Dementia is characterized by deterioration in mental function and impairment in daily activities. Alzheimer's disease is the most common cause and is a progressive neurodegenerative disorder. It involves plaques and tangles of proteins in the brain that damage neurons. Risk factors include age, family history, and medical conditions. Symptoms include memory loss, language problems, and changes in behavior and mood. Diagnosis involves assessing cognitive abilities and daily function, and ruling out other potential causes through tests and scans.
Alzheimer's disease is a progressive neurologic disorder that causes the brain to shrink (atrophy) and brain cells to die. Alzheimer's disease is the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that affects a person's ability to function independently.
Alzheimer's disease is a progressive neurologic disorder that causes the brain to shrink (atrophy) and brain cells to die. Alzheimer's disease is the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that affects a person's ability to function independently.
depression ,symptoms, mechanism of depression ,classification of antidepressants , tri cyclic anti depressants and its pharmacological actions ,acute poisoning and treatment
Definition
Epidemiology
Etiology
Pathophysiology
Classification
Diagnosis
Treatment
Anti Seizure Drugs Prices in Jordan
Two Medical cases
New drug approvals
depression ,symptoms, mechanism of depression ,classification of antidepressants , tri cyclic anti depressants and its pharmacological actions ,acute poisoning and treatment
Definition
Epidemiology
Etiology
Pathophysiology
Classification
Diagnosis
Treatment
Anti Seizure Drugs Prices in Jordan
Two Medical cases
New drug approvals
Alzheimer's disease is a causes a progressive loss of brain cells leading to memory loss. In this slide we will learn about its causes,symptoms, pathophysiology, treatment, medication and risk factors.
This slide contains information regarding Dementia. This can be helpful for proficiency level and bachelor level nursing students. Your feedback is highly appreciated. Thank you!
Organic mental disorders are disturbances that may be caused by injury or disease affecting brain tissues as well as by chemical or hormonal abnormalities.
Alzheimer's disease is a progressive, degenerative disorder that attacks the brain's nerve cells, resulting in loss of memory, imagination and speaking skills, and behavioural changes. Alzheimer's disease is the most common cause of dementia, or loss of intellectual function, among people aged 65 and older.
This is a presentation I did last spring in which I discuss how the OTPF applies to Alzheimer's Dementia. I collected data from scholarly as well as non-scholarly resources. I hope you find this to be helpful.
This outlined the age-related changes in cognition:
- Structural Changes with Aging in Brain
- Cognitive Abilities Affected by Aging
- Alzheimer’s Disease
- Assessment of cognitive disorder
- Evidence Based Practice
Respiratory stimulants: types, complete discussion on indications, contraindications, assessment, patient notes and examples of stimulants both central and respiratory
Expectorants and Antitussives: types, complete discussion on indications, contraindications, assessment, patient notes and examples of expectorants and antitussives
Complete pharmacology of Non steroidal Anti inflammatory Drugs, classification, Mechanism of action, Pharmacological actions, Indications, Contraindications, Adverse effects
Pharmacology laboratory experiment, both invivo and invitro includes interpolation, matching , bracketing, three point, four point bioassays with a note on hypoglycemic activity, acute skin irritation, acute eye irritaiton, pyrogen test, gastrointestinal motility test, physiological salt solutions
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. Dementia
• Dementia describes a clinical syndrome that is characterised
by a significant deterioration in mental function that leads to
impairment of normal function.
• In healthcare, we measure ‘normal function’ by activities of
daily living (ADLs).
• These are a series of routine activities that people should be
able to do without assistance. They can be broadly divided into
personal tasks and domestic tasks.
– Personal: washing, dressing, toileting, continence, transferring (e.g.
bed to chair)
– Domestic: cooking, cleaning, shopping, managing finances, taking
medication
3. • Dementia can be caused by several conditions, which all manifest with
poor mental performance and impaired normal functioning.
• The clinical manifestations of dementia can reflect the underlying
aetiology.
– Alzheimer’s disease (AD): 50-75%
– Vascular dementia (VD): 20%
– Dementia with Lewy-body (DLB): 15-20%
– Front temporal dementia (FTD): 2%
– Rare causes: Parkinson’s disease dementia (PDD), Huntington’s disease
(HD), Prion disease, others.
4. Alzheimer's disease
• Alzheimer's disease (AD) is a progressive neurodegenerative
disorder that causes significant deterioration in mental
performance.
• This leads to impairment in normal social and occupational
function.
• It is the most common cause of dementia and unfortunately an
incurable condition that has a variable clinical course
5. Epidemiology
• Dementia is primarily a disease of older adults.
• The World Health Organisation (WHO) estimates that almost 50 million
people have a diagnosis of dementia worldwide.
• In the UK, it is estimated that > 500,000 people have a diagnosis of AD.
• The prevalence of dementia increases with age. The estimated prevalence
at 60-64 years is 0.9% compared to 41.1% in those aged 95 years and over.
• A significant proportion of patients with dementia remain undiagnosed and
up to 54% of patients with dementia require care home placement.
6. Aetiology
• The exact cause of AD remains unknown.
• The overarching theory involves environmental and genetic
risk factors that increase the chance of developing pathological
processes, which lead to dementia.
7. Causes
• Like all types of dementia, Alzheimer’s develops due to the death of brain
cells. It is a neurodegenerative condition, which means that the brain cell
death happens over time.
• In a person with Alzheimer’s, the brain tissue has fewer and fewer nerve
cells and connections, and tiny deposits, known as plaques and tangles,
build up on the nerve tissue.
• Plaques develop between the dying brain cells. They are made from a
protein known as beta-amyloid. The tangles, meanwhile, occur within the
nerve cells. They are made from another protein, called tau.
• The Alzheimer’s Association have produced a visual guide to show what
happens in the process of developing Alzheimer’s disease
8. Risk factors
• Unavoidable risk factors for Alzheimer’s disease include:
– Aging
– Having a family history of Alzheimer's disease
– Carrying certain genes
• Other factors that increase the risk of Alzheimer’s include Trusted
Source severe or repeated traumatic brain injuries and having
exposure to some environmental contaminants, such as toxic metals,
pesticides, and industrial chemicals.
9. • Modifiable factors that may help prevent Alzheimer’s
include:
– Getting regular exercise
– Following a varied and healthful diet
– Maintaining a healthy cardiovascular system
– Managing the risk of cardiovascular disease, diabetes, obesity,
and high blood pressure
– Keeping the brain active throughout life
10. Commonly recognised risk factors
– Age: older age is a major risk for AD
– Genetics: most cases of AD are sporadic. Small number of inherited
causes exist (<5%, autosomal dominant inheritance).
– Cardiovascular disease: smoking and diabetes increase
risk. Exercise decreases risk.
– Depression
– Low educational attainment
– Low social engagement and support
– Others: head trauma, learning difficulties.
11. Pathophysiology
• The neurodegeneration in AD is hypothesised secondary to altered
amyloid and tau protein metabolism.
• The brain is composed of billions of neurons.
• The normal functioning of theses neurons is dependent on
surrounding supportive structures such as microtubules and the
protein tau, which stabilise these microtubules.
• Pathological changes that occur in AD leads to interruption of key
neuronal process including communication, metabolism and repair.
12. • The two key pathological changes in AD are senile plaques
and neurofibrillary tangles:
1. Senile plaques (SP): deposits of beta-amyloid (aggregation of protein
with a beta-sheet secondary structure). Dense, insoluble. Occur
outside of neurons (i.e. extracellular).
2. Neurofibrillary tangles (NFT): aggregations of
hyperphosphorylated tau proteins. Typically occur in areas of the
brain involved in memory. Promote neuronal cell death. Form inside
neurons (i.e. intracellular)
13. • Both SP and NFT are characteristic of AD but no path
gnomonic.
• They can be seen in other neurodegenerative conditions. SP is
also seen in normal ageing.
• Therefore, it is the amount of these pathological changes and
the topographic location within the brain (e.g. hippocampus
and medial temporal lobes) which is characteristic of AD.
14. • The amyloid deposition hypothesis is supported by
identification of genetic mutations in the amyloid precursor
gene APP leading to early-onset AD, and evidence of neuronal
apoptosis on treatment of cells with beta-amyloid.
• However, some patients with severe AD do not have evidence
of amyloid deposition on autopsy, and other patients who had
no evidence of dementia have amyloid deposition.
15. • Several additional mechanisms are part of the pathological
processes in AD.
• Alongside SP and NFT, these result in neuronal cell death that
leads to memory failure, personality changes and problems
with activities of daily living (hallmarks of dementia).
16. Clinical features
• Dementia can be difficult to identify due to the insidious and non-specific
symptoms.
• Many clinical features are attributable to dementia. Some are characteristic
of all dementias whereas others are typical of a particular type, like AD.
• There is usually a slow onset of symptoms and lack of insight with
accommodation to cognitive or functional changes.
• It is best to consider clinical features in the following domains: cognitive
impairment, behavioural and psychological symptoms of dementia (BPSD),
disease-specific features and activities of daily living.
17. – Cognitive impairment
– Poor memory
– Language problems: receptive and expressive dysphasia
– Problems with executive functioning: planning and problem solving
– Disorientation
– BPSD
– Agitation and emotional lability
– Depression and anxiety
– Sleep cycle disturbance
– Disinhibition: social or sexually inappropriate behaviour
– Withdrawal/apathy
– Motor disturbance: wandering is a typical feature of dementia
– Psychosis
18. Disease-specific features
– AD: early impairment of memory. Manifests as short-term memory loss
and difficulty learning new information.
– VD: typically a ‘stepwise’ decline in function. Predominant gait,
attention and personality changes. May have focal neurological signs
(e.g. previous stroke)
– DLB: parkinsonism (tremor, rigidity, Bradykinesia, postural
instability). Fall, syncope and hallucinations predominant feature
– FTD: marked personality change and behavioural disturbances.
Memory and perception relatively preserved.
19. Activities of daily living
– Loss of independence: increasing reliance on others for
assistance with personal and domestic activities
– Early stages: problems with higher level function (e.g.
managing finances, difficulties at work)
– Later stages: problems with basic personal care (e.g.
washing, eating, toileting) and motor function (e.g.
walking, transferring)
20. Cognitive assessment
• A formal mental status examination should be completed using
a recognised cognitive assessment tool.
• There are multiple cognitive assessment tools, which are
designed to test different areas of higher cortical functioning.
• Cognitive domains assessed include:
• Attention and concentration
• Recent and remote memory
• Language
• Praxis: planned motor movement (e.g. perform a task)
• Executive function
• Visuospatial function
21. • There are a variety of different cognitive assessment tools that range
from basic screening tools, to in-depth assessments of each
cognitive domain.
• Here we summarise some of the main tools.
1. Mini-cog
– Overview: a three item word memory and clock drawing. Screening tool
in general practice.
– Time: 2-4 minutes
– Setting: General practice
– Cut-off for dementia: 5/8
22. 2. Abbreviated mental test score (AMTS)
• Overview: a ten item scoring tool predominantly used in hospital settings
(e.g. hospital ward).
• Time: < 5 minutes
• Setting: hospital ward and General practice
• Cut-off for dementia: 6-8/10
3. Mini-mental state examination (MMSE)
• Overview: an eleven item tool. Measures cognitive function. Extensively
studied and well-validated. Copyrighted.
• Time: ≤ 10 minutes
• Setting: Memory clinic, hospital-setting
• Cut-off for dementia: 24/30
23. 4. Montreal cognitive assessment scale (MoCA)
• Overview: test several domains including executive function, attention, some
language, memory and Visuospatial skills.
• Time: 10 minutes
• Setting: memory clinic, hospital-setting
• Cut-off for dementia: 26/30
5. Addenbrookes cognitive examination - III
• Overview: longer cognitive assessment tool that assess five domains: attention,
memory, verbal fluency, language and Visuospatial abilities. Based on the ACE-R,
which was originally designed to classify different kinds of dementia
• Time: 15-20 minutes
• Setting: memory clinic
• Cut-off for dementia: 82-88/100
24. Diagnosis
• It is essential to exclude all alternative causes before making a diagnosis of
dementia.
• Patients with suspected dementia are usually referred to a memory clinic.
• At memory clinic, patients undergo a formal history and examination
(including medication review), full complement of baseline investigations
including bloods and neuroimaging to exclude an underlying cause, and
formal cognitive assessment.
• In AD, this may be reflected by the lack of other neurological symptoms,
absence of major cardiovascular risk factors and predominant impairment
in memory, thinking and behaviour.
25. Diagnostic criteria
• There is a diagnostic criteria for dementia based on the Diagnostic and
Statistical Manual of Mental Disorders (DSM-V).
• We have simplified this into three key components:
– Functional ability: inability to carry out normal functions.
Represents a decline from previous functional level
– Cognitive domains: impairment involving ≥2 cognitive domains
(see chapter on cognitive assessment)
– Differentials excluded: clinical features cannot be explained by
another cause (esp. psychiatric disorders and delirium)
26. Mild cognitive impairment
• This describes cognitive deficits in one or more of the major
cognitive domains, but the deficit is insufficient to interfere
with independence in daily activities.
• Mild cognitive impairment is an increasingly important term
because it helps identify patients at risk of progression
to dementia.
• Patients should have regular follow-up and be advised to
undertake healthy brain activities (e.g. exercise, socialising).
27. Differential diagnosis
• Dementia is a clinical syndrome that reflects deterioration
from an underlying cause, the most common being AD.
• The main differentials to exclude in a patient with features of
dementia are the three ‘D’s’:
– Depression (and other psychiatric disorders): psychosis can be a feature of
dementia.
– Drugs: consider drugs with anti-cholinergic effects (e.g. anti-histamines,
anti-psychotics, anti-epileptics)
– Delirium: acute confusional state. May be prolonged recovery following
episode.
28. Severity
• The severity of dementia can be determined based on the level of
functional inability.
• Severity of dementia is determined using cognitive assessment tools
(e.g. MMSE/MoCA) or rating/assessment tools (e.g. clinical
dementia rating - CDR).
• In general, dementia can be divided into mild, moderate or severe.
• Mild: MMSE 21-26, MoCA 18-25, CDR 1
• Moderate: MMSE 10-20, MoCA 10-17, CDR 2
• Severe: MMSE <10, MoCA <10, CDR 3
29. Investigations
• Baseline investigations are essential to exclude an
alternative diagnosis.
• Typical baseline investigations involve a routine set of
blood tests and neuroimaging.
• Bloods
– Full Blood Count
– Erythrocyte Sedimentation Rate (ESR)
– Urea And Electrolytes
– Bone Profile
– Hba1c
– Liver Function Tests
– Thyroid Function Tests
– Serum B12 And Folate Levels
30. • Other
– ECG
– Virology (e.g. HIV)
– Syphilis testing
– CXR
• Neuroimaging
– Typically magnetic resonance imaging (MRI) but CT may be used if
MRI not available or unsuitable. Important to exclude an alternative
diagnosis (e.g. brain tumour) and can be used to help characterise the
type of dementia (e.g. small vessel disease in VD).
31. Management
• Pharmacological therapy can be used in patients with AD, but it is
only a small part of overall management.
• The management of AD, and dementia as a whole, should involve a
full assessment of the biological, psychological and social needs of
the patient.
• With significant deterioration in normal activities of daily living,
patients will become dependent on others.
• This means help from families, organisation of carers, and with
more advancing symptoms, need for care home placement.
32. TREATMENTS
• There is no known cure for Alzheimer’s disease. It is not
possible to reverse the death of brain cells.
• Treatments can, however, relieve its symptoms and improve
quality of life for the person and their family and caregivers.
• The following are important elements of dementia care:
– Effective management of any conditions occurring alongside
Alzheimer's
– Activities and daycares programs
– Involvement of support groups and services
33. Medications for cognitive symptoms
• No disease-modifying drugs are available for Alzheimer’s
disease, but some options may reduce the symptoms and help
improve quality of life.
• Drugs called cholinesterase inhibitors can ease cognitive
symptoms, including memory loss, confusion, altered thought
processes, and judgment problems.
• They improve neural communication across the brain and slow
the progress of these symptoms.
34. • Three common drugs with Food and Drug Administration (FDA)
approval to treat these symptoms of Alzheimer’s disease are:
– Donepezil (Aricept), to treat all stages
– Galantamine (razadyne), to treat mild-to-moderate stages
– Rivastigmine (Exelon), to treat mild-to-moderate stages
• Another drug, called memantine (Namenda), has approval to treat
moderate-to-severe Alzheimer’s disease.
• A combination of memantine and donepezil (Namzaric) is also
available
35. Emotion and behaviour treatments
• The emotional and behavioural changes linked with Alzheimer’s disease
can be challenging to manage.
• People may increasingly experience irritability, anxiety, depression,
restlessness, sleep problems, and other difficulties.
• Treating the underlying causes of these changes can be helpful. Some may
be side effects of medications, discomfort from other medical conditions, or
problems with hearing or vision.
• Identifying what triggered these behaviors and avoiding or changing these
things can help people deal with the changes.
• Triggers may include changing environments, new caregivers, or being
asked to bathe or change clothes.
36. • It is often possible to change the environment to resolve obstacles
and boost the person’s comfort, security, and peace of mind.
• The Alzheimer’s Association offer a list of helpful coping tips for
caregivers.
• In some cases, a doctor may recommend medications for these
symptoms, such as:
– Antidepressants, for low mood
– Antianxiety drugs
– Antipsychotic drugs, for hallucinations, delusions, or aggression
37. There are multiple facets to management.
1. Assess capacity and advanced care planning: ideally completed when
patients still retain capacity. Consideration of advance statements/decisions
and appointment of lasting power of attorney.
2. Physical and mental health: consider co-existing anxiety and depression.
Manage physical health needs as normal. Consider delirium if any acute
deterioration.
3. Driving: must inform the DVLA. Check website for guidance.
38. 4. Non-pharmacological: programmes to improve/maintain cognitive
function (e.g. structured group cognitive stimulation programmes).
Also exercise, aromatherapy, therapeutic use of music/dancing,
massage.
5. Managing BPSD: non-pharmacological interventions. Consider
referral to old-age psychiatry if difficult to control.
Pharmacological therapy should be used on specialist advice.
6. Care plans: people with dementia require a care manager and care
plan. This includes details on diagnosis, treatment, environmental
modifications and review plans.
39. 7. End-of-life care: focus on physical, psychological, social
and spiritual needs. Oral nutrition encouraged as long as
possible. Long-term feeding (i.e. NG feeding, gastrostomy
tube) inappropriate in severe dementia. No evidence for
increased survival or reduced complications. Resuscitation
discussions.
40. Pharmacological therapy
• Medical therapy for the treatment of dementia should be
initiated by a specialist in treating patients with dementia.
• The two main drugs are acetyl cholinesterase inhibitors and N-
methyl-D-aspartic acid receptor antagonists.
• Pharmacological agents are primarily indicated in patients with
AD.
• They should not be used in patients with mild cognitive
impairment.
41. Cognitive enhancers
• These are a heterogeneous group of drugs developed for use in
dementia and other cerebral disorders.
• They do elicit pharmacological effects, but widely different
mechanisms of action are claimed.
• Therapeutic benefits are limited, and at the best, short-lasting.
42. The indications of cognition enhancers include:
1. Alzheimer’s disease (AD) and multi-infarct dementia (MID).
2. Mild cognitive impairment (MCI) or‘ common symptoms’ of the elderly;
dizziness and episodic memory lapses.
3. Mental retardation in children, learning defects, attention deficit disorder.
4. Transient ischaemic attacks (TIAs), cerebrovascular accidents, stroke.
5. Organic psycho syndromes and sequelae of head injury, ECT, brain surgery.
43. • A variety of drugs have been briskly promoted by
manufacturers and wishfully prescribed by physicians.
• The mechanism by which they are believed to act are:
1. Increasing global/regional cerebral blood flow
2. Direct support of neuronal metabolism.
3. Enhancement of neurotransmission.
4. Improvement of discrete cerebral functions, e.g. Memory.
45. Choice of therapy depends on severity:
– Mild-to-moderate AD: acetyl cholinesterase inhibitors (e.g. donepezil,
Rivastigmine).
– Moderate-to-severe AD: N-methyl-D-aspartic acid receptor antagonist
(e.g. memantine). May be used in combination with acetyl
cholinesterase inhibitors.
46. • Acetyl cholinesterase inhibitors are associated with small
improvements in cognition, neuropsychiatric symptoms, and
ADLs in patients with mild-to-moderate AD. However, there is
conflicting evidence on there impact on long-term outcomes
(e.g. need for care home, effect on critical ADLs).
• Memantine has modest effects in patients with moderate-to-
severe AD in terms of reducing functional decline.
47. PROGNOSIS
• There is no cure for dementia and it is considered a life-limiting condition.
• It is estimated that one in three people over the age of 65 will die with
dementia and the estimated median survival after diagnosis is 3-9 years
(variable).
• Progression of dementia has been estimated by WHO, which is based on
each stage of severity.
• Development of delirium on a background of dementia is associated with
more rapid progression.
– Mild: first 2 years
– Moderate: next 2-4 years
– Severe: 4-5 years onwards