Complaint Presentation and its RelationElizabeth Lenihan (EL) is a 79 year old retired doctor.
She is mentally and physically capable. Her blood pressure is normal. She has no previous fractures, is not on medications, does not drink excessively or smoke. She lives with her 85 year old husband who suffers from arthritis and her 43 year old daughter who has down syndrome. She had come to her GP looking to medicated for the pain as she slipped and fell on ice, fracturing her right forearm; a Colles fracture. She has been to the hospital and has the arm in a cast, but paracetamol seems ineffective at relieving the pain. Elizabeth has the position of primary care giver for her arthritic husband and hers down syndrome daughter. The first port of call was a Dexa scan to observe for Osteoperosis. EL was started on a regimen of Biphosphonate, Aledronic acid, Calcium and Vitamin D. Describe briefly, with examples, how ageing may occur at the following levels
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C. Cellular
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- Once formed free radicles and ROS interact with fatty acids, DNA, proteins and cholesterol molecules to in turn produce many more free radicles, a process that is highly destructive to neighboring cells.
- DNA, lipid layers, cellular proteins are as a result damaged. Potential down-stream diseases such as CVD, Cancer, macular degeneration (e.g. Dinitrophenol use surge -> The compound once used for weight-loss liberated massive amount of ROS causing blindness).
D. System
- The capacity of various processes to utilise oxygen decreases steadily throughout our life
- Growth rate and rate of substitutions in DNA correlate to an organisms metabolic rate
- At an endocrinological level the hormone production decrease or many systems as we age also itself having a role to play in the characteristics of elderly disease and disorder susceptibility (Coronary atherosclerosis, osteoporosis, AD, Amemia)
- In a similar fashion to decreased estrogen production during menopause, HGH and Testosterone both show a marked decline one third of the way into our lives ("Somatopause" and "Adrenopause")
- Lifestyle factors such as decreased exercise and activity with age reduce the protective effect at all of the above levels
Describe briefly the theories of why we age (wear and tear, evolutionary, non-adaptive evolution).
Mutation accumulation
Cellular senescence is the phenomenon by which normal diploid cells cease to divide.
In culture cells reach "replicative senescence" once they hit their maximum number of cellular divisions.
The phenomenon is the result of telomere shortening, ultimately triggering a DNA damage response.
Elevated reactive oxygen species can also induce this response in cells.
The Mutation Accumulation theory of aging holds the non-adaptive evolutionary standpoint that the occurance of senescence is a feature only appearing in modern humans (or animals in zoos) with an environment where life expectancy has been artificially extended.
Antagonistic Pleiotropy
Pleiotropy occurs when one gene influences two or more seemingly unrelated phenotypic traits.
Antagonistic pleiotropy describes the above influence on two or more phenotypic traits where at least one of these traits is beneficial to the organism's fitness and (at least) one is detrimental to the organism's fitness.
In this theory pleiotropic genes with good early effects would be favored by selection even if these genes had bad effects at later ages: i.e., a small beneficial effect early in life outweighs a late deleterious effect even if the latter results in senescence and death.
Disposable Soma "Wear & Tear"
The Disposable Soma theory, like the antagonistic pleiotropy theory, holds an evolutionary adaptive standpoint for the basis of aging. It describes an organism as benefiting by investing any spare resource into reproduction or survival, rather than into repair capacity, even though this means that damage will eventually accumulate to cause aging.
These theories are not mutually exclusive. Their combination provides a consistent working hypothesis.
Cellular senescence is the phenomenon by which normal diploid cells cease to divide.
In culture cells reach "replicative senescence" once they hit their maximum number of cellular divisions.
The phenomenon is the result of telomere shortening, ultimately triggering a DNA damage response.
Elevated reactive oxygen species can also induce this response in cells.
The Mutation Accumulation theory of aging holds the non-adaptive evolutionary standpoint that the occurance of senescence is a feature only appearing in modern humans (or animals in zoos) with an environment where life expectancy has been artificially extended.
Antagonistic Pleiotropy
Pleiotropy occurs when one gene influences two or more seemingly unrelated phenotypic traits.
Antagonistic pleiotropy describes the above influence on two or more phenotypic traits where at least one of these traits is beneficial to the organism's fitness and (at least) one is detrimental to the organism's fitness.
In this theory pleiotropic genes with good early effects would be favored by selection even if these genes had bad effects at later ages: i.e., a small beneficial effect early in life outweighs a late deleterious effect even if the latter results in senescence and death.
Disposable Soma "Wear & Tear"
The Disposable Soma theory, like the antagonistic pleiotropy theory, holds an evolutionary adaptive standpoint for the basis of aging. It describes an organism as benefiting by investing any spare resource into reproduction or survival, rather than into repair capacity, even though this means that damage will eventually accumulate to cause aging.
These theories are not mutually exclusive. Their combination provides a consistent working hypothesis.
Describe the disposable soma theory of ageing.
Describe the psychology of bereavement with reference to adult grief responses and the stages of mourning.
Grief/Mourning/bereavement
Multifaceted response to loss – particularly resulting from the death of someone to whom a strong bond or affection was formed
Loss of a family member, friend, acquaintance or status
The grieving process is complex and there exists no catch all stage or phase models. Two prevailing models in psychology exist with the former explaining individual response types and the later describing stages of grief itself.
Bonanno’s Four Trajectories of Grief (in lieu Death, tragedy)
George Bonanno: Prof of Clinical Psychology at Columbia
Multifaceted response to loss – particularly resulting from the death of someone to whom a strong bond or affection was formed
Loss of a family member, friend, acquaintance or status
The grieving process is complex and there exists no catch all stage or phase models. Two prevailing models in psychology exist with the former explaining individual response types and the later describing stages of grief itself.
Bonanno’s Four Trajectories of Grief (in lieu Death, tragedy)
George Bonanno: Prof of Clinical Psychology at Columbia
- Resilience: relative stability in light of highly disruptive circumstances.
- Recovery: normal functioning that transitions to a period of depression or PTSD for several months but returning to normality.
- Chronic Dysfunction: several years of prolonged suffering and inability to function.
- Delayed Grief or Trauma: seemingly normal adjustment with a delayed transition to a period of depression.
- Denial: “I feel fine” defence mechanism of refusing to accept the reality of the situation. Important to be clear cut and straight about the truth of a person’s condition so that the family can move through this stage as quick as possible.
- Anger: Blame displacement. Feelings of anger and even rage with themselves or others.
- Bargaining: “I will donate/give my life savings if...” Spiritual negotiation, self-improvement as a bargaining tool.
- Depression: Certainty of death begins to be understood. Severe despondency and dejection set in as a realisation occurs in the events which have unfolded. Inadequacy, guilt, loss of appetite energy disturbances also characterise this affect.
- Acceptance: The terms of the situation have begun to settle in. “ Everything is going to be ok”
Briefly discuss the diagnosis of depression.
- Depression is a disorder of mood which has a core set of symptoms.
- These are pathological sadness, hopelessness, apathy, anhedonia, irritability, and feelings of distress.
- Cognitive symptoms can also manifest as can volitional and physical symptoms.
- An overall breakdown in functioning is commonly seen with special emphasis on the affective sphere.
- Co-expressed disorder. e.g. with anxiety, or schizophrenia
- Through clinical interview
- Verbal & Non-verbal techniques used
- ICD-10: International Classification of Disease
- Severity of episode is based on number of symptoms, type of symptoms and intensity of the symptoms in tandem with the degree of functional deterioration.
- Depression (Unipolar) can be diagnosed as one of three degrees
- Mild
- Moderate
- Severe
- In any of these cases two of three outlined depressive symptoms must be present for at least two weeks during the episode, must not be the result of suctance abuse or an organic mental disorder and
- Depressive mood
- Marked loss of interest or pleasure in acivities that were normally pleasurable
- Loss of emotional reaction to stimulating events in life
- Increase in susceptibility to fatigue
- Loss of apetite
- Weight loss of at least 5% in the last month
- Depression worse in the morning
- Psychomotor retardation/agitation
- Notable decrease in libido
Differential diagnosis of the major depressive disorder
Other diseases*
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Prescription Drugs
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Substances
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Outline factors you should consider when prescribing drugs for the older adult
- Individuals age at different rates - "chronological" vs" biological age"
- Is your patient healthy elderly or frail elderly
- Elderly individuals are more likely to have an adverse drug reaction.
- Polypharmacy nature of the lederly patient - are they already on medications?
- Age related Co-morbidities: CVD, Hyperlipidaemia, Hypercholestaemia, Diabetes
How may advanced age affect drug metabolism?
Morphine and Benzodiazepine drugs can be particularly hazardous for elderly individual due to their extensive metabolism
Briefly describe the physiology of normal bone formation
General Anatomy and Physiology of Long Bones & Process of Bone Formation
Bone Formation
Bone formation first begins at the 8th week of gestation.
The initial bones to form are the flat bones such as the skull and face followed by the mandible and clavicles. The bones form directly from mesenchyme (intraembryonic tissue)
Intramembranous Ossification
Ossification center appears within fibrous connective tissue membrane
Central Mesenchymal cells differentiate into Osteoprogenitor Cells.
Cbfa 1 is then expressed which is a molecular switch for Osteoblast differentiation.
Bone formation first begins at the 8th week of gestation.
The initial bones to form are the flat bones such as the skull and face followed by the mandible and clavicles. The bones form directly from mesenchyme (intraembryonic tissue)
Intramembranous Ossification
Ossification center appears within fibrous connective tissue membrane
Central Mesenchymal cells differentiate into Osteoprogenitor Cells.
Cbfa 1 is then expressed which is a molecular switch for Osteoblast differentiation.
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- Compact bone begins to form on the circumfrence as spicules at the site of the periosteum thicken in size.
- This is later replaced with mature Lamellar bone.
- Trabeculae remain internally.
- Vasculature becomes red bone marrow.
Endochondral Ossification
Part 1
Part 1
- Mesenchymal cells under the influence of FGF and BMPs become Chondroblasts and produce the Cartilage matrix.
- The forms a Cartilage Model with the general shape of bone.
- Fomration of bony collar around the hyaline cartilage model.
- Cells no longer produce collagen and are now bone forming cells called osteoblasts.
- Bony Collar is then fomed around the Diaphyseal portion of the developing bone.
- The Chondrocytes enlarge in the mid region of the 'cartilage model'.
- These Cells produce Alkaline Phosphatase and the 'cartilage model' undergoes calcification.
- Calcification inhibits diffusion of nutrients and chondrocytes die.
- At the same time several blood vessels grow through the periosteal collar.
- Mesenchymal cells migrate along penetrating blood vessels (BVs) abd become Osteoprogenitor Cells.
- Hematopoietic Stem Cells also enter through BVs.
- Osteoprogenitor Cells become Osteoblasts and lay down Osteoid on Calcified Cartilage Matrix.
- This area is called the primary Ossification center.
- Formation of Secondary Ossification Centers Occurs.
- Formation occurs first at the Proximal Epiphysis than is followed at the Distal Epiphysis.
- Bone marrow cavity is established.
Process of Bone Resorption and Formation |
Including the endocrine and dietary components
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Various Cells of Bone Tissue
- Mesenchymal Stem cells -produce-> Osteoprogenitor Cells -which differentiate into->Osteoblasts*
- *This Occurs with the help of Core Binding Factor Alpha-1
- Osteoblasts then secrete Collagen Type I and Bone Matrix Proteins (BMPs) to make Osteoid(s).
- Bone Matrix Proteins contain Calcium Binding Proteins
- Both Vitamin C and Alkaline Phosphatase (high phosphate source) are key components in the formation of osteoblasts.
- Osteoblasts become trapped within bone matrix eventually becoming osteocytes.
- Osteocytes are maintenance cells that keep bone matrix in homeostasis. They are trapped in the lacuna and extend out processes through canaliculi.
- Osteoclasts are the cells responsible for bone resorption. They are large multinucleated cells that secrete HCl into the resorption bay and in doing so cause degradation of the mineral bone component.
Describe the pathology and management of osteoporosis.
Processes of Osteoperosis, Osteopenia and related pathologies along with their management option
Osteopenia Definition
Osteopenia is a medical condition in which the protein and mineral content of bone tissue is reduced causing an overall thinning of the bone & reduction in mass. Precedes the more severe osteoporosis. |
Osteoperosis Definition
Osteoperosis is a proressive bone disease that is characterised by decreased bone mineral density that leads to porous fragile bones which are at a higher risk of fracture. |
Epidemiology
The higher the peak bone mass (at adolescence) the lower the risk of osteoporosis
Pathophysiology
Diuretics, anticonvulsants & asthma medications interfering with calcium absorbency
Diagnosis
Management Options for Osteoporosis
Fist point of call.. As always
Lifestyle & Diet
>ATP analogues that accumulate within Osteoclasts promoting their apoptosis thus preventing bone resorption
(1st generation only).
>Interfere with anchoring of cell surface proteins to Osteoclast membrane (necessary for attachment to bone)
>Bind to Hydroxyapatite.
>Also have an inhibitory effect on Osteoblasts but overall effect on bone turnover is favorable
Side effects
>Diarrhea (most common)
>Nausea
>Rash
"Anabolic therapy of Bone"
Parathyroid hormone - binds to Osteoblasts
Increases the expression of RANKL
Decreases the expression of OPG
Long term use more associated with bone resorption
Calcitonin - slows release of calcium from bones into blood stream, activates osteoblasts
Hormone replacement therapy, either directly with estrogen - stimulates Osteoprotegrin production which in turn increases mineral density
Estrogen receptor modulation such as Raloxifene - Inhibits bone resorption
Denosumab - Fully human mAb. Anti-RANKL. inhibits RANKL which signals bone removal.
Dexa Scans are recommended every couple of years.
- Affects 55% of Americans 50 years of age and older
- 80% of which are women
- Asymptomatic until precipitated through bone fracturing (where otherwise unlikely with healthy bone)
- Most commonly Wrist, Spine, Shoulder and Hip
- Vertebral collapse - causing back pain, stooped posture
The higher the peak bone mass (at adolescence) the lower the risk of osteoporosis
Pathophysiology
- Bone resorption formation negatively skews with age, with the former exceeding the later in a timer dependent manner, particularly following menopause in women due to estrogen drop off.
- Trabecular bone, which is the sponge like bone near the ends of long bones, undergoes the most remodeling, so when the remodeling is imbalanced, the tubercular site is where fractures occur.
- Women over 50 and men over 70 years of age
- Post menopausal
- Secondary Osteoporosis in cases where an underlying disease is the causative factor
- Medical Factors
- Previous fractures give rise to new ones
- G.I. disease (Ca2+/Vitamin D absorption)
- Thalassemia & Pernicious anemia (hematological disorders)
- Renal and Liver Disease
- Hypogonadal States
- Long term Glucocorticoid therapy
Diuretics, anticonvulsants & asthma medications interfering with calcium absorbency
Diagnosis
Management Options for Osteoporosis
Fist point of call.. As always
Lifestyle & Diet
- Smoking cessation
- Alcohol reduction (moderation)
- Increased Calcium and Vitamin D intake (1000IU/day) intake
- Resistance/weight bearing exercise program along with balance retention training
- Bisphosphonates - aledronate, risedronate
>ATP analogues that accumulate within Osteoclasts promoting their apoptosis thus preventing bone resorption
(1st generation only).
>Interfere with anchoring of cell surface proteins to Osteoclast membrane (necessary for attachment to bone)
>Bind to Hydroxyapatite.
>Also have an inhibitory effect on Osteoblasts but overall effect on bone turnover is favorable
Side effects
>Diarrhea (most common)
>Nausea
>Rash
"Anabolic therapy of Bone"
Parathyroid hormone - binds to Osteoblasts
Increases the expression of RANKL
Decreases the expression of OPG
Long term use more associated with bone resorption
Calcitonin - slows release of calcium from bones into blood stream, activates osteoblasts
Hormone replacement therapy, either directly with estrogen - stimulates Osteoprotegrin production which in turn increases mineral density
Estrogen receptor modulation such as Raloxifene - Inhibits bone resorption
Denosumab - Fully human mAb. Anti-RANKL. inhibits RANKL which signals bone removal.
Dexa Scans are recommended every couple of years.
Dexa Scan Description and its result interpretations (T scores/ Z scores)
Define DEXA and how bone mineral density is used to derive T- and Z- scores in order to diagnose osteoporosis and osteopenia.
Works on the principal that Calcium in bone attenuates passage of X-Ray beams (photons) in proportion to the amount of mineral present.
Results
Osteopenia indicated if T-score is between -1 and -2.5
Results
- BMD measurement (expressed in grams of hydroxyapatite/cm^2)
- T-Score (SD measure related to health individual of primer age)
- Z-Score (SD measure related to person of similar age & sex)
Osteopenia indicated if T-score is between -1 and -2.5
The Anatomy of the Forearm and Wrist
- The two long bones of the forearm are named the Radius and Ulna
Then there are the Carpal bones which give flexibility to the wrist (think double jointed.
Proximal Row
- Scaphoid: Largest bone, articulates with the radius.
- Lunate: Broader anteriorly than posteriorly, also articulates with the radius.
- Triquetrum: articulates with distal radio-ulnar joint
- Pisiform: lies on triquetrum
- Trapezium: articulates with 1st and 2nd metacarpal, scaphoid and trapezoid.
- Trapezoid: articulates with 2nd metacarpal, trapezium, capitate, scaphoid.
- Capitate: articulates with 3rd metacarpal, trapezoid, scaphoid, lunate, hamate.
- Hamate: hook of hamate extends anteriorly and articulates with 4th and 5th metacarpal, capitate, triquetral.
- and of course Some Lovers Try Positions That They Can't Handle
Types and Terminologies of Fractures and their Management (with Emphasis on Wrist)
Describe common fractures of the wrist and outline their basic orthopaedic management.
General Outline of Fracture types
Common fractures of the wrist:
Colles Fracture – a fracture of the distal 2 cm of the radius as well as commonly the ulnar styloid process
The fragment of the radius is displaced dorsally and is referred to as a dinner fork deformity
Normally the radius projects further distally than the ulna, but with the fracture the relationship is reversed because of the shortening of the radius
Smith Fracture – A reverse colles fracture – Fracture of the distal radius but with volar displacement (dorsal in colles)
Bennett Fracture – fracture of dislocation of the base of the first metacarpal (thumb) – dorsolateral dislocation occurs with this fracture
Scaphoid Fracture – patient presents with tenderness in anatomical snuffbox – must be clinically diagnosed as fracture will usually not turn up on x-ray straight away – need to re-x-ray approx. 10 days later to observe fracture – consequence of this fracture is avascular necrosis due to cut off of blood supply to scaphoid is proximal → distal
Additional Fractures
- A Greenstick fracture is an incomplete fracture in which the bone is bent. This type occurs most often in children.
- A transverse fracture is when the broken piece of bone is at a right angle to the bone's axis.
- An oblique fracture is when the break has a curved or sloped pattern.
- A comminuted fracture is when the bone breaks into several pieces.
- A buckled fracture, also known as an impacted fracture, is one whose ends are driven into each other. This is commonly seen in arm fractures in children.
- A pathologic fracture is caused by a disease that weakens the bones.
- A stress fracture is a hairline crack.
Common fractures of the wrist:
Colles Fracture – a fracture of the distal 2 cm of the radius as well as commonly the ulnar styloid process
The fragment of the radius is displaced dorsally and is referred to as a dinner fork deformity
Normally the radius projects further distally than the ulna, but with the fracture the relationship is reversed because of the shortening of the radius
Smith Fracture – A reverse colles fracture – Fracture of the distal radius but with volar displacement (dorsal in colles)
Bennett Fracture – fracture of dislocation of the base of the first metacarpal (thumb) – dorsolateral dislocation occurs with this fracture
Scaphoid Fracture – patient presents with tenderness in anatomical snuffbox – must be clinically diagnosed as fracture will usually not turn up on x-ray straight away – need to re-x-ray approx. 10 days later to observe fracture – consequence of this fracture is avascular necrosis due to cut off of blood supply to scaphoid is proximal → distal
Additional Fractures
- Chauffeur's fracture – radial styloid process
- Galeazzi's fracture – radius with dislocation of the ulna
- Monteggia's fracture – ulna with dislocation of the radius
- GRUM – Galeazzi-Radius, Ulna-Monteggia
Common Causes of Falls in the Elderly
Briefly describe the causes of falls in older people and outline how you could differentiate between these.
Inflammation of joints
Hypotension (orthostatic changes)
Auditory & Visual abnormalities
Tremor
Equilibrium (balance) problem
Foot Problems
Arrhythmia, heart blocker or valvular disease
Leg-length discrepancy
Lack of conditioning (general weakness)
Illness
Nutrition
Gait disturbance
Investigations:
Prevention:
Multidisciplinary health and environment risk evaluation & risk factor screening
Muscle strengthening, balance retention and group exercise programs
Home hazard assessment and modifications (remove rugs, insert shower bars etc.)
Prescription of Vitamin D 1000IU, daily
Tapering/gradual discontinuation of psychotropic medication / General review of medications
Management of postural hypotension (a form of low blood pressure that happens when you stand up from sitting or lying down), heart rate, and rhythm abnormalities
Optimization of footwear and eyesight
Hypotension (orthostatic changes)
Auditory & Visual abnormalities
Tremor
Equilibrium (balance) problem
Foot Problems
Arrhythmia, heart blocker or valvular disease
Leg-length discrepancy
Lack of conditioning (general weakness)
Illness
Nutrition
Gait disturbance
Investigations:
- Full history and physical exam
- Comprehensive geriatric assessment to identify all possible causes
- CBC, Electrolytes, creatine, glucose, calcium, TSH, B12, urinalysis, cardiac enzymes, ECG, Head CT
Prevention:
Multidisciplinary health and environment risk evaluation & risk factor screening
Muscle strengthening, balance retention and group exercise programs
Home hazard assessment and modifications (remove rugs, insert shower bars etc.)
Prescription of Vitamin D 1000IU, daily
Tapering/gradual discontinuation of psychotropic medication / General review of medications
Management of postural hypotension (a form of low blood pressure that happens when you stand up from sitting or lying down), heart rate, and rhythm abnormalities
Optimization of footwear and eyesight
Social and Home Supports & the Issues Surrounding them
Strategic Goals
- Empower older people, their families and other consumers
- Enable them to remain in their own homes
- Help them to stay active & healthy
- Ensure that their rights are acknowledged
- Prevent neglect
Services AvailableCommunity intervention team (72 hours and within limited radius)
Mental Health Services: Psychogeriaticians Elder Abuse Case workers Social Workers for Elderly Services - Pension theft, emotional abuse, neighbor priest or resident report Housing adaptions - county council Hospital Liaison Services Medical Assessment Services - NWHB Rehabilitation Units Respite Facilities in Community Nursing Units - 2 weeks every 12 weeks Assessment Beds Categories A and B -On route to long term care vs. further assessment/slow rehab to return to individual living Inter-Agency Co-operation Bereavement Counselling Services - loss of spouse or partner Palliative Care Services Private Agencies The Brackets
Anybody over 65 years old with a medical card/long term illness card is entitled to receive the public health nursing service, home help service (HSE/Voluntary) or Home Care Package where required.
If you do not have a medical card then you will be assessed on a 'case-by-case' basis. |
Priorities for the HSE
Primary Care TeamGP
Nurse Physio O.T. Social Worker Home Help May also Include Dietitian Podiatrist Psychogeriatician |
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