
patients, nutritional evaluations may also be needed.
1) Make sure you are sitting or standing upright.
2) Put on the nose clip.
3) Hold the IMT by the handle grip.
4) Place the mouthpiece in your mouth, making sure you put your
lips over the outer shield to make a good, airtight seal.
5) Breathe out as far as you can then take a fast, forceful breath in
through your mouth. Take in as much air as you can, as quickly as
possible, whilst expanding your chest.
6) Breathe out slowly and with minimal effort, letting your shoulders
relax.
7) Pause and then take another fast, forceful breath in.
8) Repeat this fast, forceful breath
55
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist
Basic of geriatrics and internal medicine for physiotherapist

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Basic of geriatrics and internal medicine for physiotherapist

  • 1. By Dr. Doha Rasheedy Associate Professor of Geriatric Medicine Basic Geriatrics and internal medicine for physiotherapist
  • 2. Content Title Page No. Chapter 1  Ageing .....................................................................................………..2  Age related physiological changes........................................………..5 Chapter 2  Disease presentations in Elderly…………...........................………..12  Comprehensive Geriatric Assessment………… .................………..14  Delirium, Dementia, Depression…………...........................………..17  Health promotion in elderly…………..................................………..28  Geriatric pharmacology…………........................................………..29  Sarcopenia………… ..............................................................………..33  Frailty………… .....................................................................………..37  Osteoporosis………… ...........................................................………..42  Sleep disorders………… .......................................................………..48 Chapter 3  Chronic respiratory diseases………… ................................………..52  Hypertension………… ..........................................................………..56  Orthostatic hypotension…………........................................………..59  Congestive heart failure…………........................................………..61  Metabolic syndrome………… ..............................................………..64  Obesity………… ....................................................................………..67  Dyslipidemia…………...........................................................………..70  Diabetes Mellitus…………....................................................………..72  Constipation………… ...........................................................………..76  Arthritis………… ..................................................................………..78  Anemia…………....................................................................………..82  Chronic liver disease………… .............................................………..84
  • 3.  Chronic Kidney Disease………… ........................................………..87 Chapter 4  Immobilization………….......................................................………..94  Falls………….........................................................................………..102  Dizziness…………..................................................................………..108  Fatigue………… ....................................................................………..123
  • 4. CHAPTER (1): AGEING PROCESS Definition of Ageing Types of Ageing Theories of Ageing Ageing of different Body systems 1
  • 5. Ageing Process Definition of ageing:  Physiological ageing (normal ageing): is a complex process of progressive reduction in the function of all body organs. This process may be summarized in the expression “homeostenosis”. It reflects alteration of organ structure and function with time alone and in the absence of supervening disease processes.  Physiological ageing is an inevitable changes can be explained from both biologic and psychosocial perspectives.  Processes influencing ageing include gene variations and differences in expression and environmental factors.  Age and disease are closely associated phenomena. Secondary ageing then refers to those aspects of the aged state that are attributable to disease. Characters of the ageing process: Aging is characterized by being Universal, Cumulative, Unidirectional, Heterogeneity, Intrinsic, and Deleterious. Characters of ageing process Universal All humans age Cumulative the effects of aging are irreversible and accumulate over time Unidirectional For example, a postmenopausal woman cannot become ovulatory again. Heterogeneity occurs at different rates among individuals and within individuals Intrinsic Because even under the best environmental conditions an individual ages, aging is intrinsic to the organism. Deleterious aging is harmful, resulting in decreased vitality and an increased vulnerability to disease and environmental stresses Ageing is different from Cellular senescence is the process by which a cell loses its ability to divide, grow, and function, ultimately leading to cell death. Fig 1: Predictors of the Ageing process 2
  • 6. Theories of ageing (biological) Fig 2: examples of biological theories of ageing Cellular senescence/ telomere theory:  Replicative senescence is a specific type of cellular senescence that ultimately results from loss of telomeres (specialized structures composed of a repeating DNA sequence and located at the ends of each linear chromosome).With each cell division, a small amount of DNA is lost at each chromosome end, resulting in shorter telomeres, altered telomere structure, and eventual replicative senescence.  Activation of the telomerase enzyme will regenerate telomeres, prevent replicative senescence, and immortalize human primary cell cultures Free Radical theory:  Free radicals are reactive oxygen species (ROS) are highly reactive molecules that can damage all sorts of cellular components.  ROS can originate from exogenous sources such as ultraviolet (UV) and ionizing radiations or from several intracellular sources: (phagocytosis, fatty acid degradation, drug detoxification by liver, ATP utilization).  Toxic accumulation of ROS interfere with cell communication, disturb DNA, RNA and protein synthesis, lower energy levels and generally impede vital chemical processes.  To protect against oxidation there are many different types of antioxidants, from vitamins C and E selenium, CoQ10 and lipoic acid to enzymes such as superoxide dismutase (SOD), catalase, and glutathione peroxidase. Briefly, antioxidant enzymes are capable of degrading ROS into inert compounds through a series of chemical reactions. 3
  • 7. The Neuro-endocrine Theory  Hypothalamo-pituitary-adrenal (HPA) axis is the master regulator that control the onset and termination of each life stage. It is also responsible for the maintenance of the internal “homeostasis” (steady state) despite the continuing changes in the environment.  During life span, chronic exposure to severe stress from a multitude of physical, biological, or emotional stimuli may exhaust or weaken the capacity to adapt and lead to the so-called “diseases of adaptation” and death . Aging would then result from “a decreasing ability to survive stress.  Evidence to this theory: the cortisol hormone which is considered to be responsible for stress is one of the few hormones that increases with age. The immunosenescence theory:  The immune system must control and eliminate foreign organisms and substances in the host body while at the same time recognizing and therefore sparing from destruction the molecules (cells and tissues) from oneself. In most elderly humans, immunosenescence is characterized by a decreased resistance to infectious diseases, a decreased protection against cancer, and an increased failure to recognize self (hence, autoimmune pathology. The disposable soma  The somatic cells are only preserved to maintain reproductive functions. After reproduction somatic cells become disposable. Antagonistic pleiotropy  The theory of antagonistic pleiotropy is based on two assumptions. First, it is assumed that a particular gene may have an effect not on one trait only but on several traits of an organism (pleiotropy). The second assumption is that these pleiotropic effects may affect individual fitness in opposite (antagonistic) ways.  Such genes will be maintained in the population due to their positive effect on reproduction at young ages despite their negative effects at old age (their negative effects in later life will look exactly like the aging process) Error catastrophe  Gene expression accuracy diminishes with age. This culminates in a higher proportion of abnormal proteins.  There is a certain rate of error tolerance of a cell, exceeding which the cell fails in its ability to sustain and function normally.  Thus, accumulation of errors in the genomic replication machinery beyond a certain threshold might lead to erroneous dysregulation of the protein synthesis, folding and expression mechanisms which ultimately might bring about deterioration in the functionality of the cell. 4
  • 8. Types of Ageing: Chronological The number of years a person has lived since birth. Biological age changes in physical structures and functions that affect either ability to survive or appearance Social How a person perceives the aging process and how it relates to the society in which they live Psychological age changes in mental processes and behavior The elderly are special population with special needs:  Physiological Changes in the Elderly (Normal Aging is not a disease)  Multiple comorbidities and multiple medications: The incidence of chronic diseases increases with ageing e.g. dementia, Parkinsonism, stroke, heart diseases leading to polypharmacy.  Overlapping Variables (physiological, social, psychological, environmental variables) &multiple diseases): heterogeneous Population: Need for Individualized Treatment:  Atypical presentations of diseases  They need different assessment approach (see comprehensive geriatric assessment) through Multidimensional, Interdisciplinary, Geriatric team  The goal of elderly care is maintaining function &quality of life:" To add life to years NOT only years to life Age related physiological changes:  Aging and disease are not synonymous. Although the aging process makes individuals more vulnerable to illness and disease, pathology is not inevitable with age. Aging alone generally does not cause symptoms.  The major age-related biologic change is a diminished reserve capacity and the inability to maintain homeostasis in the face of stressors such as a disease or adverse environmental factors such as excessive heat. Body system Physiological change Clinical implications General body composition The percent of body water (TBW) decreases with aging ↑risk of dehydration Pharmacokinetic effect Lean body mass decreases because of muscle loss Slower gait speed, weaker hand grip Pharmacokinetic effect Increased percent of body fat (until around 70, then decreases) Pharmacokinetic effect Decreased bone mass Changes in Resting Energy Rate Decreased Basal Metabolic Rate Vision loss of rods and cones ↓ light sensitivity, color perception, dark adaptation, night vision (stressor) 5
  • 9. The lens becomes denser, thicker, and less elastic. ↑ risk of cataract Hearing loss of hair cells in the organ or Corti and loss of cochlear nerve cells Difficulty in speech discrimination esp. in noisy environments (stressor). ↑ difficulty to determine the source of sound Smell and taste ↓the number of taste buds and olfactory receptors. Smell is more affected than taste with age and declines rapidly after age 50 ↑ risk of malnutrition ↓ quality of life Difficult compliance on therapeutic diets Immunity Thymic involution and attenuated T- cell-mediated Immunity, ↓T cells lead to reactivation of quiescent infections, such as TB and varicella. decline in delayed-type skin- hypersensitivity reactions to injected antigens (anergy) in many frail aged subjects ↓production of antibody by B cells ↑ risk of infection. ↓efficacy of vaccination Autoantibodies occur more frequently (e.g. antiphospholipid antibodies) and are associated with vascular disease Their significance in older people is uncertain. Cardiovascular system Loss of cardiac myocytes secondary to apoptosis, with compensatory hypertrophy of remaining cells. Changes in stroke volume and diastolic function Accumulation of intracellular lipofuscin and extracellular amyloid. Increased intercellular collagen. leading to reduced LV diastolic compliance Loss of pacemaker cells Increase risk of sick sinus syndrome Patchy fibrosis of the conduction system Increase risk of heart block Reduced baroreceptor sensitivity Increased risk of orthostatic hypotension. ↓ β-adrenergic receptors number & sensitivity Lead to altered response to beta blockers Beta-adrenergic-mediated vasodilatation decreased while Alpha-adrenergic- mediated vasoconstriction unchanged leading to hypertension Increased vascular stiffness Increases risk of systemic hypertension Respiratory system Calcification of the intercostal cartilages; arthritis of the costo- vertebral joints Rigidity and stiffness of the wall increases and chest wall compliance decreases Gradual atrophy of intercostal muscles (loss of muscle mass) Greater contribution from diaphragmatic and abdominal muscles and may lead to diaphragmatic fatigue The cilia beat decreases with age and there is a reduction in number of cilia Reduces clearance of debris and pathogens Increases chance of infection 6
  • 10. Thickening of the alveolar basement membrane Decrease gas-diffusing capabilities, increase in ventilation/perfusion heterogeneity. Arterial oxygenation declines. Ventilation control Diminishes Diminishes response to hypercapnia and hypoxia Endocrine system Marked decrease in dehydroepiandrosterone (DHEA) Decreased free and bioavailable testosterone Decreased production of vitamin D by skin and activation in kidney Decreased GH, IGF1 Increased cortisol level Increased risk of frailty, sarcopenia, and osteoporosis. ↓ Aldosterone secretion Increased risk of Orthostatic hypotension Musclo-skeletal system Muscle Marked decrease in muscle mass (sarcopenia) due to loss of muscle fibers Decreased myosin heavy chain synthesis Decreased innervation, increased number of myofibrils per motor unit Infiltration of fat into muscle bundles Bone Slower healing of fractures Decreasing bone mass in men and women, both trabecular and cortical bone Decreased osteoblast bone formation Joints Disordered cartilage matrix Modified proteoglycans and glycosaminoglycans Gastrointestinal ↓ Saliva production ↑ Oral infections, ↑ Gum disease Decreased liver size and blood flow Hepatocytes accumulate secondary lysosomes, residual bodies, and lipofuscin Impaired clearance by liver of drugs that require extensive phase I metabolism Reduced inducibility of liver mixed- function oxidase enzymes Mild decrease in bilirubin Mild decrease in stomach acid production, probably due to nonautoimmune loss of parietal cells Impaired response to gastric mucosal injury Decreased mucus secreting cells Slowed gastric emptying Prolonged gastric distention,↑ Postprandial satiety Decreased pancreatic mass and enzymatic reserves Insulin resistance Decrease in effective colonic contractions Increased risk of constipation 7
  • 11. ↓ Calcium absorption ↑ Bone loss Skin Epidermal turnover rates decrease by 30% to 50% by the age of 70 Rougher skin with decreased barrier function, delayed wound healing. The dermal- epidermal junction fattens Resulting in decreased contact between the two layers. As a result the two layers may easily separate, making older skin more likely to tear and blister. Basal and peak levels of cutaneous blood flow are reduced by about 60% compromised vascular responsiveness during injury or infection Collagen synthesis decreases and degradation increases Loss of the connective tissue matrix and impaired wound healing. Elastic fibers decrease in number and size decreased skin elasticity Subcutaneous fat decreases with age Decreasing its ability to protect deeper structures from injury. Decreased Langerhans cells Increased risk of infections Hematologic Bone marrow reserves decreased Failure to response to high demand e.g infections , hemorrhage, hemolysis Kidney ↓ Kidney size, mass, and number of functional glomeruli Decreased creatinine clearance and GFR 10 ml/decade affecting drug excretion ↓ Number/length of functional renal tubules ↓ Concentrating/diluting capacity, ↑ Fluid and electrolyte abnormalities ↓ Renal blood vessel elasticity ↓ Renal blood flow ↓ Vitamin D activation Vitamin D deficiency Decreased serum renin and aldosterone Increased risk of Volume depletion and hypokalemia Peripheral nervous system Loss of spinal motor neurons Decreased size of large myelinated fibers Increased heterogeneity of axon myelin sheaths Decreased vibratory sensation, especially in feet Decreased thermal sensitivity (warm– cool) Decreased sensory nerve action potential amplitude Central nervous system 1. Small decrease in brain mass, Nonrandom loss of neurons to modest extents 2. Decreased brain blood flow and impaired autoregulation of perfusion 3. Decreased density of dendritic connections, synapses. 4. Increased numbers of scattered neurofibrillary tangles and senile plaques 5. Decreased myelin and total brain lipid 6. Altered neurotransmitters, including dopamine and serotonin Decline in fluid intelligence Slowed central processing and reaction time Affected working memory, divided attention 8
  • 12. 9
  • 13. QUIZ 1: 1. Age-related changes in the cardiovascular system among older adults include: A. Adrenergic receptors number-Decreased βA. B. Decreased systolic blood pressure C. Increased maximal heart rate during exercise D. Increased β-adrenergic receptors sensitivity E. Increased cardiac output under stress 2. Age related changes in vision include A. Increase color Sensitivity B. Decrease dark Adaptation C. Decrease intraocular pressure D. Increase risk of iridocyclitis E. Decreased risk of cataract 3. The following can cause decrease appetite among elderly A. Decrease taste sensation B. Decrease intestinal motility C. Loss of teeth D. Cognitive impairment 4. Elderly are more prone to develop infections because A. Decrease T cell immunity B. Increased environmental factors C. Cognitive impairment D. Iron deficiency Anemia 5. Elderly develop sarcopenia due to all of the following except A. Decreased myosin heavy chain synthesis B. Decreased innervation, increased number of myofibrils per motor unit C. Infiltration of fat into muscle bundles D. Excess mitochondrial ATP production 10
  • 14. CHAPTER (2): GERIATRIC MEDICINE Disease presentations in Elderly Comprehensive Geriatric Assessment Delirium, Dementia, Depression Health promotion in elderly Geriatric pharmacology Sarcopenia Frailty Osteoporosis Sleep disorders 11
  • 15. The definition of an atypical presentation of illness is: when an older adult presents with a disease state that is missing some of the traditional core features of the illness usually seen in younger patients. 1. Examples for altered presentations of diseases  Dwindles (Functional decline)  Weakness  Falls  Immobility  Incontinence  Cognitive Change  Mood Change 2. Examples for non-specific presentations of diseases: e.g. Fatigue which can be a presentation of any of the following: Organic conditions Cardiopulmonary (heart failure, COPD, IPF) Neurological (MS, Parkinsonism) metabolic/ (DM, hypothyroidism toxic (chronic lead exposure) infections (HCV, HBV, HIV) Deficiency states (Vitamin D deficiency) neoplasm Psychogenic: depression Drugs: beta-blockers, diuretics, chemotherapy 3. Examples for silent presentations of diseases: During preoperative assessment, the presence of ECG changes suggestive of previous myocardial infarction in elderly patient without history suggesting coronary ischemia. Osteoporosis is usually silent until fracture occurs. Prevalence of atypical presentations in elderly: Atypical presentations were found in approximately 20% of elderly patients in the Emergency Department (ED), with (35%) of older adults with infectious diseases presented atypically. 12
  • 16. Silent MI in elderly, detected incidentally on electrocardiogram (ECG) is high, ranging between 38% and 60%. Consequences of atypical presentations in elderly: Delayed diagnosis, misdiagnosis, and mismanagement with increased morbidity. Presentations of ischemic heart disease in elderly: Typical Pain is usually substernal chest pain/discomfort with exercise, relief by nitroglycerin or rest Non specific Fatigue , Shortness of breath silent Minimal or no chest pain, no shortness of breath or acute confusion, silent ECG or Echo findings Altered Acute confusion Syncope Acute functional decline Attack of Epigastric pain Attacks of back pain Attacks of jaw pain Attacks of neck pain Presentation of Pneumonia Typical Productive cough of purulent sputum The temperature may rise to 38.9°–39.4°C Non specific Minimal cough, no sputum production, no fever No leucocytosis May appear tired or confused Altered Dwindles, delirium Causes of atypical presentations in elderly: • The aging process: fever is usually absent in elderly due to lower basal body temperature, thermoregulatory center aging, lower skeletal muscle mass • Multiple Co-morbidities: presence of severe osteoarthritis of the knee with reduced physical performance may delay the presentations of heart failure and peripheral arterial disease until symptoms are present during minimal activity or even at rest. • Poly-pharmacy: (use of beta blockers mask tachycardia in anemia or infections) Remember: New onset functional decline is a manifestation of an acute illness in elderly. 13
  • 17. Comprehensive Geriatric Assessment Comprehensive geriatric assessment (CGA) is a multidimensional, interdisciplinary diagnostic process to determine the medical, psychological, and functional capabilities of a frail elderly person in order to develop a coordinated and integrated plan for treatment and long-term follow up. Interdisciplinary Team - Team Members Overview  Nurse  Physician trained in Geriatrics  Dietitian  Physical Therapist  Social Worker  Patient, Family members, caregiver  Psychologist  Speech-Language specialist  Audiologist  Occupational Therapist Assessment Domains Medical (Medical illnesses, surgical history, medications, nutrition, dentition, Vision, Hearing, Pain, impotence, Sleep, health promotion, Geriatric giants: Urinary incontinence,, Frailty) Psychiatric (Cognitive status, Emotional status) Functional status (Activities of daily living ADLs, Instrumental activities of daily living IADLs) Physical (Balance and gait, Falls) Environmental (Social, financial status, Environmental hazards). Geriatric depression scale – 15items 1 - .‫دلوقتى‬ ‫حياتك‬ ‫عن‬ ‫راضى‬ ‫انت‬ 2 - .‫واهتماماتك‬ ‫نشاطاتك‬ ‫من‬ ‫كثير‬ ‫قللت‬ ‫انت‬ 3 - .‫فاضية‬ ‫حياتك‬ ‫ان‬ ‫حاسس‬ ‫انت‬ 4 - .‫وزهقان‬ ‫متضايق‬ ‫انك‬ ‫بتحس‬ ‫الغالب‬ ‫فى‬ 5 - ‫الغالب‬ ‫فى‬ .‫عالية‬ ‫بتكون‬ ‫معنوياتك‬ 6 - .‫تحصلك‬ ‫ها‬ ‫وحشة‬ ‫حاجة‬ ‫ان‬ ‫خايف‬ ‫انت‬ 7 - .‫مبسوط‬ ‫انك‬ ‫بتحس‬ ‫الغالب‬ ‫فى‬ 8 - .‫الحيلة‬ ‫قليل‬ ‫انك‬ ‫بتحس‬ ‫الغالب‬ ‫فى‬ 9 - .‫جديدة‬ ‫حاجات‬ ‫تعمل‬ ‫تخرج‬ ‫انك‬ ‫عن‬ ‫البيت‬ ‫فى‬ ‫تقعد‬ ‫بتحب‬ 10 - .‫االخرين‬ ‫من‬ ‫اكثر‬ ‫الذاكرة‬ ‫فى‬ ‫مشاكل‬ ‫عندك‬ ‫انك‬ ‫بتحس‬ ‫انت‬ 11 - .‫عايش‬ ‫لسة‬ ‫انك‬ ‫حلوة‬ ‫حاجة‬ ‫دى‬ ‫ان‬ ‫بتعتقد‬ ‫انت‬ 12 - .‫ليك‬ ‫مناسبة‬ ‫مش‬ ‫بطريقة‬ ‫الحياة‬ ‫عايش‬ ‫انك‬ ‫شايف‬ ‫انت‬ 13 - .‫ونشاط‬ ‫حيوية‬ ‫عندك‬ ‫ان‬ ‫حاسس‬ ‫انت‬ 14 - .‫منها‬ ‫ميئوس‬ ‫دى‬ ‫حالتك‬ ‫ان‬ ‫حاسس‬ ‫انت‬ 15 - ‫اغلب‬ ‫ان‬ ‫حاسس‬ ‫انت‬ ‫منك‬ ‫احسن‬ ‫حواليك‬ ‫اللى‬ ‫الناس‬ 14
  • 18. Mental State Examination (MMSE) - Mini ‫المختصر‬ ‫العقلية‬ ‫الحالة‬ ‫فحص‬ 1 - ( )‫(االهتداء‬ ‫التوجه‬ 10 ) ‫إيه؟‬ ‫فصل‬ ‫فى‬ ‫احنا‬ ‫لى‬ ‫تقولى‬ ‫تقدر‬ ‫؟‬ ‫كام‬ ‫سنة‬ ‫احنا‬ ‫لى‬ ‫تقول‬ ‫تقدر‬ ‫إيه؟‬ ‫شهر‬ ‫فى‬ ‫احنا‬ ‫لى‬ ‫تقول‬ ‫تقدر‬ ‫إيه؟‬ ‫النهاردة‬ ‫لى‬ ‫تقول‬ ‫تقدر‬ ‫؟‬ ‫النهاردة‬ ‫تاريخ‬ ‫لى‬ ‫تقول‬ ‫تقدر‬ ‫؟‬ ‫دلوقت‬ ‫فين‬ ‫احنا‬ ‫؟‬ ‫الكام‬ ‫الدور‬ ‫فى‬ ‫احنا‬ ‫؟‬ ‫إيه‬ ‫حى‬ ‫تتبع‬ ‫أنت‬ ‫؟‬ ‫إيه‬ ‫محافظة‬ ‫تتبع‬ ‫أنت‬ ‫فى‬ ‫احنا‬ ‫؟‬ ‫إيه‬ ‫جمهورية‬ 2 - ( : ‫المعلومات‬ ‫تسجيل‬ 3 ) ‫قولك‬ ‫ها‬ 3 ‫واحفظهم‬ ‫ورائى‬ ‫وكررهم‬ ‫كلمات‬ ‫كورة‬ - ‫شجرة‬ - ‫كرسى‬ 3 - ( : ‫والحساب‬ ‫االنتباه‬ 5 ) ‫من‬ ‫أكثر‬ 5 : ‫دراسة‬ ‫سنوات‬ ‫اطرح‬ 7 ‫من‬ 100 ‫منه‬ ‫اطرح‬ ‫والباقى‬ 7 ‫بعد‬ ‫وتوقف‬ ‫نازل‬ ‫وأنت‬ 5 ( ‫مرات‬ 93 - 86 - 79 - 72 - 65 ) ‫من‬ ‫أقل‬ 5 ‫د‬ ‫سنوات‬ : ‫راسة‬ ‫اطرح‬ 3 ‫من‬ 20 ‫منه‬ ‫اطرح‬ ‫والباقى‬ 3 ‫بعد‬ ‫وتوقف‬ 5 ‫مرات‬ : ‫قادر‬ ‫غير‬ ‫كان‬ ‫إذا‬ ‫بالعكس‬ ‫األسبوع‬ ‫أيام‬ ‫قول‬ 4 - ( : ‫الذاكرة‬ ‫استرجاع‬ 3 ) ‫الـ‬ ‫لى‬ ‫قول‬ 3 ‫كده‬ ‫قبل‬ ‫قولناهم‬ ‫اللى‬ ‫كلمات‬ ‫كورة‬ - ‫شجرة‬ - ‫كرسى‬ 5 - : ‫اللغـة‬ )‫األشياء‬ ‫هذه‬ ‫عن‬ ‫واسأل‬ ‫والساعة‬ ‫القلم‬ ‫على‬ ‫(شاور‬ ‫ده‬ ‫إيه‬ ( 2 ) ( ‫عاجبانى‬ ‫حاجة‬ ‫وال‬ ‫والمانى‬ ‫والكانى‬ ‫ورائى‬ ‫كرر‬ 1 ) ‫من‬ ‫مكون‬ ‫ألمر‬ ‫المريض‬ ‫استجابة‬ 3 ( ‫حركات‬ 3 ) .‫األرض‬ ‫على‬ ‫وحطها‬ ‫االثنين‬ ‫بإيديك‬ ‫اثنين‬ ‫وطبقها‬ ‫اليمين‬ ‫بإيدك‬ ‫دى‬ ‫الورقة‬ ‫امسك‬ ‫نقو‬ ‫أو‬ ‫ونفذه‬ ‫المكتوب‬ ‫اقرأ‬ ( )‫عينك‬ ‫(غمض‬ ‫له‬ ‫ل‬ 1 ) ( .‫مفيدة‬ ‫جملة‬ ‫قل‬ ‫أو‬ ‫معنى‬ ‫لها‬ ‫مفيدة‬ ‫جملة‬ ‫اكتب‬ 1 ) ( : ‫الشكل‬ ‫هذا‬ ‫ارسم‬ 1 ) 15
  • 19. ‫اليومية‬ ‫األنشطة‬ ‫تأدية‬ ‫على‬ ‫القدرة‬ ‫قياس‬ ADL ‫بمفرده‬ ‫بمساعدة‬ ‫كاملة‬ ‫بمساعدة‬ :‫االستحمام‬ ‫تستطيع‬ ‫هل‬ :‫وخلعها‬ ‫مالبسك‬ ‫ارتداء‬ ‫تستطيع‬ ‫هل‬ ‫التبول‬ ‫تستطيع‬ ‫هل‬ :‫والتبرز‬ ‫االنتق‬ ‫تستطيع‬ ‫هل‬ :‫الكرســـى‬ ‫او‬ ‫السرير‬ ‫والى‬ ‫من‬ ‫ال‬ :‫والتبرز‬ ‫التبول‬ ‫فى‬ ‫التحكم‬ ‫تستطيع‬ ‫هل‬ :‫والشراب‬ ‫الطعام‬ ‫تناول‬ ‫تستطيع‬ ‫هل‬ IADL ‫بمفرده‬ ‫بمساعدة‬ ‫كاملة‬ ‫بمساعدة‬ 1 - ‫التليفون؟‬ ‫استعمال‬ ‫تستطيع‬ ‫هل‬ 2 - ‫طعامك؟‬ ‫تجهيز‬ ‫تستطيع‬ ‫هل‬ 3 - ‫هل‬ ‫لها؟‬ ‫تمشى‬ ‫أن‬ ‫من‬ ‫أبعد‬ ‫ألماكن‬ ‫الذهاب‬ ‫تستطيع‬ 4 - ‫المنزل؟‬ ‫بأعمال‬ ‫القيام‬ ‫تستطيع‬ ‫هل‬ 5 - ‫المالبس؟‬ ‫أو‬ ‫البقالة‬ ‫شراء‬ ‫تستطيع‬ ‫هل‬ 6 - ‫بك؟‬ ‫الخاصة‬ ‫األدوية‬ ‫تناول‬ ‫تستطيع‬ ‫هل‬ 7 - ‫بالمال؟‬ ‫التعامل‬ ‫تستطيع‬ ‫هل‬ ‫بنفسك‬ ‫مالبسك‬ ‫غسيل‬ ‫تستطيع‬ ‫هل‬-8 16
  • 20. Delirium (Acute Confusional State) Delirium is a serious disturbance in mental abilities that results in confused thinking and reduced awareness of the environment (inattention), and altered level of consciousness.. The start of delirium is usually rapid — within hours or a few days. Causes  Drugs: sedatives, anticholinergic drugs, drug withdrawal  Infection (eg: chest infection, urinary tract infection)  Urine retention– Fecal impaction  Metabolic: hypoglycemia-hyperglycemia, end organ disease (uremia, hepatic encephalopathy, respiratory failure)  Electrolytes disturbance: ↓ Na, Ca  Myocardial infarction(MI)  Pain Clinical picture: ACUTE ONSET, FLUCTUATING COURSE, SECONDARY TO MEDICAL condition, INATTENTION, DISORGANIZED THINKING (The Confusion Assessment Method CAM) 1. Inattention:  inability to stay focused on a topic or to switch topics  inability to stay focused on a topic or to switch topics 2. Altered consciousness:  Increased; irritability and excitability  Decreased; apathy, decreased consciousness and decreased response to stimuli 3. Cognitive impairment  Poor memory, particularly of recent events  Disorientation — for example, not knowing where he is  Rambling or nonsense speech  Trouble understanding speech 4. Neuropsychiatric findings;  Hallucinations  Illusions  Delusions  Emotional distress  sleep disturbances Types: hyperactive, hypoactive, mixed  Hyperactive delirium. Probably the most easily recognized type, this may include restlessness (for example, pacing), agitation, rapid mood changes or hallucinations, and refusal to cooperate with care. 17
  • 21.  Hypoactive delirium. This may include inactivity or reduced motor activity, sluggishness, abnormal drowsiness, or seeming to be in a daze.  Mixed delirium. This includes both hyperactive and hypoactive signs and symptoms. The person may quickly switch back and forth from hyperactive to hypoactive states. Complications delirium: 1. Iatrogenic complications (eg: antipsychotic use, mechanical constraints) 2. Incontinence 3. Complications of bed ridden (eg: deconditioning, pressure ulcers, aspiration) 4. Malnutrition 5. Hospitalization 6. Long-term care admission 7. Falls 8. Functional decline Management of delirium: 1. Identify and remove or treat underlying cause (may be life threatening MI, hyponatremia) 2. Provide general supportive measures:  Keep patient in quiet, well-lit room (eg, night lights)  Ensure safe environment and strict supervision  Avoid excessive noise, stimulation  Reorientation: o Encourage familiar faces (family members) at bedside for reassurance o Provide orientation (eg, calendar, clock) o Correct sensory impairment (eg, vision, hearing)  Nutrition and good hydration  Enhance mobility and range of motion  Care of bowel and bladder 3. Control of disruptive behavior  Use physical restraints only as last resort to maintain patient safety (eg, prevent patient from pulling out tubes, catheters)  For acute agitation or aggression: use a high-potency antipsychotic such as haloperidol (Haldol) 0.5-2mg po or IM. Role of physical therapy in prevention and management of delirium:  Early mobilization and walking following surgeries  Minimizing use of immobilizing equipment  Individual active mobilization strongly encouraged, Progress through range-of-motion, sitting, standing, walking, ADLs  Assisted walking for frail patients routinely performed by PT 18
  • 22. Delirium and dementia Dementia and delirium may be particularly difficult to distinguish, and a person may have both. In fact, delirium frequently occurs in people with dementia. But having episodes of delirium does not always mean a person has dementia. So a dementia assessment should not be done during a delirium episode because the results could be misleading. Dementia is the progressive decline of memory and other thinking skills due to the gradual dysfunction and loss of brain cells. The most common cause of dementia is Alzheimer's disease. Some differences between the symptoms of delirium and dementia include: Onset. The onset of delirium occurs within a short time, while dementia usually begins with relatively minor symptoms that gradually worsen over time. Attention. The ability to stay focused or maintain attention is significantly impaired with delirium. A person in the early stages of dementia remains generally alert. Fluctuation. The appearance of delirium symptoms can fluctuate significantly and frequently throughout the day. While people with dementia have better and worse times of day, their memory and thinking skills stay at a fairly constant level during the course of a day. Because symptoms of delirium and dementia can be similar, input from a family member or caregiver may be important for a doctor to make an accurate diagnosis. 19
  • 23. Dementia Dementia is a syndrome of acquired (not learning difficulties), chronic (lasts months to years), global (not just memory or just language problems), progressive impairment of higher brain function, in an alert patient (not drowsy), which interferes with social and functional abilities. What are the higher brain functions?  Learning and Memory (e.g. free recall, cued recall)  Aphasia (e.g. word-finding difficulty)  Apraxia (inability to perform motor tasks, such as cutting a loaf of bread, despite intact motor function)  Agnosia (inability to recognize objects despite intact sensory function)  Impaired executive function (poor abstraction, mental flexibility, planning, and judgment). Different causes of dementia Reversible causes of dementia Irreversible causes of dementia  Thyroid disease  Vitamin B 12 deficiency  Depression  Tumors  Hypercalcemia  Subdural heamatoma  Normal pressure hydrocephalus  Syphilis- HIV  Drugs(anticholinergic) Degenerative disorders:  Alzheimer disease  Lewy body dementia  Frontotemporal dementia Vascular dementia Mixed dementia Infections:  AIDS-related dementia  Creutzfeldt–Jakob (C-J) disease Toxins:  Chronic alcholism Pathology of Alzheimer disease Differential Diagnosis 1. Amyloid plaques 2. Neurofibrillary tangles 3. Loss of synapses and dendrites 4. Cerebral atrophy eventually occurs; however, atrophy is not strongly correlated with clinical severity. Acetylcholine is the main neurotransmitter that is deficient 20
  • 24. Delirium Depression Age related memory loss: • Much milder symptoms • Not substantially progressive • Does not impair function Mild cognitive impairment • May represent a transitional state between normalcy and dementia but some cases may not progress to Dementia • Either amnestic or non-amnestic MCI • No functional impairment 21
  • 25. Alarming signs: 1. People with dementia often forget things and never remember them. 2. Asking the same question over and over 3. Difficulty in performing familiar tasks. 4. Problems with language. 5. Time and place disorientation. 6. Misplacing things. 7. Poor judgment Consequences of dementia Malnutrition, safety issues, fall risk, functional decline, incontinence, Delirium, depression, sleep disorders, aspiration, immobility, Caregiver stress. Means of Confirmation or Diagnosis Definitive diagnosis is made upon autopsy. Exclude reversible causes Laboratory Tests Cerebrospinal fluid (CSF) for protein analysis Neuropsychological testing Mini mental state examination Imaging Computed tomography (CT) of the brain Magnetic resonance imaging (MRI) of the brain Single-photon emission computed tomography (SPECT) for hypoperfusion in the parietal and temporal regions Positron emission tomography (PET) scan for abnormal brain proteins Treatment Memory issues: not curative may delay progression Cholinesterase inhibitors: donepezil Memantine: Namenda Behavioural and psychological symptoms BPSD:  Behavioural symptoms that may occur in dementia include wandering, aggression and agitation. Psychological symptoms include anxiety, depression and hallucinations. The mainstay of treatment for BPSD is non-pharmacological and approaches include orientation, reassurance, and complementary therapies.  Antipsychotic drugs may have a role but should only be prescribed by specialists.  Acetylcholinesterase inhibitors are increasingly used for their effect on BPSD. 22
  • 26. Depression Depression is not a normal response to the aging process (It is a disease). It is very common problem in elderly with 25% of patients at primary care report depressive symptoms. Effects of depression  Depression is associated with poorer self-care and slower recovery after acute medical illnesses.  It can accelerate cognitive and physical decline and leads to an increased use and cost of health care services.  Less effective rehabilitation  Lower quality of life, higher level of chronic pain, and increased disability (is the fourth leading cause of disability in the United States).  The mortality rate coincided with the level of depression even when controlling for other factors. Types of depression  Primary depression is not triggered by any other psychological or medical cause. Rather, this type of depression is triggered by psychological instability, genetic predisposition.  Secondary depression is caused by one or more negative life events such as illness, this kind of depression is triggered by a medical condition as thyroid gland disorder and by a psychiatric illness as schizophrenia. Symptoms of depression and how old age can modify its presentation? 1. Depressed mood and/or lack of interest or pleasure in usual activities  The older adults may be more likely to express a loss of pleasure than to specifically complain of depression 2. Feelings of worthlessness or inappropriate guilt  Less common in older adults than in younger adults 3. Diminished ability to concentrate or make decisions  Often manifested as a complaint of memory problems—adults of all ages with moderate-to-severe depression complain of problems with concentration and memory, but depressed elders, in contrast to younger adults, exhibit impairment on psychological testing even when they do not have a comorbid dementing disorder 4. Fatigue Common regardless of age 5. Psychomotor agitation or retardation  Older persons may exhibit either of these symptoms 6. Insomnia or hypersomnia  Older persons rarely, if ever, exhibit hypersomnia—a symptom that is much more common in adolescence and young adults 7. Significant decrease or increase in weight or appetite 23
  • 27.  Older adults rarely gain weight or experience an increase in appetite during a depressive episode 8. Recurrent thoughts of death or suicidal ideation  Although thoughts of death are not uncommon in older adults, suicidal ideation among depressed elders is less frequent than among the depressed who are younger but more risky. 9. More likely to express somatic complaints  65% have hypochondriacal symptoms Medical Conditions and medications Causing Depression Medical disorders • Autoimmune (SLE, RA) • Cerebrovascular (CVS) • Chronic pain • Degenerative Disease PK, Alzheimer • Endocrine DM, hypothyroidism • Metabolic cirrhosis, uremia • Neoplasms • Infections chronic: TB, HCV, HIV Drugs ▫ Non steroidal anti- inflammatory ▫ Propranolol ▫ Cimetidine ▫ Clonidine ▫ Benzodiazepines ▫ Steroids ▫ Tamoxifen ▫ Chemotherapy Screening for depression is performed as a part of comprehensive geriatric assessment by many tools: 1. Geriatric Depression Scale - 15 2. Zung Self-Rated Depression Scale 3. Patient Health Questionnaire-2 INTERVENTIONS • Seek out medical illness, Recognize medical side effects • Rehab services to maximize remaining function and retrain impaired ADL’s • Involve family and caretakers • Psychotherapy • Medications: Best to use Selective Serotonin Reuptake Inhibitor Citalopram (Celexa) and Escitalopram (Cipralex) least side effects and drug interactions but may cause hypernatremia and sexual dysfunction. • Electro-convulsive therapy 24
  • 28. Exercise has been shown to benefit patients with mild to moderate mood disorders, especially anxiety and depression. 1. Aerobic and resistive exercises release endorphins from the pituitary gland which are responsible for  Relieving pain  Improving mood.  Lower cortisol levels which have been shown to be elevated in patients with depression. 2. Additionally, exercise increases the sensitivity of serotonin in the same way antidepressants work, allowing more serotonin to remain in the nerve synapse. 3. Depression symptoms can be decreased significantly after just one session but the effects are temporary. An exercise program must be continued on a daily basis to see continued effects. 4. As a person continues to exercise they may experiences changes in their body type which can help to improve self-esteem and body image issues they may have been having. 5. Regular exercise program can enhance social integration 6. Some other benefits of regular physical exercise include: (general benefits apply to all patients) a. Reduces/prevents functional declines associated with ageing b. Maintains/improves cardiovascular function c. Aids in weight loss and weight control d. Improves function of hormonal, metabolic, neurologic, respiratory, and hemodynamic systems e. Alteration of carbohydrate/lipid metabolism results in favourable increase in high- density lipoproteins f. Strength training helps to maintain muscle mass and strength g. Reduces age-related bone loss; reduction in risk for osteoporosis h. Improves flexibility, postural stability, and balance; reduction in risk of falling and associated injuries i. Psychological benefits (preserves cognitive function, alleviates symptoms/behaviours of depression, improves self awareness, promotes sense of well-being) j. Improves immune function k. Reduces age-related insulin resistance l. Improves sleep pattern 25
  • 29. WHAT IS YOUR DIFFERENTIAL DIAGNOSIS? 5. Delirium 6. Depression 7. Dementia Why delirium most likely?? 1. Acute onset 2. Confusion But other criteria needs to be confirmed and further history and examination needed 75 years old female underwent coronary artery bypass graft surgery 3 days ago. She lays in bed most of the day and is not interacting with staff, which is impairing her recovery. She is confused, and appears sad and unmotivated. Is she depressed???.” WHAT OTHER INFORMATION WOULD YOU LIKE TO KNOW ABOUT MRS. x ? 1. Past psychiatric history 2. Past medical history 3. Current medications 4. Pre-morbid cognitive status Now that you have collateral information, you summarize the case: – 76 year old female post-CABG – Decreased level of consciousness – Confused and disoriented – Amotivated and apathetic – Fluctuation of symptoms – No prior history of depression – No prior history of dementia – What is the diagnosis? – What is the subtype? Hypoactive delirium – WHAT SHOULD YOUR NEXT STEP BE? Search for the cause, exclude life threatening condition first  You now attempt to see Mrs. X to obtain her history and observe her current mental status.  She is dressed in a hospital gown lying in bed, looking older than her stated age. Her eyes are closed, and you have a difficult time rousing her.  Her words are slurred and difficult to understand.  She is unable to respond appropriately to your questions.  She appears to be picking at things in the air.  You are unable to assess her mood, but her affect is restricted. She is confused, and when asked where she is mumbles something about “being in Newfoundland”.  You attempt to perform an MMSE, but Mrs. X is unable to pay attention long enough to complete the test As you are unable to obtain much information from Mrs.x, what should you do now? OBTAIN COLLATERAL You review the medical chart and speak with Mrs. x’s daughter to obtain collateral information. You find out the following information. No prior psychiatric problems – No history of depression Past medical history: Angina, Hypertension, Dyslipidemia, Hearing impairment (Uses hearing aid), Hysterectomy (1985), Smoker (30 pack years) Medications Atenolol 25 mg BID. Atorvastatin 20 mg OD, Aspocid 81 mg OD, Multivitamin ī tab OD, Amitriptyline 10 mg HS, Ramipril 5 mg OD*, Ranitidine 150 mg OD*, Hydromorphone 2-4 mg on demand Receiving approx. 6 mg/day Pre-morbid cognitive functioning – Mrs. x has occasionally been forgetting names of friends/family over the past year, but there are no other memory deficits. – She is independent for all IADL’s/ADL’s – She scored 30/30 on a recent MMSE done at her GP’s office – Her family now find her drowsy and confused, which gets worse later in the day Real case scenario 26
  • 30. Possible causes to investigate:  Drugs: sedatives, anticholinergic drugs, drug withdrawal  Infection (eg: chest infection, urinary tract infection)  Urine retention– Fecal impaction  Metabolic: hypoglycemia-hyperglycemia, end organ disease (uremia, hepatic encephalopathy, respiratory failure)  Electrolytes disturbance: ↓ Na, Ca  Myocardial infarction(MI)  Pain Role of rehabilitation in a case of delirium: Care of immobile patient: • Pressure ulcer prevention: – Proper positioning, change positions at least every two hours – Air mattress, keep skin dry and clean • For contracture prevention – Do stretching and range-of-motion exercises to each of the joints every day, and several times a day (active better than passive). – Maintain proper body alignment, therapeutic splints. – Pain control, treatment of spasticity. • For muscle weakness, atrophy prevention – Muscle strength can be maintained without loss or gain with daily muscle contractions of 20% or more of maximal tension for several seconds each day. – Functional electrical stimulation and biofeedback training can increase or maintain muscular strength in those muscles with less than antigravity strength. • For cardiac deconditioning prevention: – Isotonic exercise prevent fluid shift – Tilt table therapy – Elastic leg wrapping – Fludrocortisone therapy • Thrombo-embolisation prevetion: – Anticoagulation, elastic stocking, intermittent pneumatic compression. • Airway Secretions Elimination – Oral, nasal, or transtracheal suctioning – Chest percussion and postural drainage – Flutter mucus clearance devices – Mechanical vibration devices to the chest wall – Regular deep breathing, coughing • Maintain an adequate fluid intake to prevent: thick secretion ,constipation, UTI, renal stones, dehydration, clotting • Laxative use • Nutritional support • OCCUPATIONAL THERAPY IN THE MANAGEMNET OF IMMORBILE OLDER PATIENTS – Assessment of mobility(Bed mobility, Transfers, Wheelchair propulsion) – Assessment of other ADL using actual or simulated environments – Visit home for enviornmental assessment and recommentations for adaptation – Recommend and teach use of assisitive devices (cane, crutches) – Recommend and teach use of safety devices (e.g., grab bars and railing, raised toilet seats, shower chairs) Support delirious patient: – orienting environment :easy-to-read calendars and clocks – Presence of family members can be helpful , frequent interaction , Frequent verbal orientation – Support for confusion or hallucinations , encouraged to express fears and discomforts – Adequate lighting and reasonable noise level – Devices available - eye glasses and hearing aids, Avoid sensory deprivation and overload – Manage pain, Support normal sleep pattern You perform an appropriate work-up and order investigations. You obtain the following ABNORMAL results: Na 152 BUN 25 All other results are normal This suggests dehydration and hyponatremia that was corrected by fluid therapy 27
  • 31. Health promotion in elderly Disease prevention The goal of preventive medicine in older people should be not only reduction of morbidity and mortality but also preservation of function and quality of life. Attempts to prevent diseases of old age should start in youth. Even in the very elderly, preventive interventions can limit disease and disability. However, selecting appropriate interventions requires consideration of: 1. Life expectancy 2. Patient’s preferences 3. Direct and indirect harm of the intervention 4. Goals of care Levels of prevention Primary Prevention of disease by targeting cause and risk factors 1. Life style modifications:(Diet- Physical activity- Safety and injury prevention- Smoking cessation 2. Immunizations influenza vaccine 3. Chemoprophylaxis aspocid, omega 3 for cardiovascular risk reduction, vitamin D and calcium for osteoporosis prevention Secondary the early detection of disease before it becomes symptomatic 1. Screen for malignancy: mammography to detect early breast cancer, colonoscopy to screen for cancer colon) 2. Screen for medical conditions: DM, obesity, malnutrition 3. Screen for geriatric giants: incontinence, sleep problem, dementia, depression Tertiary Managing established diseases (e.g. tight control of DM) to prevent complications e.g. MI, diabetic foot PREVENTING DISABILITY: While there may be little that can be done to prevent the occurrence of a disease in an elderly person, much can be done to minimize the impact of that disease (Proper treatment, Rehabilitation, occupational therapy). 28
  • 32. Pharmacotherapy in elderly Many older patients are prescribed multiple drugs, take over-the-counter drugs, and are then prescribed additional drugs to treat the side effects of medications they are already taking resulting in polypharmacy (usually defined as consuming ≥ 5 medications). The elderly are the biggest consumer of the drug industry, Elderly account for 1/3 of prescription drug use, while only 13% of the population. The Effects of Aging on pharmacokinetics: Several age-related biological and physiological changes are relevant to pharmacology. Except for changes in renal function, however, the effects of these age-related changes on dosages of specific drugs for individual patients are variable and difficult to predict Parameter Absorption Decreases in absorptive surface Decreased splanchnic blood flow Increased gastric pH Altered gastrointestinal motility not clinically significant as they do not affect the absorption of most drugs Distribution  body water  Vd for hydrophilic drugs e.g. ethanol, lithium  lean body mass  Vd for drugs that bind to muscle e.g. digoxin  fat stores  Vd for lipophilic drugs e.g. diazepam  plasma protein (albumin)  % of unbound or free drug (active) e.g. , phenytoin, warfarin Metabolism Decreases in liver blood flow, Decreases in enzyme activity, Decreases in enzyme inducibility Reduced liver volume and enzyme activity means that hepatic metabolism of many drugs decreases. To prevent toxic accumulation doses should be reduced or the dosing interval increased Excretion Decreases in renal blood flow, Decreases in glomerular filtration rate Decreases in tubular secretory function Serum creatinine alone not accurate in the elderly to reflect GFR  lean body mass  lower creatinine production Cockroft-Gault formula formula for estimating creatinine clearance Cr clearance=(140-age)(IBW)/creatinine(72) (multiply by 0.85 for women) The Effects of Aging on pharmacodynamics: 1. Generally, lower drug doses are required to achieve the same effect with advancing age. 2. Change in receptor numbers, affinity can increase or decrease drug sensitivity: HR response to beta-blockers 3. Changes in homeostatic mechanisms can increase or decrease drug sensitivity.  sensitivity to warfarin due to a greater decrease in clotting factor synthesis Other factors affecting drug prescription in elderly: 1. Multiple morbidities: e.g. NSAIDs may cause acute decompensation in patients with chronic heart failure.(drug- disease interaction) 2. Multiple medications leading to drug-drug interactions: ACEIs and aldactone causes hyperkalemia 3. Psychological factors: depressed patients may have their stable conditions exacerbated due to non-adherence to treatment 4. Social factors: economic problems and Problems with transportation may interfere with obtaining the medications. 29
  • 33. 5. Diminished hearing, impaired vision, poor literacy, and poor short-term memory can interfere with patient education and adherence to treatment regimens. POTENTIALLY INAPPROPRIATE MEDICATIONS FOR OLDER PERSONS: Multiple tools are available to clinicians that can assist in making information readily available to avoid adverse drug reactions and interactions. 1. The Beers Criteria: developed to assist healthcare providers in improving medication safety in older adults. The criteria were originally published in the Archives of Internal Medicine in 1991 and were updated in 1997 and again in 2003,2012,2015. Last edition on 2019 https://onlinelibrary.wiley.com/doi/full/10.1111/jgs.15767 2. STOPP criteria (Screening Tool of Older Persons’ Potentially Inappropriate Prescriptions) Principles of Prescribing in the Elderly:  Consider non-pharmacologic agents  Start with a low dose and titrate slowly  Avoid starting 2 agents at the same time  Reach therapeutic dose before switching or adding agents  Review meds regularly (at least q3 months)  Avoid prescribing to treat side effect of another drug  Use 1 medication to treat 2 conditions, Use simplest regimen possible  Adjust doses for renal and hepatic impairment  Use least expensive alternative.  Monitor for adverse drug reactions, drug-disease, drug-drug, and nutrients-drug interaction.  Avoid inappropriate drug prescription for old age using The Beers Criteria or similar tools. NB: example of nutrients drug interactions: 1. Tyramine, a component of cheese and a potent vasoconstrictor, can cause hypertensive crisis in some patients who take monoamine oxidase inhibitors and eat cheese. 2. Foods with vitamin K (arugula, avocado, green beans, Cucumber), produce blood-clotting substances that reduce the effectiveness of oral anticoagulants (Warfarin). 30
  • 34. Safe analgesic prescription in elderly: World Health Organization (WHO) analgesic “pain ladder” is a good model to follow for the treatment of acute pain in older adults: 1. Mild pain should be treated with non-opiates (e.g., acetaminophen). 2. Moderate pain (pain score 4–7) should be treated with an oral opioid (e.g., oxycodone). 3. Severe pain (pain score 8–10) should be treated with an opioid (preferably parenteral) that can be easily titrated. Acetaminophen:  It is the safest analgesic when it is used with the recommended dosage.  Most mild or moderate pain in the elderly is of musculoskeletal origin and responds well to acetaminophen given around-the-clock.  This agent is well tolerated in older patients provided that both renal and hepatic functions are normal. The daily dose of acetaminophen should not exceed 2 gm.  Risks of hepatic toxicity with acetaminophen are minimal and have primarily been observed with long- term use.  Nonetheless, acetaminophen should be avoided in patients with liver disease or a history of heavy alcohol use.  Unfortunately, it is not as effective for inflammatory pain, Nonsteroidal anti-inflammatory drugs (NSAIDs):  All commonly used NSAIDs are on the Beers list of inappropriate medications for older adults. Even short-term use of NSAIDs should be considered unacceptable in older adults with diabetes, impaired kidney function, or taking medications that may impair kidney function (diuretics, ACE inhibitors) or metformin.  Both renal and gastrointestinal toxicity from NSAIDs are dose- and time-dependent. The patient’s risk factors for side effects and recent history of NSAID exposure should be reviewed prior to administering or prescribing NSAIDs.  Gastric acid suppression with a proton pump inhibitor should also be considered.  Because of their association with a lower incidence of gastrointestinal bleeding, selective cyclooxygenase-2 (COX-2) inhibitors (coxibs) have been viewed as a safer alternative to the other NSAIDs; however, concern about their association with heart disease and stroke has dampened their acceptance and resulted in the withdrawal of rofecoxib (Vioxx) from the market.  Prolonged use of NSAIDs in the elderly should be avoided whenever possible. Opioid analgesics:  Administration of opioid analgesics to manage chronic non-cancer pain in the elderly has become acceptable; these agents are effective in treating patients with moderate to severe nociceptive pain.  True addiction in the elderly is uncommon, and the possibility of addiction should not be used as justification for undertreatment of the elderly for pain.  Morphine sulfate and oxycodone hydrochloride, now available in both short-acting and sustained- release preparations, are commonly used. Short-acting opioids can be used in treatment of patients with intermittent pain, whereas sustained-release opioids should be given for continuous pain (with short-acting preparations available for breakthrough pain). The dosage of sustained-release opioids can be titrated based on the frequency of use of the short-acting preparation. 31
  • 35.  For patients who may not be able to take oral preparations periodically, opioids are available as parenteral, sublingual, suppository (oxymorphone hydrochloride), and transdermal (eg, fentanyl patch) products.  Physicians should anticipate, prevent, and manage side effects. o They should initiate prevention of constipation through the use of stool softeners and other prophylactic bowel regimens whenever opioid therapy is used in the elderly. o When opioid therapy is initiated, sedation and delirium are commonplace until tolerance develops. o Although respiratory depression occurs uncommonly, tolerance develops rapidly. If needed, naloxone hydrochloride could be used for profound respiratory depression and sedation; care must be taken when reversing this adverse effect since an antagonist action that is too powerful could propel the patient on long-term opioid therapy into withdrawal. It is advisable that patients take a maintenance dose for several days before they resume driving. o Antiemetics such as prochlorperazine or metoclopramide may be needed early on with the initiation of opioid therapy. o Falls, dizziness, and gait disturbances are not uncommon; therefore, preventive precautions are often recommended, such as the use of an assistive device. o Eventually, for most patients, the analgesic effect of opioids is preserved while tolerance develops to most side effects (eg, respiratory depression, sedation, nausea, and vomiting). However, because tolerance does not develop to gastric hypomotility, patients need to take stool softeners for as long as they are on opioid therapy. Chewing or crushing sustained- release opioids must be avoided as doing so can cause rapid absorption of the entire dose resulting in overdosing. o Certain opioids should be avoided in elderly patients when possible. Propoxyphene is thought to be no more effective than aspirin or acetaminophen, but it is associated with ataxia, dizziness, and neuroexcitatory effects due to drug accumulation.22 Meperidine hydrochloride should not be used because of the accumulation of a nephrotoxic metabolite. Methadone hydrochloride should also be avoided in the elderly because it has a long and variable half-life, which makes titration difficult. In addition, the analgesic action is shorter than that of respiratory depression1 so patients whose methadone dosage is too low may increase their daily amount, which increases the risk of death from respiratory depression.  Transdermal fentanyl, contraindicated in opioid-naïve patients, should also be used with extreme caution in the elderly. It has a variable absorption rate in older adults and a long residual effect even when the patch is removed.  Tramadol hydrochloride, an analgesic that has some opioid properties and is used for mild to moderate pain, should be used with caution in the elderly because it may cause dizziness and reduce the seizure threshold. Adjuvant Medications  Anticonvulsants, steroids, topical local anesthetics, and antidepressants are such agents that may be used alone or in combination with nonopioid or opioid analgesics.  Adjuvant medications are particularly useful in managing neuropathic pain. 1. Tricyclic antidepressants such as amitriptyline hydrochloride (cardiotoxic) 2. Anticonvulsants such as gabapentin and carbamazepine are thought to be more effective and safe, anticonvulsant pregabalin is effective and easier to tolerate than gabapentin. 3. Serotonin norepinephrine-reuptake inhibitor (SNRI) in duloxetine, has been shown to be effective for the treatment of patients with neuropathic pain and seems to be well tolerated in the elderly. 32
  • 36. Sarcopenia Definition: a progressive and generalized loss of skeletal muscle mass and strength with a risk of adverse outcomes such as physical disability, poor quality of life, and death. Both low muscle mass and function are fundamental criteria for sarcopenia diagnosis. Prevalence: – The prevalence in 60–70-year-olds is reported as 5–13%. – The prevalence ranges from 11 to 50% in people >80 years. – Highly related to frailty and osteoporosis. Although it is primarily a disease of the elderly, its development may be associated with conditions that are not exclusively seen in older persons. It can be divided in primary (or age related) and secondary sarcopenia. Sarcopenia can occur secondary to • A systemic disease, especially one that may invoke inflammatory processes, e.g. malignancy or organ failure. • Physical inactivity also contributes to development of sarcopenia, whether due to a sedentary lifestyle or to disease-related immobility or disability. • Inadequate intake of energy or protein, which may be due to anorexia, malabsorption, limited access to healthy foods or limited ability to eat. • Stages pre-sarcopenia, sarcopenia, and severe sarcopenia Operational definition of sarcopenia by The European Working Group on Sarcopenia in Older People (EWGSOP) in 2019 • Low muscle strength (Criterion 1) • Low muscle quantity or quality (Criterion 2) • Low physical performance (Criterion 3) 1. Probable sarcopenia is identified by Criterion 1. 2. Diagnosis is confirmed by additional documentation of Criterion 2. 3. If Criteria 1, 2 and 3 are all met, sarcopenia is considered severe. 4. The ‘presarcopenia’ stage is characterized by low muscle mass without impact on muscle strength or physical performance 33
  • 37. Acute and chronic sarcopenia Acute sarcopenia is that lasted less than 6 months, while sarcopenia lasting ≥6 months is considered a chronic condition. Acute sarcopenia is usually related to an acute illness or injury, while chronic sarcopenia is likely to be associated with chronic and progressive conditions and increases the risk of mortality. Differentiation is done by periodic clinical assessment. Mechanisms underlying sarcopenia 1. Loss of both slow and fast motor units, with an accelerated loss of fast motor units. 2. Myosteatosis 3. Age-related muscle denervation 4. Increased protein degradation/decreased protein synthesis 5. Increased inflammatory cytokine expression (IL-6 and TNF-alpha) 6. Decreased GH and IGF-I production 7. Increased oxidative damage 8. Insulin resistance, which occurs with aging and obesity, plays an important role in decreasing available glucose and protein for muscle anabolism. 34
  • 38. Sarcopenia diagnosis stepped approach: Screening: with SARC-F if score > 4 suggest sarcopenia Muscle mass measurement: Computed tomography (CT) and magnetic resonance imaging (MRI), Dual energy X-ray absorptiometry (DXA), Bioimpedance analysis (BIA). Muscle strength assessment: Grip strength, chair stance test Assessment of physical performance: Timed up and Go test, Short physical performance battery (SPPB). 35
  • 39. Management: 1. Physical activity is the primary treatment of sarcopenia (also prevention). – Resistance exercise improves skeletal muscle strength and mass – Aerobic exercise may also show some benefit 2. Nutritional interventions combined with exercise: • adequate intake of protein • vitamin D, • antioxidant nutrients • long-chain polyunsaturated fatty acids 3. No specific drugs have been approved for the treatment of sarcopenia, however; many drugs were considered for potential benefits without enough clinical evidence: vitamin D (only if <50 nmole) , dehydroepiandrosterone, growth hormone, growth hormone-releasing hormone, combined testosterone-growth hormone, insulin- like growth factor-1, testosterone (in hypogonadism), and angiotensin-converting enzyme inhibitors. 36
  • 40. Frailty in Older Persons Frailty can be defined as an age-associated declines in physiologic reserve and function across multi-organ systems, leading to increased vulnerability for adverse health outcomes. Clinical implications of frailty: • It is a warning sign for high risk of adverse health outcomes. • The explanation for downward spiral in many elderly patients after acute illness. • Frailty has been widely utilized as a mortality risk assessment tool. Reflects biological age that predicts mortality better than chronological age. • Frailty is often described as a transitional phase between successful ageing and disability. • Frail elderly need specific management: Regardless of age, a frail person may be unable to withstand aggressive medical treatment that could benefit a nonfrail person. Epidemiology: • Although exact definitions and screening methods vary, approximately 15 % of the US population over age 65 and living in the community are considered frail. • In 15 studies that included 44,894 participants identified a prevalence of frailty of 9.9 %; when psychosocial aspects were included in the definition, prevalence was 13.6 % among eight studies that included 24,072 participants. • Prefrail individuals, generally identified with a physical frailty type tool , are more common in these population studies, with prevalence ranging from 28 to 44 %. • Of those individuals who were prefrail, over 10 % went on to become frail over the next 3 years. The biology of frailty is explained by two models: 37
  • 41. 1. Phenotypic frailty • A cycle of physiological decline was hypothesized that included interrelated and reinforcing declines in metabolism, nutrition utilization, and skeletal muscle that in sum drove worsening vulnerability. • Triggers of this cycle of decline included acute illnesses, some medications, and aging related biological changes in genetic predisposed elderly. • These physiological impairments result in the five clinical characteristics of frailty: weakness, low energy, slow walking speed, low physical activity and weight loss.(Fried criteria for frailty diagnosis) • The presence of any three of these phenotypes indicates that a person is ‘frail’; one or two phenotypes indicate that the person is ‘prefrail’ and absence of these characteristics indicates the person is ‘robust’. 2. Deficit-driven frailty • Frailty as an aggregate of illnesses, disability measures, cognitive and functional declines that has been termed deficit-driven frailty. According to this model, the more deficits or conditions that an individual has, the more frail the individual is. • In this diagnostic approach, almost any conditions or deficits are interchangeable in index tools. • This conceptual basis has also been widely utilized to develop risk assessment tools that tally a broad range of comorbid illnesses, mobility and cognitive measures, and environmental factors to capture frailty. Initiators (triggers) of frailty: Aging Genetics Environmental factors (UVR, Pollution), Drugs Internal stressors (inflammatory, malignancy, malnutrition) 38
  • 42. The mechanisms of frailty Chronic inflammatory pathway activation Decline in skeletal muscle function and mass(Sarcopenia) Endocrinal changes contribute to frailty 1. Serum levels of the proinflammatory cytokine IL-6 and C-reactive protein (CRP), as well as white blood cell and monocyte counts, are elevated in frail older adults. 2. IL-6 acts as a transcription factor and signal transducer that adversely impacts skeletal muscle, appetite, adaptive immune system function, and cognition and contributes to anemia. 3. Immune system activation may trigger the clotting cascade, with a demonstrated association between frailty and clotting markers (factor VIII, fibrinogen, and D-dimer). 4. there is evidence linking a senescent immune system to chronic CMV infection and frailty. 1. chronic inflammation 2. age-related changes in α-motor neurons, 3. poor nutrition 4. ↓growth hormone (GH) production, sex-steroid levels, and physical activity. 5. Age-related insulin resistance causes an increase of fat infiltration into muscle and a decline in muscle strength. 6. Mitochondrial dysfunction in aging skeletal muscle causes oxidative damage and the decline of energy generation to maintain function properly 1. Decreased growth hormone and insulin-like growth factor-1 levels in later life (IGF-1) 2. Decreased levels of the adrenal androgen dehydroepiandrosterone sulfate (DHEA-S). 3. Chronically increased cortisol levels, blunted diurnal variation of cortisol. 4. Evidence is mixed that lower levels of the reproductive hormones estrogen and testosterone contribute to frailty. 5. there is stronger evidence that links decreased 25(OH) vitamin D levels to f 6. railty Management • Once a frail or prefrail patient is identified there are no succinct guidelines on how to best mange them. • Diagnosis, differential diagnosis (rule out underlying medical or psychological issues that may be driving signs and symptoms of frailty) Diagnosing frailty: 39
  • 43. 40
  • 44. • Laboratory Testing (in order to rule out treatable conditions, A suggested initial screen, based on the differential diagnosis, might include: Complete blood count, basic metabolic panel, liver biochemical tests, including albumin, vitamin B12, vitamin D, and TSH). Exercise • Exercise is believed to be the most effective intervention in older adults to improve quality of life and functionality. However, data on specific exercise interventions designed to improve outcomes in patients with frailty are limited. • The demonstrated benefits of exercise in older adults include increased mobility, enhanced performance of activities of daily living (ADL), improved gait, decreased falls, improved bone mineral density, and increased general well-being. Nutritional Supplementation • In treatment of weight loss, oral nutritional supplements between meals (low-volume, high caloric drinks or puddings) may be helpful in adding protein and calories. • Vitamin D supplementation for those with low serum vitamin D levels (< 20 ng/ml)is effective for fall prevention, improving balance, and preserving muscle strength. • those taking leucine-enriched whey protein plus vitamin D had significant improvement in physical frailty related measurements • Whey protein, omega 3 fatty acids rich items, amino acid glutamine, carnitine have been suggested for their useful role. Pharmacotherapy • Not adequately evaluated. • Such hormonal therapy as testosterone, while it improves muscle strength, has significant systemic side effects. Estrogen-replacement therapy in postmenopausal women also has an unfavorable safety profile. • Even growth hormone, DHEA, testosterone when deficient, may be considered • Friedlander et al reported that IGF-1 therapy had a beneficial impact on bone density, muscle strength, or physical function in elderly women with no clinical IGF-1 deficiency. • Currently available anti-inflammatory agents, while not formally evaluated in clinical trials in treating the frailty syndrome, also have significant adverse effects, particularly in the elderly. Statin has no effect in management of frailty. • While vitamin D and angiotensin-converting enzyme inhibitors have favorable pharmacological and safety profiles, their clinical utility in the prevention and treatment of frailty has yet to be investigated 41
  • 45. Osteoporosis • Osteoporosis is: ‘progressive loss of bone mass associated with change in bone micro- architecture, leading to enhanced bone fragility and a consequent increase in fracture risk’. Epidemiology: • It is estimated that 1 in 3 women and 1 in 12 men over the age of 50 years worldwide suffer from osteoporosis. Above age of 60, one in two women and one in three men will have a minimal trauma fracture because of osteoporosis. • Associated with excess morbidity and mortality – 33% of people die and 35% require help to walk one year after a hip fracture. Pathophysiology • The risk of osteoporosis depends on the peak bone mass attained in young adult life and the rate of bone loss in later years. • The peak bone mass, excessive bone resorption and inadequate formation of new bone remodeling are the three main mechanisms by which osteoporosis develops. • Achieving peak bone mass depends on adequate nutrition, appropriate intake of calcium and vitamin D, exercise and regular menstrual cycles. • Remodeling is: A normal process continually taking place within bone to repair micro damage through continuous bone formation and resorption. • Stages of bone remodeling are: 1. Activation of osteoclasts from circulating precursor cells, mediated by receptor binding of NF- κB (RANK) ligand. 2. Aggregation and adherence of osteoclasts to regions of active bone resorption on the trabecular plate. 3. Osteoclastic breakdown of bone matrix, releasing calcium, minerals and active growth factors. 4. Simultaneous osteoblastic deposition of osteoid with subsequent mineralization as calcium and phosphate (hydroxyapatite) is deposited. • In postmenopausal women, there is a shift towards bone resorption, leading to net bone loss. Osteoclasts function in a less regulated manner, perforating through the trabecular plate. There is then no framework for osteoblast activity and structural integrity is lost. This loss of connectivity between the trabecular plates is typical of the microstructural changes associated with osteoporosis. 42
  • 46. Risk Factors for primary osteoporosis Causes of secondary osteoporosis  female gender  current smoker  alcohol intake >3 units/day  low calcium and vitamin D deficiency  Low body mass index (<19 kg/m2). Endocrinal: hyperthyroidism/ hyperparathyroidism/ Cushing rheumatoid arthritis chronic malabsorption or malnutrition (e.g. coeliac) Chronic liver disease. Renal failure Hematological diseases: multiple myeloma, Leukemia Drugs: heparin, phenytoin, steroids • In men the major causes of secondary osteoporosis are hypogonadism and corticosteroid therapy. Possible symptoms: • Osteoporosis remains asymptomatic till fracture occurs. • Back pain, caused by a fractured or collapsed vertebra • Loss of height over time • A stooped posture (kyphosis) • Fragility fractures • The fracture sites in osteoporosis, the wrist, the hip and the vertebra, have relatively high trabecular bone to cortical bone ratio Risk stratification tools • The FRAX tool (http://www.shef.ac.uk/FRAX/) was developed by the World Health Organization as a free-online resource to calculate 10-year fracture risk. These calculations help to inform decisions about treatment alongside investigations. Investigations • Blood tests – FBC, UE, LFT, TFT, Ca, PO4, vitamin D, PTH, coeliac serology, myeloma screen. • Dual-energy X-ray absorptiometry (DEXA) scanning is: The gold-standard investigation used to establish a formal diagnosis of osteoporosis by measuring bone mineral density (BMD). • Reported as a T score, corresponding to the number of standard deviations (SDs) above or below the bone mineral density for an average 25-year-old. A T-score of 2.5 SDs below normal represents osteoporosis. • Z score, corresponding to the number of SDs above or below the bone mineral density in age-matched controls. 43
  • 47. • A whole-spine X-ray may be helpful to establish the presence of asymptomatic fractures. Up to one-third of vertebral fractures fall into this group. • Bone turnover markers such as serum C-terminal telopeptide (CTX) levels are used in specialist clinics to establish compliance and effectiveness of treatment. Management • Diet rich in calcium and vitamin D • Exercise • Stopping smoking • Reducing alcohol Pharmacological • All patients with osteoporotic fractures, or at risk of sustaining them, should be commenced on vitamin D supplementation. Co-administration of calcium will depend on baseline serum calcium levels and dietary intake. • Bisphosphonates are the mainstay of treatment. These inhibit osteoclastic bone resorption. Because the processes are linked, impaired bone resorption results in reduced bone formation and turnover as a whole is reduced. Usually patients receive bisphosphonates for 3–5 years. Beyond this, benefits of therapy must be balanced against risk of atypical subtrochanteric fracture and osteonecrosis of the jaw. Continuation after 3 years depends on a reassessment of fracture risk and up-to-date • Teriparatide, denosumab and raloxifene are reserved for specific indications 44
  • 48. Recommendations for Prescribing Exercise to Patients with Osteoporosis: Weight-bearing aerobic exercises and muscle-strengthening exercises have been shown to be an integral part of osteoporosis prevention, as well as a part of the treatment process. All three components of an exercise program are needed for strong bone health: weight-bearing aerobic exercise such as jogging, brisk walking, stair climbing; muscle strengthening exercise with weights; and balance training such as Tai Chi. Any form of resistance training should be site specific i.e. targeting areas such as the muscle groups around the hip, the quadriceps, dorsi/plantar flexors, rhomboids, wrist extensors and back extensors. Precautions: 1. As many patients may present with comorbidities, it may be necessary to tailor the exercise prescription accordingly. 2. There are currently no established guidelines regarding contraindications for exercise for people with osteoporosis. The general recommendation is to prescribe moderate intensity exercise that does not cause or exacerbate pain. 3. Exercises that cause twisting (e.g. golf swing), bending or compression of the spine (e.g. rowing or other dynamic abdominal exercises including sit-ups) should also be avoided. 4. Exercises that involve high-impact loading should be avoided. Low impact weight-bearing activity is characterized by always having one foot on the floor. Jumping (both feet off floor) is termed high impact training. 45
  • 49. QUIZ: Kindly comment on the following DXA reports 46
  • 50. 47
  • 51. Sleep problems Normal age related changes in sleep:  Decreased sleep efficiency (time asleep divided by time in bed)  Decreased total sleep time  Stable or increased sleep latency (time to fall asleep)  Earlier bedtime and earlier morning awakening  More arousals during the night  More daytime napping  Decreases in deeper stages of sleep stage 3 and stage 4 sleep.  Stages 1 and 2 (the lighter stages of sleep) increases. Common sleep problems include: 1. Insomnia: difficulty initiation or maintaining sleep for at least 3 nights per week (primary or secondary to psychiatric, medical problems, or medications. 2. Sleep disordered breathing: Obstructive sleep apnea, Central sleep apnea, mixed 3. REM behavioral disorder: enactment of dreams 4. Circadian rhythm related sleep disorder: jet lag, advance phase disorder 5. Restless leg syndrome, and periodic limb movements. Consequences of sleep disorders: Depression, poor quality of life, day time fatigue and somnolence, falls, irritability, and cognitive impairment. Resistant hypertension may occur in cases with chronic insomnia. Sleep disordered breathing: is also an independent risk factor for hypertension and is associated with obesity, pulmonary hypertension, and cardiac arrhythmias. The respiratory events may cause oxyhemoglobin desaturation, which may cause morning headaches and decreased cognitive functioning. Types: 1. Insomnia: acute<3months- chronic >3 months may be primary or secondary It occurs 2ry to psychiatric disorders e.g. depression, generalized anxiety disorder or medical problems e.g. pain due to arthritis and neuropathy, nocturnal dyspnea and cough in heart failure, nocturia, and GERD. Insomnia can be secondary to medications use e.g alpha methyldopa, levodopa/carbidopa, diuretics, beta- blockers, glucocorticoids, Decongestants, SSRI. Main treatment is treating cause and behavioral therapy (sleep hygiene), short term pharmacotherapy if other lines fail. Short-acting agents (Eszopiclone, zaleplon) are recommended for problems with initiating sleep • Lower associations with falls and hip fractures • But produce the most pronounced rebound and withdrawal syndromes after discontinuation Intermediate-acting agents (tenazepam)are recommended for problems with sleep maintenance Other sedating drugs: • Low doses of sedating antidepressants such as mirtazapine or trazodone at bedtime • Sedating antihistamines (eg, diphenhydramine) • Valerian is an herbal product with mild sedative action • Melatonin receptor agonists 48
  • 52. 2. Obstructive apneas are caused by an anatomic obstruction of the airway during sleep. Patients attempt to breathe and may appear to be choking or gasping for breath; Bed partner may report loud snoring, cessation of breathing, and choking sounds during sleep. Main treatment = nasal CPAP = continuous positive airway pressure and surgical correction of the obstruction. Weight loss in obese patients with SDB can significantly reduce or eliminate the respiratory events. Oral appliances have been developed for both obstructive sleep apnea and snoring. 3. Central apneas are caused by failure of the central nervous system respiratory centers. Central apnea is common in patients with heart failure or stroke. Treatment is limited to treatment of heart failure. 4. Periodic limb movement: Debilitating, repetitive, stereotypic leg movements that occur in non- REM sleep. May present as difficulty maintaining sleep or excessive daytime sleepiness its diagnosis requires polysomnography. Good response to dopamine agonist. 5. Restless legs syndrome: The diagnosis of restless legs syndrome is based on the patient’s description of symptoms. The patient’s complaint is usually of nighttime leg discomfort or difficulty in initiating sleep. There may be a family history of the condition and, in some cases, an underlying medical disorder (eg, iron deficiency anemia, or renal or neurologic disease). Treatment mainly by iron replacement and dopamine agonist. Association between poor sleep quality and neurologic conditions, rehabilitation outcomes, and mortality • Emerging evidence suggests that poor sleep quality may also contribute to the development of neurologic conditions e.g. Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative diseases. • Sleep disturbances are likely present in many individuals receiving PT services, which may exacerbate their condition and slow recovery and impact their outcomes. Poor nighttime sleep quality) was associated with less functional recovery. • As sleep contributes to the modulation of pain, thus; addressing sleep disturbances may potentially impact pain severity. • Lower survival rates among the elderly during inpatient post-acute rehabilitation was associated with self-reported poor sleep quality. Furthermore, healthy individuals (age range 30–70 years) who sleep less than 6 hours or more than 8 hours each night had a higher risk for mortality compared with those with adequate sleep (6–8 hours) Role for Physical Therapist 1. Assess overall sleep health and screen for risk of sleep disorders. 2. Refer for additional assessment if individual is identified as at increased risk for a sleep disorder: to sleep lab (polysomnography) 3. Provide sleep hygiene education. 4. Provide an appropriate exercise program. 5. Consider positioning to promote sleep quality. 6. Address bed mobility issues. Screening for Common Sleep Disorders Pittsburgh Sleep Quality Index (PSQI): https://www.med.upenn.edu/cbti/assets/user- content/documents/Pittsburgh%20Sleep%20Quality%20Index%20(PSQI).pdf Epworth Sleepiness Scale (ESS): http://www.sleepapnea.org/assets/files/pdf/ESS%20PDF%201990- 97.pdf 49
  • 53. Sleep hygiene: • Maintain a regular rising time • Maintain a regular bedtime, unless not sleepy • Decrease or eliminate naps, unless necessary • Exercise daily, but not immediately before bedtime • Do not use bed for reading or watching television • Relax mentally before going to sleep • If hungry, have a light snack (except with symptoms of gastroesophageal reflux or medical contraindications), but avoid heavy meals at bedtime • Limit or eliminate alcohol, caffeine, nicotine. • Control the nighttime environment with comfortable cool temperature, quiet, and darkness • Try a fan or other “white noise” machine • Wear comfortable bed clothing • If unable to fall asleep within 30 minutes, get out of bed and perform soothing activity (avoid bright light) • Get adequate exposure to bright light during the day. • Bathing before sleep has been demonstrated to enhance the quality of sleep in older people, perhaps related to changes in body temperature with bathing. Exercise • Acute and chronic exercise has a moderate positive benefit on sleep characteristics by increasing slow-wave sleep (deep stages) and total sleep time and decreasing sleep onset latency. • Moderate-intensity exercise has also been shown to improve sleep in healthy, sedentary people aged 50 and older who reported moderate sleep complaints at baseline. However, strenuous exercise should not be performed immediately before bedtime. • Exercise should be conducted in the morning or early afternoon but not in the evening. • Meditative movement, including tai chi, and yoga, also appears to improve sleep quality • The exact mechanism of how exercise improves sleep characteristics remains unknown: 1. One theory is that exercise raises body temperature, which triggers heat-loss mechanisms and leads to sleep onset. 2. Another theory suggests that exercise uses energy and produces “wear and tear” on the body, which leads to sleep to recuperate and restore energy. 3. It is also possible that exposure to bright light while exercising outside and the production of inflammatory cytokines in response to exercise may influence sleep characteristics and sleep quality. 4. Changes in depressive symptoms, improvements in physical function, and weight loss have also been associated with improvements in sleep due to exercise. Positioning for Sleep and Addressing Bed Mobility to Facilitate Sleep Quality • Education about positioning for sleep in a pain-free or pain-reduced position may limit sleep disruption. For example, an individual with low back pain may benefit from instruction to sleep side-lying with a pillow between his knees or to sleep supine with pillows under his knees to reduce the lordosis of the back. • The therapist should address the difficulty with transfers and bed mobility. Adequate bed mobility is needed to change position while sleeping, and improved ease with changing position with sleep may reduce sleep disruptions. 50
  • 54. CHAPTER (3): APPROACH TO COMMON MEDICAL PROBLEMS Chronic respiratory diseases Hypertension Orthostatic hypotension Congestive heart failure Metabolic syndrome Obesity Dyslipidemia Diabetes Mellitus Constipation Arthritis Anemia Chronic liver disease Chronic kidney disease 51
  • 55. Chronic respiratory diseases (CRDs) Chronic respiratory diseases (CRDs) are diseases of the airways and other structures of the lung. Some of the most common are asthma, chronic obstructive pulmonary disease (COPD), occupational lung diseases and pulmonary hypertension. Risk factors: 1. Smoking is the most common risk factor. 2. Genetics: cystic fibrosis, alpha 1 antitrypsin deficiency. 3. Other risk factors include: air pollution, occupational chemicals and dusts, and frequent lower respiratory infections during childhood 4. Connective tissue diseases. Airway diseases are classified into two groups Obstructive disorders Restrictive disorders Characterized by: reduction in airflow. Shortness of breath in exhaling air. Air will remain inside the lung after full expiration Characterized by reduction in lung volume Difficulty in inhaling air Due to stiffness of lung tissue or limited chest wall expansion COPD Asthma Bronchiectasis Interstitial lung disease Marked obesity Scoliosis Neuromuscular disorders Clinical presentations can vary with each category:  Chronic obstructive airway disease: includes both (emphysema and chronic bronchitis): chronic productive cough, dyspnea, fatigue that may progress to respiratory failure and cyanosis. Peripheral oedema, cor pulmonale, respiratory failure and polycythemia may develop in patients with COPD.  Asthma: condition of airway hyper-responsiveness with reversible airflow obstruction that results in intermittent symptoms of difficult breathing, wheezing, dyspnea, chest tightness, and non- productive cough. Coughing often occurs at night or early in the morning. There are two forms of bronchial asthma (allergic extrinsic and non-allergic intrinsic asthma). Early in the course of the disease, the chest is usually free in between the attacks.  Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD is a group of respiratory diseases affecting the interstitium of the lungs. It may occur as an abnormal repair process to a variety of injuries to the lungs leading to scarred and thickened alveoli. This makes it more difficult for oxygen to pass into the bloodstream. The disease presents itself with the following symptoms: shortness of breath, nonproductive coughing, fatigue, and weight loss, which tend to develop slowly, over several months. Etiologies could be idiopathic, secondary to connective tissue disease e.g. Sarcoidosis, SLE, Rh A, secondary to lung exposure to inorganic inhalation: silicosis, asbestosis, or organic as Hypersensitivity pneumonitis (Extrinisic allergic alveolitis).  Pulmonary hypertension: Is abnormally elevated pressure in the pulmonary circulation. Symptoms of pulmonary hypertension include: shortness of breath, tiredness, feeling faint or dizzy, chest pain (angina), palpitations, edema, and ascites. The symptoms often get worse during exercise. There are five classes. 52
  • 56. o Class one pulmonary arterial HTN either 1. have no identifiable cause and is then referred to as idiopathic pulmonary hypertension (formerly called primary pulmonary hypertension). 2. Or Drug- and toxin-induced (e.g., methamphetamine use) 3. Or associated with conditions: Connective tissue disease, HIV infection, Portal hypertension, Congenital heart diseases, Schistosomiasis o Class 2 – Pulmonary hypertension secondary to left heart disease o Class III – Pulmonary hypertension due to lung disease, chronic hypoxia (COPD, Obstructive sleep apnea, ILD). o Class IV – chronic arterial obstruction: Chronic thromboembolic pulmonary hypertension. o class V :Pulmonary hypertension with unclear or multifactorial mechanisms: Sarcoidosis, sickle anemia, glycogen storage disease  Pulmonary hypertension is diagnosed by measuring the pulmonary pressures by either echocardiogram or right heart catheterization. Investigations to evaluate respiratory system: Plain chest x-rays are most useful in identifying abnormalities in the heart, lung parenchyma, chest wall, pleurae, diaphragm, mediastinum and hilum. Usually, a chest x-ray is the initial test performed to evaluate the lungs. Sputum microscopy and serology are useful for the diagnosis of infections of the lungs. Flow rate and lung volume measurements are used to differentiate obstructive from restrictive pulmonary disorders, to characterize disease severity and to measure responses to therapy. Obstructive lung disorder is characterized by a decrease in the flow rate, whereas restrictive lung disorder is a reduction in lung volume. Arterial blood gas exchange analysis is useful in assessing accurate measures of PaO2, PaCO2 and blood pH. A Ventilation and perfusion scan, also called a v/q lung scan, is a type of medical imaging using scintigraphy and medical isotopes to evaluate the circulation of air and blood within a patient's lungs in order to determine the ventilation/perfusion ratio. The ventilation part of the test looks at the ability of air to reach all parts of the lungs, while the perfusion part evaluates how well blood circulates within the lungs. CT scan: CT scans of the chest define intrathoracic structures and abnormalities more clearly than do chest x-rays. CT angiography using a bolus of intravenous contrast is employed to highlight pulmonary arteries, useful in the diagnosis of pulmonary embolism. Treatment: Treatments for each chronic respiratory disease vary and the ideal solution is the reduction and avoidance of risk factors. Neither asthma nor chronic obstructive pulmonary disease (COPD) can be cured but treatments can reduce symptoms, prevent escalation and improve quality of life. 1. Smoking cessation 2. Supplemental oxygen should be prescribed for patients with PaO2 of 55 mmHg or less. Oxygen should also be used in patients whose O2 saturation drops below 90% during exercise or sleep. 53
  • 57. 3. Asthma: based on avoidance of triggers, Bronchodilators (salbutamol inhalers and steroid inhalers, such as beclometasone) using spacers or dry powder preparations, long acting β-agonist (salmeterol) inhalers, and theophylline are effective. 4. COPD: use of bronchodilators, antibiotics, inhaled corticosteroids, mucolytics. 5. ILD is multiple conditions, hence treatment is different for each disease. If a specific occupational exposure cause is found, the person should avoid that environment. If a drug cause is suspected, that drug should be discontinued. Many cases due to unknown or connective tissue-based causes are treated with corticosteroids, such as prednisolone. Some people respond to immunosuppressant treatment. 6. Pulmonary hypertension: treat the cause, diuretics, anticoagulation, vasodilators (prostacyclin, sildenafil, calcium channels blockers), Endothelium antagonists are the newest medications used for this condition. These include bosentan and ambrisentan. Role of physiotherapy: 1. Proper assessment and exclude acute on top of chronic conditions as infection, acute exacerbation of COPD or acute asthma attack. 2. Screen for other comorbidities e.g. hypertension, IHD, or DM. 3. Stop smoking. 4. Nutritional counseling. 5. Vaccination pneumococcal, influenza. 6. Control environmental exposure to air pollution. 7. warm up and use of bronchodilators to avoid exercise- induced bronchospasm in asthma 8. Diaphragmatic breathing (to retrain the patient to use the diaphragm more than the chest muscles). 9. Positioning changes can be used to address ventilation and perfusion mismatches and to help with postural drainage. 10. Inspiratory muscle training is specifically directed at inspiratory muscles. It is usually performed by breathing in against a measured resistance using a specific device. It is uncertain how much, or if, inspiratory muscle training adds to a whole- body exercise programme, but it is known to be effective alone and is potentially useful for individuals who are unable to cycle or walk. 54
  • 58. 11. More efficient coughing techniques can be taught to help expel secretions. This will help prevent pooling of secretions, subsequent infections, or air trapping. Manual chest therapy, including percussion or a vibrator, can help mobilize secretions. 12. A pulmonary rehabilitation program should include endurance and/or reconditioning exercises. For these the therapist needs to monitor the patient’s heart rate and oxygen saturation. The heart rate should be limited, generally as a percentage of an age-adjusted maximal heart rate (this is especially important for patients with additional cardiac disease). 13. Oxygen saturation should be monitored as well as the patient’s perceived exertion. Exercise should be discontinued for O2 saturation below 90%, significant increases in exertion or dyspnea, chest pain, or tachycardia or irregular heart rate. 14. Therapy should be performed 3–5 days per week. Walking is a fundamental part of a pulmonary rehabilitation, and patients should be encouraged to walk outside of therapy (with appropriate precautions and oxygen supplementation if required). 15. An exercise bicycle may also be beneficial for home use. An important part of therapy is for patients to learn their abilities and limitations so they can safely exercise at home. Physical or occupational therapists should also help develop an upper body exercise program. 16. Occupational therapists may be helpful in assessing activity of daily living (ADL) impairments and with prescribing assistive devices. Respiratory therapists can help instruct patients in the proper use of medications and mobilization of secretions and teach them breathing techniques. In pulmonary patients, nutritional evaluations may also be needed. 1) Make sure you are sitting or standing upright. 2) Put on the nose clip. 3) Hold the IMT by the handle grip. 4) Place the mouthpiece in your mouth, making sure you put your lips over the outer shield to make a good, airtight seal. 5) Breathe out as far as you can then take a fast, forceful breath in through your mouth. Take in as much air as you can, as quickly as possible, whilst expanding your chest. 6) Breathe out slowly and with minimal effort, letting your shoulders relax. 7) Pause and then take another fast, forceful breath in. 8) Repeat this fast, forceful breath 55