Geriatrics LITMED PDF
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This document discusses the importance of an interdisciplinary approach in treating older patients, highlighting the principles of geriatric medicine, and the characteristics of diseases common in older adults. It also explores the assessment of elderly patients in geriatric care.
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1. Importance of interdisciplinary approach in treatment of aged patients. (L5.5A) Health of elderly is impacted by physical, mental and psychosocial factors (social isolation, economic deprivation, decreased capacity for carrying out activities necessary for independent living)...
1. Importance of interdisciplinary approach in treatment of aged patients. (L5.5A) Health of elderly is impacted by physical, mental and psychosocial factors (social isolation, economic deprivation, decreased capacity for carrying out activities necessary for independent living) An interdisciplinary approach permits to improve the quality of life of the patients and the outcomes of care such as increased survival rates, maintaining autonomy and decreased institutionalization rates. Interdisciplinary team can include [don’t memorise, just bullshit the functions lol] Team Member Functions Patient and his family - Medical doctor Diagnoses, management, assessment of care, identification of home care needs, documentation, support /communicate / participate with other members, quality of care evaluation Nurse Identify health problems, health and self care teaching, coordination and case management of complex care needs, medication administration, wound / catheter care and teaching, operative care, lab services Social worker Psychosocial assessment, counselling, referrals to community resources, assistance with long term planning, day care programs / nursing home placement, housing, guardianship Physiotherapist Teaching and assisting with mobility, assistive devices, therapy exercises for ROM/strength/endurance, pain management using TENS etc, lifting/handling techniques Occupational therapist Regain or retain independent living activity ability (feeding, dressing, toileting, meal prep, shopping etc.) Speech therapist Language/cognitive-linguistic evaluation and treatment, swallowing evaluation, communication for tracheostomy / ventilator patients Psychiatrist, psychologist - Clinical pharmacologist - 2. The principles of geriatric medicine; the principles of working with older patients (L5.5A) Elderly patients are treatable AND teachable (and they teach us about ageing) The goal of treating is to maintain or improve functional level and quality of life (rather than simply prolong) Interdisciplinary approach is needed for physical, functional, social and psychological assessment - which includes teamwork from an interdisciplinary geriatric team: Physician, nurse, social worker, physiotherapist etc.. Role of family is critically important as well Care of elderly requires special training in geriatrics and gerontology Prioritize problems, and interventions applied ONLY when benefits outweigh risks Periodic medication monitoring is important 3. The main characteristics of diseases in the older adults (L5.5A) 1. The acute illnesses displayed are NOT very acute (they are masked by chronic diseases and aging processes) 2. The onset of symptoms, seeking help and diagnosing are often delayed because of sedentary lifestyle, attributing the symptoms to aging and absence of typical symptoms and signs of disease 3. Multiple diseases are NOT rare - several chronic and acute diseases together can occur 4. Polypharmacy - polymedication. Elderly patients often use 10 and more medications. 5. Adverse drug reactions are almost twice as common as in younger patients 6. Deterioration of functional ability is the final common outcome for many disorders in the elderly. Hence this could be an early, subtle sign of untreated illness characterized by the absence of typical symptoms and signs of disease. 7. The course of diseases is longer and recovering slower. Step-wise rehabilitation in hospital, hospice, at home or elderly home is often needed 8. Poor correlation between functional impairment and diseased organ or tissue. (For example, Incontinence - not bladder dysfunction, but due to diuretics; Falls - not by musculoskeletal disease but by cardiac arrhythmias, Confusion - not by encephalitis but by pneumonia) 9. Focus on all presenting problems (series of i’s) rather than just diagnoses: immobility, instability, incontinence, intellectual impairment, infection, impairment of vision and hearing, irritable colon, isolation, inanition, impecunity, iatrogenesis, insomnia, immune deficiency, impotence. 4. Assessment of the elderly patient (L5.5A) Comprehensive geriatric assessment (CGA): a systematic, multi-disciplinary evaluation of elderly by a team of health professionals. Differs from a standard medical evaluation by: 1) including nonmedical domains; 2) by emphasizing functional capacity and quality of life; 3) incorporating a multidisciplinary team. Assessment and Evaluation is complex (physical, functional, social, psychological evaluations) as problems of the elderly patients are complex. The overall care by CGA teams can be divided into six steps: 1. Data-gathering 2. Discussion among the team,including the patient and/or caregiver as a member of the team 3. Development of a treatment plan with the patient and/or caregiver 4. Implementation of the treatment plan 5. Monitoring response to the treatment plan 6. Revising the treatment plan Data gathering: History The history may be difficult to obtain - hearing and memory deficits. The interview of older patients frequently includes family members, caregivers, neighbours. Old medical records can give valuable information. Psychosocial History: includes assessment of: Housing Relationships with family and friends Expectations of family and other carriers Economic status Ability to perform activities of daily living Social activities and hobbies Mode of Transportation Nutritional history, immunizations, and activity level List of consumed drugs (OTC + prescription meds) smoking and alcohol Physical examination Examination Changes in older adults BP Measurements routinely - in the supine and Orthostatic Hypotension is common in the elderly and upright positions predisposes to syncope and falls. Hearing and vision testing Hearing (cerumen props); vision (cataracts, refractive errors, glaucoma) Examination of the oral cavity after denture may reveal erosions, ulcers, or carcinoma. removal Examination of the carotids, abdominal aorta, Aneurysms and peripheral vascular disease. and peripheral arteries via US Breast examination annually; Pelvic examination Increased risk of carcinoma once in 2 years. Rectal examination + Annual stool examination Occult Bleeding, BPH, Hemorrhoids may be otherwise for occult blood in patients > 50 years missed Examination of the feet for calluses, warts, ingrown toenails, foot deformities, infections, vascular problems, onychogryphosis and joint disease. Physical finding Physiological correlation Pseudohypertension Non- compressible, calcified brachial artery Orthostatic Hypotension Poor baroreceptor sensitivity Systolic hypertension Ridgid aorta Early Systolic Murmur Aortic Stenosis causing Turbulence End Expiratory Crackles Decreased Elastic Recoil Diagnostic tests Test Changes in older adults CBC Unchanged ESR Normal Urinalysis incidence of bacteriuria and pyuria. Creatinine May be normal even when creatinine clearance CrCl Decreases Serum Albumin Decreases or normal FSH / LH Increases ABG (pO2 ) Decreases Head CT Mild or no cerebral atrophy and dilated ventricles Comprehensive Functional Assessment: Assessment of physical and psychosocial function are the most accurate measure for identifying new disease and monitoring progress of treatment. In geriatric medicine a large number of standard functional assessment scales are used. They help identify problems that may otherwise be missed. Core components: Functional status: Barthel’s Index and IADL instrumental activities of daily living Nutrition: Mini nutritional assessment (MNA-SF; MNA);Nutritional Risk Screen 2002 (NRS) Falls risk: Get up and Go test; Sharpened (tandem) Romberg test Cognitive: Mini Mental State Examination (MMSE); clock drawing test (CDT) Emotional: Geriatric Depression Scale (GDS) Perceptive: Hearing, speech, vision. Other: polypharmacy, , financial concerns, goals of care, advanced care preferences social support Social status: directly related to health and health needs. Social status may determine impact of disease and need for healthcare 5. Geriatric care system (medical and social) (L5.12) Medical Care Social Care Institutional (5% of older people) State mental hospital Sheltered or organized housing Acute care hospital Care/ residential home Long-term care in hospital Sheltered homes Rehabilitation centre Congregate housing Skilled nursing facility Retirement villages Hospices Community (95% of older people) Outpatient services Adult day care Visiting nurse Respite care Mental health counseling Occupational therapy Chiropody (feet) Meals on wheels Home help services Environmental alterations ramps, grab bars, raised toilet seats Increased social contacts clubs,day centres, voluntary organisations Electronic alarm systems Community support services Social services: provide practical social, emotional and financial support to help patients remain in the community, to age in place. Major social indicators: living alone, difficulties in managing personal care, difficulties in managing the environment, financial need, needs of carers, gaps in services. Instruments to assess social support: The family APGAR, The friends APGAR, The Social Dysfunction Rating Scale, Older Americans Resources and Services (OARS), Multidimensional Functional Assessment Questionnaire, Social Resources, Zarit Burden Interview, Caregiver Strain Index 6. Dehydration syndrome: prevalence, consequences, diagnosis, treatment, prevention (L5.6) Dehydration syndrome Definition and A complex condition resulting in a reduction of the total body water. types Levels of dehydration: Types of dehydration: Mild - loss of 1-2% of Hypertonic (hypernatremic)* - loss of H O, water insufficient intake; Osmotic pressure Moderate - 2-5% Hypotonic (hyponatremic) - loss of electrolytes. Severe - > 5% [e.g. with prescription of diuresis] Isotonic (isonatremic) - equal loss of water and electrolytes. osmotic pressure and sodium conc. [e.g. vomiting, diarrhea, blood loss, sweating] * most common type among elderly & in hospital settings. Prevalence Community: 16-28% Long Term Care (LTC): 25% among those hospitalized from LTC Hospitals: 40% during hospitalization Risk Factors Environmental - Heat/dry weather, dehydration Physiological - sense of thirst, ability to hold Na H O due to kidney function aging - muscle mass content of H O in the body Diseases - Acute: Fever, diarrhoea, vomiting, trauma, urgent surgery, infection - Chronic: Diabetes, hypertension, obesity, mobility problems, dementia, depression, visions problems, dysphagia Nutrition - Inadequate H O intake; salt, sugar and caffeine; insufficient fruits and vegetables, excessive protein intake. Drugs - Diuretics, laxatives, ACEI,polypharmacy Social - Neglect, social isolation, lack of support, dependency on caregiver Psychological - Lack of understanding the importance of water Symptoms Thirst when plasma osmolarity is higher than 292mOsmol/kg Decreased sensitiveness of thirst sensation is specific for older adults, and thirst appears when plasma osmolarity is 296mOsmol/kg Dry skin/mouth/tongue/lips/eyes, headache, lethargy, dizziness, confusion skin turgor, weakness, oliguria ml, dark urine, weight loss, Bb, hyposweating, weak pulse, temperature ℃. Diagnosis Plasma urea/creatinine ratio useful when kidneys function well, but in elderly raised ratios may also be due to renal failure, bleeding, heart failure, sarcopenia, etc. Bioelectrical impedance (insufficiently in acute changes) Change in body weight (useful for rapid dehydration and rehydration: reduction of 4 % of body weight within 7 days may be considered to be clear sign of dehydration) Serum measures: Osmolarity (Gold standard), Sodium and tonicity Osmolarity: → > 295 mOsm/kg (normal: 280 295 mOsm/kg , 280 295 mmol/kg SI units) → 295 to 300 mOsm/kg ➝ mild or preclinical dehydration → > 300 mOsm/kg ➝ dehydration. Others: → Increased or normal sodium (>145 mmol/L) → Increased urea in blood (>25 mmol/L) → Hyperglycemia → Increased hematocrit (>55 %.) Management Rehydration: - Per os - Intravenous infusion - Subcutaneous infusion (hypodermoclysis) interstitial infusion - If a patient does eat: he/she must drink 1200-1500 ml liquids. - If patient does not eat: liquids must constitute 2500 ml during 24 hours - In hyperosmolarity, hypotonic infusion (5% glucoses 0.2% NaCl) Pathogenesis Prevention Identify risk factors and problems Education Dietician and speech therapist (e.g. safe swallowing techniques) Adequate liquid intake Technique applications reminders 7. Frailty syndrome: prevalence, criteria, consequences, prevention, treatment (L5.6) Frailty syndrome Definition Clinically recognizable status of older persons, for whom coping with chronic or acute stressors becomes ineffective due to decreased physiologic reserve related to aging changes and impaired organs’ functioning. Medical syndrome with multiple causes and predisposing factors with decreased muscle strength, endurance and decreased physiologic response, which increases risk for adverse outcomes, dependency and/or death. Prevalence - By sex: female 9.6%. Male 5.2% - By age: Advanced age is a risk factor Frailty index 𝒅𝒆𝒇𝒊𝒄𝒊𝒕𝒔 𝒐𝒇 𝒕𝒉𝒆 𝒑𝒆𝒓𝒔𝒐𝒏 𝒇𝒓𝒂𝒊𝒍𝒕 𝒊𝒏𝒅𝒆 𝒂𝒍𝒍 𝒅𝒆𝒇𝒊𝒄𝒊𝒕𝒔 Frailty index counts deficits. A deficit is a thing that is wrong with a person (symptom, sign, disease, disability). Frailty index = proportion of deficits accumulated over time. Simple calculation: - Zero deficits from the list of 50: FI = 0/50 =0 - Ten deficits from the list of 50: FI= 10/50 = 0.2 Other frailty index: - walking speed test, chair stand test, balance test. 4m walking speed test: Taking more than 5 sec to walk 4m predicts future: - Disability - Long-term care - Falls - Mortality Clinical picture Nonspecific symptoms: of frailty Fatigue, unexplained weight loss, frequent infections Falls: Key features of physical frailty are impairment in gait and balance Delirium: Rapid deterioration of orientation and related to adverse outcomes Fluctuating disability: Unstable and changing health status “good day” “bad day” Pathogenesis Multiple disfunction, causing impairment in homeostasis, decrease in physiologic reserve and increase susceptibility for disorders This frequently manifests as inadequate response to stressors and deterioration of function Management Aim of interventions & 1. To avoid, postpone, recover and decrease frailty syndrome; Prevention 2. To avoid or decrease adverse outcomes for those with frailty syndrome. Methods: 1. Physical exercise (best evidence) a. Reduces hospitalization and institutionalization b. Cost effective c. Improves function, gait speed, chair rising, climbing stairs, balance, decreases depression and fear of falling 2. Nutrition a. Malnutrition death risk and complication b. Protein supplement muscle mass and strength complication c. Frailty common obesity 3. Drugs 4. Vitamin D (Optimal concentration in blood 30 40 ng/ml (75 100 nmol/l))+ 8. Principles of drug therapy in the older adults (L5.5B) (TL:DR - be careful and make sure that the patient actually is capable of following the regime) General principles: Know the pharmacology of the drugs. Use a few drugs well rather than many drugs poorly. Generally use lower doses for the elderly β-blockers are an exception) Monitor for adverse drug reactions, drug interactions, and unwanted drug side effects. Obtain an accurate list of all the patient’s medications ask the patient to bring you all the medications). Encourage the destruction of outdated or leftover medications. Enlist the patient as a co-therapist in measuring clinical outcome, noting adverse effects & proposing potential changes in treatment plan. Establish a need for drug treatment Many situations do not require drug treatment. Consider prescribing exercise, physical therapy, counselling, change in diet, or relaxation. Establish realistic treatment goal: “Prioritize therapy” Limit the number of drugs used. Use extra caution in selecting drugs for patients with a positive history of drug allergy Set a therapeutic end point & check periodically to see if you have reached it. P e c ibe d g a ia e f he elde l Be careful with or completely avoid drugs with a low therapeutic index. Determine preparation dosage based upon the patient’s age, general condition ability to handle the drug. Adjust dose if there is known hepatic or renal impairment. Consider side effects: Many psychotropic drugs have anticholinergic, sedative, hypotensive, or extrapyramidal side effects. Drugs that may produce depression in the elderly include: antihypertensives, indomethacin, benzodiazepines, steroids, levodopa, -blockers, digoxine, phenothiazines. Drugs with anticholinergic side effects that may produce impaired cognitive performance, glaucoma, urinary retention in the elderly include: antidepressants, phenothiazines, antihistamines, antipsychotics, antiarrhythmics. Review the drug regimen frequently (for drug interactions and alike): Titrate dose up or down in small steps. Monitor plasma drug level (digoxin, theophylline, anticonvulsants, aminoglycosides, antiarrhythmics). Discontinue those drugs that precipitate adverse side effects or are no longer needed. Consider drug toxicity when new symptoms occur. For those with arthritis request that drugs be dispensed in easy-to-open bottles. A liquid may be more suitable than tablets for a patient who has difficulty swallowing. Request that labels be written in capital letters for the visually impaired. Educate the patient and family: Make dosage regimen as simple as possible. Supply written instructions. For complicated dose regimens recommend using a calendar, diary or special dispensing container. 9. Polymorbidity (L5.6E) The lecture has a clinical case that you might want to see. Definition: chronic diseases in the same patient Prevalence 65 74 years 63% 75 84 years 77% years Risk factors: Age Lower social status The accumulation of chronic conditions as a result of genetics, lifestyle choices, environmental factors, treatment of prior conditions (e.g. heart failure as an adverse consequence of chemotherapy regimens) Most common overlapping conditions/combinations: Cardiovascular/metabolic disorders including hypertension & diabetes mellitus (30% of women; 39% of men) Anxiety/depression/somatoform disorders & pain including depression & osteoporosis (34% of women; 22% of men) Neuropsychiatric disorders including chronic stroke & dementias (6% of women; 0.8% of men) Factors affecting management of heart failure with significant comorbidities: CVD Co-existing Prevalence of Common issues during management Conditions combination Hypertension 85.6% Orthostatic hypotension Risk of falls with treatment Optimal tolerated medical therapy limited with chronic kidney disease Ischemic Heart 72.1% Intolerance of beta-blocker therapy due to fatigue Disease Exertional symptoms due to mobility impairment Intolerance of statins due to muscle aches Heart healthy diet may increase unintentional weight loss Atrial Fibrillation 28.8% Anticoagulation monitoring Toxicity with impaired renal or hepatic clearance Anticoagulation and antiplatelet therapy increases bleeding risk Dizziness from medications (Propafonone, Flecanide) Nausea and reduced appetite (Amiodarone, Warfarin) Adherence to diet for Coumadin therapy may reduce compliance with heart healthy diet Chronic Non-Cardiac Prevalence of Common issues during management Coexisting Conditions combination Chronic Kidney Disease 44.8% Diuretic resistance Risk of contrast induced nephrotoxicity with angiography Bleeding risk with antiplatelet therapies Stroke risk Advanced kidney disease will limit heart failure therapies volume retention General fatigue, vomiting loss of appetite will weight loss sarcopenia Chronic Obstructive 30.9% Intolerance of β-blockers Pulmonary disease β-agonist therapy may increase heart rate (COPD) Steroid treatment may promote fluid retention Exacerbation of COPD & heart failure common & difficult to discriminate primary trigger Geriatric Prevalence of Common issues during management Syndromes combination Incontinence 50% Anticholinergic effects of incontinence treatment may confusion impair cognition Medications may dry mouth leading to PO intake Assessment of fluid balance utilizing input:output ratio impaired Compliance with diuretic therapy through fear of incontinence Social activities and physical activity Risk of falls due to urgency Mobility > 57% Physical activity increases cardiovascular risk, increased frailty, and Impairment Risk of falls Mobility impairs compliance with daily weights and access to heart healthy diet Falls 35% Mobility due to fear of falls Risk of injury with antiplatelet and anticoagulation therapy Weight loss 7 9% Side effects of medications may calorie intake metallic taste, nausea, vomiting, GI upset) Impaired pharmacodynamics leading to overdosing of standard medications and side effects Consequences of polymorbidity At the micro level (individual): Loss of biopsychosocial functions, quality of life Mental health disorders Polypharmacy At the macro level (health care system): Mortality Frequent, not always rational use of health services High need for human and material resources Control/management of polymorbidity - ame a Q e i 10. Pharmacokinetics and pharmacodynamics in the older persons (L5.5B) Pha mac d amic d g effec b d 1. Additive or antagonistic response 2. Therapeutic, eg. antihypertensives, cancer chemotherapy, pain management. 3. Harmful, eg., in patients receiving several drugs with anticholinergic effect Pha mac ki e ic b d effec d g Absorption GI absorption may be inhibited (to various extents) by: Drugs with large surface area (eg. antacids) Binding resins (eg. cholestyramine) Drugs which affect GI motility Drugs which affect GI pH (eg. antacids, iron, kaolin-pectin, cholestyramine, colestipol) Distribution Drugs may compete with each other for binding sites on proteins or tissues (lasts for a few days). That is not clinically important, unless: The displaced drug is highly bound The displaced drug has limited VoD (volume of distribution). The displaced drug is slowly eliminated The displaced drug has low therapeutic index, Eg. dramatic in hypoprothrombinemia when phenylbutazone is added to warfarin (warfarin displaced from pl. protein binding sites + inhibition of hepatic w. metabolism). Eg. of precipitant drugs: sulphonamides, phenytoin, NSAIDs, sulphonylureas. Metabolism Can be or by the concurrent administration of other drugs. Effect on metabolism of drugs Examples “Enzyme-inducers” drug metabolism effect Barbiturates, Carbamazepine, Phenytoin, takes 1- weeks to kick in “takes longer” to Primidone, Rifampicin disappear) “Enzyme-inhibitors” All of these are due to P450 3A4 activity: Metabolism concentration drug Amiodarone, fluoxetine, Chloramphenicol, response possible toxicity isoniazid, Cimetidine, Ciprofloxacin, Diltiazem, Mostly occurs from using drugs that are Erythromycin, Valproic acid, ketoconazole, broken down by the same subtype of cytochrome propoxyphene, quinidine, Sulphonamides, P450. Inhibition of drug metabolism begins fairly verapamil quickly & is usually maximal by the time steady state concentration is reached. Renal excretion - pH, nephrotoxicity & competition Part of renal excretion affected Examples of drugs Alkalinisation of the urine ionization of drugs Quinidine that are weak bases: lipid solubility drug Methadone reabsorption from renal tubule into the blood Sympathomimetics plasma drug concentration. But if the drug is a weak acid the urinary pH Salicylates renal excretion plasma levels. Nephrotoxic Elimination of other drugs by Aminoglycosides, amphotericin B, pentamidine glomerular filtration Many drugs are excreted via active tubular Amphotericin B, Cephalosporins, Methotrexate, secretion Competition for excretion NSAIDs, Penicillins, Probenecid, Salicylates, Thiazides 11. Pain in the elderly (classification, prevalence, diagnosis, pharmacological and non- pharmacological treatment) (S7.8) Classification of pain Functional Pain: Pain without obvious origin, but can cause pain. Inflammatory Pain: e.g. gout, rheumatoid arthritis Referred pain Prevalence 1. Estimates suggest that 20% of adults suffer from pain globally and 10% are newly diagnosed with chronic pain each year. 2. Pain prevalence increases with increasing age among older adults but a peak or plateau in the prevalence of pain by age 65 and a decline in reported pain in the old-old (75 84 years), and oldest-old (85+ years) 3. Studies have indicated that as many as 50% of older adults who live in the community and 45% to 80% of those in nursing homes suffer from this problem Diagnosis General screening as pain may not be reported - may feel that reporting pain would distract from the actual illness 1. 7 questions of pain 2. Pain scales (VAS,faces pictorial pain scale (FFPS), Mcgill Pain Questionnaire, in non- communicative patients - PAINAD) 3. Find the cause - x-ray, CT, blood tests Pain management can be pharmacological and non-pharmacological. Pharmacological Adjuvants: antidepressants, anti-seizure medications, muscle relaxants, sedatives or anti-anxiety medications, botulinum toxin Local analgesics: Lidocaine patches, Corticosteroids (IA injections for osteoarthritis), nerve block or botulinum toxin (for herpetic neuralgia) For Neuropathic pain: tricyclic antidepressants e.g. amitriptyline; SSRIs e.g. Duloxetine; anticonvulsants e.g. gabapentin Opioids Drug Dosage (no need to learn) Considerations in elderly patients Tramadol Initial Release: 25 50 mg - Can interact with serotonergic medications (eg, every 6 h antidepressants and ondansetron) Extended Release: 50 mg - Avoid use in older adults with risk of seizures every 12 h - Reduce dose in CKD Morphine Initial release: 2.5 - 10 mg - Renal impairment: clearance of active and potentially every 4 - 6 hrs as needed; neurotoxic metabolites is decreased Extended release: after 3-7 - Hydromorphone or fentanyl may be a better choice for days; 10 mg every 12 hrs older adults with renal impairment (CrCl 4 medications Certain drugs: High risk: 1. Analgesics/opioids 2. Antipsychotics 3. Anticonvulsants 4. Benzodiazepines 5. Diabetes drugs Medium Risk: 1. Antihypertensives 2. Antiarrhythmics 3. Antidepressants Low Risk: 1. Diuretics Consequences: PHYSICAL: skin tear, internal bleeding, subdural hematoma, hip fractures, rhabdomyolysis, hospitalisation, death PSYCHOLOGICAL: fear of falling, increased dependency, anxiety, loss of confidence, depression SOCIAL: social withdrawal, inability to leave home, travel or follow hobbies Evaluation: History: History of falls? Circumstances: when? how many times?: Morse fall scale Home unsafety Do you stumble on thresholds or rugs? etc. Medication BZD, Antidepressants, Antipsychotics, Cardiac medications, Hypoglycemic agents etc. Acute Chronic Underlying illness heart neurological condition, dehydration, pneumonia etc. Vision Changes in vision? cataract, glaucoma, macular degeneration , New glasses? Laboratory/Instrumental assessment: Complete blood count, electrolyte abnormalities Glucose hypoglycemia Vit D low levels lead to osteoporosis Calcium levels DEXA scan Physical examination: Visual acuity Proprioception Examine neck, back, legs, feet for pain, deformities, decreased range of motion, contractures, leg-length discrepancy Physical functional assessment: Lying to standing orthostatic test 5 times sit to stand test Timed Up and Go Test Tandem Romberg Test C g i i e a e me Montreal Cognitive Assessment Scale (MoCA) N i i a e me Mini Nutritional Assessment Scale (MNA) Prevention: Treat or Fix underlying issues of person that could cause falls: 1. Vision correction, hearing aids 2. Vitamin D supplements 3. Sensible shoes (non-skid, rubber sole, low-heeled), Using cane or walker 4. Gradual withdrawal of medications that can cause falls (Eg. psychotropics) 5. Manage orthostatic hypotension 6. Education: enough sleep, standing up slowly, no alcohol, help from family 7. Strength & Balance training 8. Multifactorial fall risk assessment Improving living space (environment) 1. Remove hazards - secure loose rugs, necessities within reach, immediately clean spills/grease, remove clutter/ less furniture in the way 2. Non-slip mats in bathroom or non-slip surfaces in general 3. Better lighting (especially near the staircase, voice controlled) 4. Assistive devices - handrails for bathtub/stairways, raised toilet seat, shower chair, fall detectors (bracelets or new Apple watch) Multifactorial Exercise Interventions - Supervised, 1-3 x/week for 12 weeks: Helps to improve: muscle strength, balance, coordination & gait Detection: Technology: 1. Fall detector bracelets or smart watches (or even necklaces) 2. Smart sensors on shoes to detect walking patterns and/or GPS 14. Peculiarities of hypothyrosis and hyperthyrosis in the aged: causes, clinical course, diagnosis, treatment (L.5.13) Hyperthyrosis Hypothyrosis Cause Common: Common: Thyroid gland nodules Chronic autoimmune thyroiditis Hashimoto‘s disease , Iatrogenic hyperthyroidism: Graves‘ disease final stage , o Iodine or iodinated containing Radioiodine therapy, intravenous contrast Resection of thyroid gland, o Thyroid replacement therapy Idiopathic hypothyreosis. o Amiodarone (causes 2 types of thyroid disease) Less common: With pre-existing Action of drugs such as amiodarone, lithium, thionamide, multinodular goitre iodine, interferon, rifampicin; With destructive thyroiditis Action of antithyroid drugs; Disorders of hypothalamus and pituitary gland. Rare: Subacute thyroiditis Graves’ disease Symptoms Course of the disease in elderly is Course of the disease in elderly is subtle and silent. subtle. Frequent symptoms: Classical signs: Arthralgia, myalgia, weakness. Tachycardia Arterial hypertension Weight loss Apathy, weakness Classical symptoms: (rare) Intolerance of cold, Other symptoms: Weight gain Constipation Muscle cramps, paresthesia, Atrial fibrillation Fatigue, depression, Nonpalpable thyroid gland, Constipation nodules Dry skin Perspiration Puffiness around the eyes Cachexia Hoarse voice Tremor, nervousness Heat intolerance In severe hypothyreosis: Anasarca (ascites, hydrothorax, Warm, moist skin pericarditis), hypothermia, hyponatremia, hyperlipidemia, Palpitation anemia. Heart failure (dyspnea) Geriatric syndromes and conditions (common): Cognitive dysfunction - dementia, Lack of appetite, weight loss, Urine incontinence, Immobility, Gait, posturality impairment (due to myopathia, ataxia), Complication Osteoporosis. Cardiomegaly, Thyrotoxic crisis (TC): A state of Myxoedema coma (hypoglycaemia, hypercapnia, decompensated thyrotoxicosis hyponatremia). o Severe hypermetabolism, fever, nausea, vomiting, neuropsychiatric changes, (delirium) congestive cardiac failure. o The most common precipitating cause is infection. Diagnosis Decreased TSH levels Increased TSH and Decreased T4 Pathognomic H symptom if TSH Norm values: < 0.01 mIU/l. TSH: 0.5- Concentration of T4, T3, and 5mIU/l thyroglobulin are high, but less high T4: 0.7- than in young people. 1.9ng/dL May be isolated T3 toxicosis. Treatment 1. Radioiodine therapy, Thyroid replacement therapy. 2. Thyrostatics (antithyroid drugs- Levothyroxine is the treatment of choice: Methimazole). 75 μg/d, (severe ischaemic heart disease or severe 3. Surgery if toxic multinodular hypothyreosis: initial levothyroxine dose is 12.5 μg d, to goitre increase dose 12.5- μg every -6 week) 4. Beta-blockers if subacute thyroiditis and for symptomatic It is recommended that the TSH must be measured 8 weeks treatment. after initiation, or a change in levothyroxine dose. Maintain TSH between and. mIU l or higher. SUBCLINICAL HYPERTHYROSIS AND HYPOTHYROSIS SUBCLINICAL HYPERTHYROSIS SUBCLINICAL HYPOTHYROSIS Definition Decreased TSH and normal T4/T3 Increased TSH and normal T4 Grades Grade 1: 0.1 -0.5 mIU/l Grade 1: TSH 4.5-9.99 mIU/l Grade 2: < 0.1 mIU/l Grade 2: TSH >10 mIU/l Hyperlipidemia increased risk of heart failure Coronary heart disease CHD When to Definitely treat at Grade 2, consider at grade 1 When TSH >7, consider treatment to reduce initiate risk of CHD mortality treatment 15. Hyponatremia in older age: prevalence, consequences, classification, treatment (L.5.6) Definition: Disorder of water balance: Occurs when more water ingested than kidneys can excrete Ability to excrete a large volume of dilute urine is compromised: Kidney Disease Diuretics Low Protein Intake Prevalence: Hyponatremia in older people: 18-26%, In older patients admitted to the emergency room 50%. Risk groups: Endurance athletes Institutionalized patients with schizophrenia People who consume large quantities of fluid but little protein People with severe kidney disease Certain drugs (diuretics, particularly thiazide; SSRIs; SNRIs) Hypovolemia or heart or liver disease Admitted to the ICU Older patients Low dietary solute intake “Tea and toast” diet Low sodium restrictive diet Beer drinkers Causes: Hypovolemia- extrarenal losses: Vomiting, diarrhea, sweating Pancreatitis Small bowel obstruction Hypovolemia - renal losses: Diuretics, osmotic diuresis Cerebral salt wasting, salt-losing nephritis Addison disease Hypervolemia: Heart failure Liver disease with cirrhosis Nephrotic syndrome Chronic kidney disease Euvolemia: Primary Polydipsia (excess water drinking even if not thirsty) Decreased Solute Excretion Diuretics Hypothyroidism Cortisol Deficiency Syndrome Of Inappropriate Antidiuretic Hormone Secretion (SIADH) Classification: 1. Mild 135-130mmol/l 2. Moderate 129-125mmol/l 3. Severe 125 mmol/l. Mild hyponatremia: Subtle neurocognitive deficits Deficits improve when plasma sodium is normalized Moderate hyponatremia: Nausea, confusion, headache, vomiting Severe hyponatremia: Delirium; impaired consciousness; seizures. Rarely: cardiorespiratory arrest Complications: seizure, coma, permanent brain damage, respiratory arrest, brainstem herniation and death. Prevention: Encourage runners to drink fluids only when thirsty, monitor body weight to avoid weight gain during exercise Check plasma sodium 1-2 weeks after initiating thiazides, SNRIs, SSRIs, Avoid thiazides in persons with high fluid or low protein intake and during acute illness Measure plasma sodium in hospitalized patients on admission Treatment: Acute severe hyponatremia 1. 3% 150 ml hypertonic NaCl (4.5g NaCl) infusion in 20 min. 2. Check Na concentration after 20 min 3. Repeat until Na concentration mmol l. Chronic asymptomatic hyponatremia, according to cause 1. H lemia d e GI l e a d ea i g Isotonic saline 2. Di e ic Discontinue use; if no improvement administer isotonic saline 3. Addi di ea e Isotonic saline; glucocorticoid and mineralocorticoid replacement 4. Gl c c ic id i fficie c Glucocorticoid replacement 5. P ima l di ia Restrict water 6. Dec ea ed l e i ake Restrict water PLUS increase electrolytes and protein in the diet 7. Hea fail e Restrict water and salt; loop diuretics in fluid overload cases 8. Ci h i i h a ci e Restrict water and salt; administer diuretics; possible albumin infusion with diuretics 9. Ne h ic d me Restrict water and salt; diuretics If clinically decreased effective circulating volume, administer albumin with diuretics 10. Ch ic kid e di ea e Restrict water and salt; loop diuretics if fluid overload present 11. SIADH: Discontinue diuretics and any drug known to cause SIADH Restrict water but not salt consider oral urea, salt tablets, furosemide with salt tablets 17. Principles of nutrition of older population, nutrient demand. (L.5.8) Principles Food must be tasty, flavourful, warm and presentable. Eating regular, frequent, slow, smaller portions. Company when eating is important. In case of lactose intolerance soy milk products. Avoid long (>12 h) fasting periods at night. Encourage older people to consume meat, fish, eggs, nuts, fruit. Nutrient Demand Energy Ageing is associated with significant energy needs due to in resting energy expenditure as a requirement result of decline in muscle mass Energy needs also result from physical activity BMR (basal metabolic rate) depends on respiration, heart rate, and contraction of muscles. WHO: Men 13.5 × M + 487 , Women 10.5 × M + 596 Additional kcal must be added to account for the patient's condition and physical activity. Protein For healthy older people: 1 1.2 g/kg/d. For older patients: 1.5 g/kg/d. Essential amino acids (histidine, leucine, isoleucine, lysine, methionine, phenylalanine, tryptophan, valine, threonine) must be ingested with food. Physical activity, glucocorticosteroids, infection, trauma, and inflammation ( increased risk of negative nitrogen balance) cause loss of lean body mass Water As a general rule, fluid intake should be ml kg body weight per day , i.e.. L. For elderly fluid balance is extremely important because they easily can develop dehydration and overhydration because of compromised renal function. Total fluid intake should be carefully monitored by frequent weight measurement and output measurements. Fats of daily calorie intake. In total, g of fats are required daily. Dairy products dominated by saturated fatty acids, but restriction is not recommended. Essential fatty acids, when consumed in large quantities: Decrease concentration of TG, increase concentration of HDL; Have an antiarrhythmic effect; Decrease risk of sudden death. Carbohydrates ~55-60% of daily calorie intake. At least 130 g must be consumed. It is recommended to increase the amount of complex carbohydrates. Salt Sodium (Na) 1500-2300 mg needed daily. 40% of salt is Na. Potassium Daily intake of potassium (3500-4700 mg) should be consumed in the form of organic potassium salts Sources: potatoes, apricots, grapes, raisins, bananas Calcium 1000-1200 mg needed daily Iron Need 8.7-10 mg/day. Ageing is associated with gradual increase in iron stores, as a consequence, iron deficiency is rare in elderly subjects and is invariably caused by pathological blood loss. In older age, iron deficiency anemia manifests mostly due to disease or restriction of meat and eggs in the diet. Iron is absorbed most easily from: veal, giblets (liver, gizzard, sweetbread, tongue, heart, giblets, brain) Vitamins Vitamin D Need around 800 UA. Main sources: salmon, sardines, dairy products (cheese, butter), mushrooms (e.g. white mushroom, portobelllo, shiitake), eggs, cod liver. Vitamin B12 μg mg for many older people. Sources: liver, tuna, dairy products (curd, cheese, yoghurt), meat, eggs. Folic acid (vitamin B9) μg. ources: leafy green vegetables (parsley,lettuce), liver, eggs, yeast. Vitamin C men: 90 mg, women: 75 mg. Sources: citrus fruits, tomatoes, potatoes, Brussels sprouts, cabbages, strawberries, cauliflower, spinach, kiwifruits 18. Insufficient nutrition of the aged: prevalence, causes, consequences. (L.5.8) Malnutrition is a negative imbalance between the supply of nutrients to the tissues and the requirement for the nutrients, due to an inappropriate dietary intake or defective utilisation by the body. Prevalence 1 26% among community-dwelling older adults, 4 43% among out-patients, 35 65% among in-patients (and ~65% in geriatric settings), 5 85% among older people in nursing institutions. Causes Physiological Decreased sense of taste and smell Worsening eyesight Increased satiety (increased sensitivity to cholecystokinin Decrease in appetite Xerostomia (dry mouth from reduced saliva flow) Hypochlorhydria (less gastric acid) Slowing of gastrointestinal peristalsis Social, psychological Isolation (economic, social) Grief, mourning, loneliness Decreased socialisation while eating Inability to travel (walk or drive) to the store Inability to buy or cook food Poverty Lack of help with eating Restrictive diets: low calorie diet, cholesterol-free diet, salt restriction, strict fasting Alcohol abuse Institutionalisation Anorexia nervosa Physical Poor dentition: edentulismus, gingivitis, periodontitis, candidosis, poor fitting dentures Cancer Medicaments (digoxin, SSRI, antacids, diuretics, laxatives, NVNU, anticonvulsants, antibiotics, ACEI, chemotherapy) Drug-induced xerostomia Disability with inactivity Dysphagia related to neurological disorders: stroke, dementia, Parkinson’s disease, myasthenia gravis, amyotrophic lateral sclerosis Other diseases with dysphagia (oesophagus disorders) Cognitive disorders (dementia, delirium) Chronic and chronic inflammatory diseases (CHF, CRD, COPD, RA) Infections (tuberculosis, AIDS) Diseases of the gastrointestinal tract: gastritis, Crohn’s disease, nonspecific ulcerative colitis, gastroparesis, obstipation, mesenteric ischaemia, etc. Consequences Increased morbidity Increased hospitalisation (43*-90**%) Re-hospitalisation Complications - falls, dizziness, deficiencies Early institutionalisation Shorter life span Impaired quality of life Increased mortality: BMI 20 breaths per minute is the earliest and most sensitive sign and may precede other signs by three to four days Complications: Pleuritis Lung abscess Empyema Respiratory failure Bacteremia (sepsis) and shock Damage of internal organs (meningitis, pericarditis, endocarditis) Mortality from pneumonia can reach 30-60 percent (increases with delirium, immobility, hypothermia, tachypnea, CRP> 100 mg / l, hypoalbuminemia, dysphagia and possible aspiration) The most common causes of death are respiratory failure, shock, and multiorganic failure Poor prognosis if: Respiratory rate >30 breaths/ minute Heart rate >125 beats/ minute Altered mental status Hypotension (systolic BP 100 mg/l Acute aggravation of comorbid chronic diseases, especially diabetes, cardiac, renal and liver Diagnostics: Lab tests include: CBC - leukocytosis may absent, renal parameters (urea, creatinine, GFR) Electrolytes, glucosis CRP is a sensitive,age- independent marker that decreases after a favourable treatment response: Procalcitonin test is more sensitive Cultures Sputum (rarely) Blood culture: if in ICU, leukopenia, chronic liver failure, pleural effusion Serological (SARS-CoV-2 RNA by RT-PCR, SARS-CoV-2 antigen tests) Blood gas X-ray (gold standard)- to check for infiltration and consolidation (can be uninformative if dementia, G-ve pneumonia or endobrachial TB) Treatment: Empiric antimicrobial regimens should cover S. pneumoniae with β-lactam medications or new respiratory fluoroquinolones Atypical pathogens should be treated with macrolides or respiratory fluoroquinolones Severe pneumonia patients admitted to the ICU should be stratified as to whether or not the patients are at risk for Pseudomonas species infection and be treated accordingly Hospitalised pts- treated for 7 10 days Atypical pathogens such as Legionella species- treated for 10 14 days For influenza infection antivirals agents (oseltamivir or zanamivir) COVID-19 - Remdesivir Prevention: Medications (steroid, PPI, antipsychotic, benzo, statin, BP): Monitor and adjust doses as needed, prescribe only when indicated Oral health (oral & tongue hygiene, prosthesis): regular oral hygiene & dental checkups Measures directed at prevention, such as vaccination for pneumococcal and influenza infections, and smoking cessation programs for at-risk patients may help to decrease the incidence and severity of pneumonia 28. Herpes zoster infection in old age: definition, prevalence, risk factors, etiopathogenesis, clinical course, complications, diagnostics, treatment, prevention. (L.5.15) Definition: due to reactivation of the varicella-zoster virus, from a latent state. (lays dormant in posterior dorsal root ganglion). Prevalence: H.Zoster accounts for 9% of infections in older people. About half of all shingles cases are in adults 60 and older. Risk factors: Anyone who has had natural infection with wild-type varicella zoster virus (VZV) or had varicella vaccination can develop herpes zoster. People with the following conditions have an increased risk for herpes zoster: Older patients cancer, especially leukemia and lymphoma, human immunodeficiency virus (HIV), bone marrow or solid organ transplants taking immunosuppressive medications, including steroids, chemotherapy, or transplant-related immunosuppressive medications. Etiopathogenesis: Pts with risk factors cell-mediated immunity decreased Reactivation of virus. Types: Thoracic dermatome, lumbar dermatome, Ophthalmic herpes zoster (V1) Other: geniculate/ Herpes zoster ( affects the 8th CN ganglia and the geniculate ganglion of the 7th (facial) CN. V3 (V1-forehead,V2,V3-cheeks and chin) Clinical course: Stabbing, sharp pain develops in the involved site to days later a rash develops, usually crops of vesicles on an erythematous base. (continue to form for up to 5 days) 1 or more adjacent dermatomes in the thoracic or lumbar region, although a few satellite lesions may also appear. Do not cross the midline of the body. Complications: Post-herpetic neuralgia (PHN) is the most common complication of herpes zoster. PHN is pain that persists in the area where the rash once was for more than 90 days after rash onset. PHN can last for weeks or months, and occasionally, for years. PHN may be sharp and intermittent or constant and may be debilitating. Diagnostics: Almost entirely clinical. If unsure- Tzanck test (Herpes skin test) can be performed to detect multinucleated giant cells Treatment: Symptomatic drying lotion, cold compress, loose clothes Anti-viral within 72 hours of first noticing the rash. Valacyclovir 1 g 3 times a day for 7 days Acyclovir 800 mg 5 times a day for 7 to 10 days PHN gabapentin, pregabalin, amitriptyline (TCA), paracetamol, opioids Prevention: If an individual is suffering with active shingles: avoid direct contact with vesicular fluid until they are crusted. Immunocompetent pts: recombinant zoster vaccine Must not give live-attenuated in immunocompromised pts!! 27. Peculiarities of urinary tract infections in old age: definition, prevalence, risk factors, etiopathogenesis, clinical course, complications, diagnostics, treatment, prevention. (L.5.7) Urinary tract infection (UTI) is broadly defined as an infection of the urinary system, and may Definition involve the lower urinary tract or both the lower and upper urinary tracts: An infection of the kidneys, bladder or urethra The definition of a symptomatic UTI generally requires the presence of urinary tract specific symptoms in the setting of significant bacteriuria with a quantitative count of colony forming units of bacteria per milliliter (CFU/ml) in one urine specimen Asymptomatic bacteriuria (ASB) is defined as the presence of bacteria in the urine, without clinical signs or symptoms suggestive of a UTI: Leading to unnecessary antibiotic treatment Asymptomatic pyuria is defined as the presence of white blood cells in the urine, in the absence of urinary tract specific-symptoms Urinary tract infection (UTI) is one of the most common infections in older adults Prevalence Approximately 25% of all infections in older adults Asymptomatic bacteriuria (ASB): Over the age of years, it is found in 10% of men and 17 20% of women Among nursing home residents reported up to had ASB Prevalence of ASB is in patients with long term indwelling catheters IDC and about with short term Abnormal defence mechanisms: inability to void completely, alkalinization of urine, suppressed Risk Factors immune system (lack of immunoglobulin production). Women are especially prone to UTIs: Shorter urethral length, Frequent vaginal colonization, Loss of pelvic floor muscle tone and associated prolapse Anatomical abnormalities Sexual activity at any age, anal intercourse Urinary incontinence Physical limitations (hygiene) Diabetes, cancer, autoimmune disorders, Co morbidities such as dementia, stroke, Parkinson’s disease, Oestrogen deficiency, Prostatic hypertrophy, Presence of foreign body (including urinary catheter, stone, suture, surgical material) Etiopathoge nesis A significant diagnostic difficulty when trying to differentiate between ASB(asymptomatic Clinical bacteriuria) and UTI in older people is that they may not have typical UTI symptoms even if they do Course have a UTI. Typical symptoms of UTI: Lower urinary tract symptoms such as dysuria, urinary frequency and urgency cystitis Back flank pain, costovertebral angle tenderness (pyelonephritis) Fever might be present as a part of clinical syndrome of pyelonephritis Urine turbidity, sediment colour and odour do not reliably correlate with the presence of infection and may be related to antibiotic overuse: Changes in urine characteristics such as colour, and odour may be attributable to dehydration, renal stones, certain types of food (e.g. asparagus) or medications (e.g. multivitamins) Atypical presentation of UTI in older patients: Confusion or delirium, Agitation, Hallucinations, Poor motor skills or loss of coordination, Dizziness, Falls Recurrent infections, especially in women who experience two or more UTIs in a six-month period Complicatio or four or more within a year. ns Permanent kidney damage from an acute or chronic kidney infection (pyelonephritis) due to an untreated UTI. Sepsis Diagnosis of UTI requires the following four components: Diagnosis 1. Clinical symptoms of infection localised to the urinary tract (urinary frequency, dysuria, flank pain, suprapubic pain, fever, malaise or acute onset of non specific symptoms of infection in the absence of symptoms suggesting infection elsewhere 2. Laboratory evidence of pyuria and bacteriuria (based on urine culture): (Isolation of a urinary pathogen at colony forming units mL in a freshly voided midstream. 3. Additional criteria: No more than two species of organisms identified on urine culture Pyuria white blood cells mm per high power field Growth of only colony forming units mL of a urinary pathogen on urine culture, in those with a catheter acquired UTI Systemic inflammation e.g. fever hypothermia, raised WBC or CRP 4. The absence of another infection or non infectious process to which the patient’s symptoms can be readily attributed Urine Culture The purpose of urine culture is to identify bacteriuria and determine sensitivity to antibiotics. Bacterial count of 10^5 CFU/mL is usually considered significant bacteriuria, but lower counts can also be relevant in patients with symptoms of UTI. Diagnosis of UTI cannot be solely based on urine culture as bacteriuria may be present in asymptomatic patients. Taking Blood Cultures is appropriate in patients with suspected sepsis: Other investigations: Imaging of the urinary tract: For patients who have not improved despite 48 72 h of antibiotic therapy For patients who have known history of obstruction like renal or ureteric calculi, ureteric stents in situ For patients who have a decline in renal function from baseline. Ultrasound of the renal tract is safe, non invasive and usually provides the clinical information required CT scan: Can identify renal calculi, pyelonephritis, haemorrhage and cortical abscesses. Chronic obstruction or urinary incontinence: May require CT intravenous pyelography and urodynamic evaluation of the bladder. These studies are not necessary for management of UTI but could be undertaken in consultation with an urologist when other causes for urinary tract symptoms are present Treatment Treatment of complicated UTI: Infection involves other parts of the renal tract apart from the urinary bladder: They often need hospitalisation and surgical intervention like nephrostomy tubes or ureteric stents. Intravenous antibiotics are usually prescribed for this group of patients Treatment can be modified based on known multi drug resistant organism colonisation or previous (within last 6 months) urine culture result Patients with complicated UTI require a 10 14 day course of antibiotic treatment Management of Catheter Associated UTI CAUTI : Consideration should be given to removing or changing the catheter as soon as possible, particularly if it has been in place for more than 7 days + Antibiotics Management of Recurrent UTI: Recurrent UTI is defined as more than four episodes of UTI in a month period Prophylactic antimicrobials to reduce the incidence and severity of recurrent UTI episodes is indicated in selected cases Treatment with intra vaginal oestrogens in recurrent UTI in post menopausal women has been Prevention shown to restore the normal vaginal flora and reduce the risk of vaginal colonisation by E. coli Cranberry products have been used with variable reported improvement in symptoms Drink plenty of liquids, especially water. Empty your bladder soon after intercourse. 26. Peculiarities of the infectious process: ageing of the immune system and changes of immune response, prevalence and consequences of infections, predisposing factors, peculiarities of clinical course, useful markers of infection. (L.5.15) Ageing of the Immunosenescence - an age-related dysfunction of the immune system which leads to immune system and enhanced risk of infection: changes of immune The total number of immune cells does not decrease with aging There is functional decline in both innate immunity and adaptive immunity (cell response mediated and humoral) Cardinal features of immune system aging: Weakened antimicrobial immunity Impaired anti vaccine response Insufficient protection against malignancies Predisposition for unopposed tissue inflammation (inflammaging): atherosclerotic disease, osteoarthritis, neurodegenerative disease Failing wound repair mechanisms Changes of immune system: Thymus gland involution Changes of cellular immunity (T cells dysfunction): T cells DNA damage More common inflammatory diseases especially respiratory Does not recognise new antigens More common atypical infections Reactivation of chronic viral infections ( Herpes Zoster) Changes of humoral immunity (B cells dysfunction): B cells neoplasms Immune response is reduced by 50 - 90% Decreased antibody production Lower vaccine efficacy Insufficient anti-cancer protection Prevalence Infections cause the majority of hospitalizations in patients over age 65 years Infection is the primary cause of death in one-third of individuals aged 65 years and older Risk of death in over age 65 years compared with younger patients: Pneumonia: 3 x Urinary tract infections: 5-10 x Common infections: UTI, Respiratory infections, unknown source, intra abdominal infections, skin infections Consequences of - Frequent cause of hospitalization infection - Bacteriemia (pneumonia) - Frequent recurrence (UTI) - Perforation and abscess (abdominal infections) - Severe disability (pressure ulcer infections) Predisposing factors Urinary: e.g. reduction of bladder capacity Pulmonary: e.g. decrease of cough reflexes and decreased mucociliary clearance Skin and soft tissue: e.g. loss of collagen from dermis and delayed wound healing GI: e.g. decreased saliva production (xerostomia), decreased intestinal motility CNS: eg. Structural and functional changes to microglial cells Endocrine: eg. increased cortisol catabolism anorexia, weight loss, decreased muscle Musculoskeletal: eg Sarcopenia Clinical course The clinical course of infections may be different Classic symptoms such as fever, leukocytosis or productive cough may absent Early symptoms of infection: poor appetite, confusion, delirium, weakness, falls An atypical course of the infectious process: No fever or leukocytosis (only neutrophilia) Acute confusion Polymicrobial flora, multiple infections simultaneously Nosocomial pathogens more common in community Weak association between infection and organ dysfunction (check lecture if you want specifics about each infection) Useful markers of Dehydration, electrolyte disbalance: infection Complaints: thirst, muscle weakness, headache, anxiety, fear Physical examination: dry mucous membranes, dry tongue and lips, soft eyeballs, confusion, If severe- coma, fever, tachycardia, weak pulse, peripheral venous filling> 5 s, postural systolic blood pressure decreases> 25 mmHg and diastolic >20 mmHg with pulse rate > 30 bpm, cervical vein congestion, weight loss, oliguria, decreased faecal moisture and volume Laboratory tests: increased osmolarity (> 295 mOsm / kg), hypernatremia, uremia, hyperglycaemia, increased hematocrit Leukocytosis: may be absent, only neutrophilia may occur (> 90%) CRP Procalcitonin test (PCT) Culture (blood, sputum, urine) Immunological, serological tests 44. Depression in old age: clinical course. (L.5.14) Diagnostic criteria of depression: 1. Depressed mood and/ or loss of interest or pleasure. 2. Plus 4 of the following (3 if both depressed mood and loss of interest or pleasure): Weight loss or weight gain. Insomnia or hypersomnia. Psychomotor retardation or agitation. Fatigue or loss of energy. Feelings of worthlessness or of guilt. Difficulty concentrating. Recurrent thoughts of death or suicidal ideation. Late - onset depression Less likely than younger patients to report feeling sad or depressed (tend to even have depression without sadness). Presents usually with: Somatic complaints: headache, fatigue, dizziness, muscle pain Low energy/motivation and loss of interest = social withdrawal Sleep & memory complaints Weight loss Irritability, anxiety More likely to have neurological abnormalities, including deficits on neuropsychological tests and neuroimaging Higher risk for subsequent dementia In addition, late-onset depression may be a distinct subtype, with: less likelihood of a family history of depression, more cognitive and neurosensory impairment, more of an association with cerebrovascular insults and white matter abnormalities, more chronicity less robust response to antidepressants than earlier onset depression. Probably the most important differences between late-life depression and depression seen earlier in the life cycle are the associations of late-life depression with medical and cognitive impairments and with other adverse life events. Suicide They are less likely to report suicidal thoughts than their younger counterparts, although the rate of suicide is alarmingly high. Persons aged 65 years and elder commit suicide at a higher rate than any other age group and the suicide attempts more often are successful than in younger adults. Depression and treatment of depression in older persons is vital to reduce the risk of suicide of this population. 45. Depression in old age: treatment principles. (L.5.14) Short-term and long-term treatment includes pharmacological and nonpharmacological management. Goals in treating depression in elderly are: Resolution of symptoms Prevention of relapse and recurrence Improvement in functional capacity Nonpharmacological interventions: Lifestyle changes: Increase physical activity, improve nutrition and increase engagements in pleasurable activities and social interactions Treatment of somatic diseases Patient and family education Psychotherapy, cognitive-behavioural therapy Electroconvulsive therapy for severe major depression (psychotic depression, who cannot tolerate antidepressants or therapy has failed) Pharmacological interventions: SSRI fi line an ide e an (initiate doses at half the usual adult dosage and then titrate slowly for a few weeks to the optimal dose if tolerated, adequate medication trial requires 6 or more weeks) Best choice in elderly: Sertraline 25-200 mg/d; Citalopram 10-60 mg/d (most common side effects: GI symptoms and sexual dysfunction) AVOID TCA! Too many side effects! (sedation, cardiac conduction abnormalities, etc) Short-acting benzodiazepines (lorazepam) to be used with precaution (can worsen cognitive function); long- acting benzodiazepines are most associated with cognitive impairment 43. Delirium: definition, importance, risk factors, prevention and treatment. (L.5.14) Definition: Etiologically nonspecific, organic cerebral syndrome characterized by concurrent disturbances of: consciousness and attention Perception, Thinking,memory, psychomotor behavior, emotion the sleep-wake schedule. The duration is variable and the degree of severity ranges from mild to very severe. Principal characteristics: - Altered consciousness - Changes in cognitive abilities - Recent and rapid onset Importance: It's the most common complication during the hospitalization in the elderly. 1/3 of older patients presenting to the emergency department 1/3 of inpatients aged 70+ on general medical units, half of whom are delirious on admission. 10-85% after hip fracture and heart surgery. Onset of some somatic diseases (MI, infection). Risk factors: Dementia syndrome is the most important risk factor. D: Drugs E: Electrolyte imbalances L: Lack of drugs (e.g. withdrawal) I: Infection (UTI or Pneumonia) R: Reduced Sensory input (e.g. vision or hearing deficits) I: Intracranial (CVA, Subdural hematoma) U: Urinary retention/ fecal retention M: Myocardial/Pulmonary (Usually causing low O2 levels) Prevention: Interventions for cognitive impairment, sleep deprivation, immobility, sensory impairment, dehydration. Focus on nonpharmacologic approaches (eg, sleep protocol involving warm milk, back rubs, soothing music) Limit or avoid psychoactive and other high-risk medications Treatment: Behavioral problems Provide “social” restraints: consider a sitter or allow family to stay in room Avoid physical or pharmacologic restraints If absolutely necessary, use haloperidol: Mild delirium: 0.25 0.5 mg po or 0.125 0.25 mg IV/IM Severe delirium: 0.5 2 mg IV/IM Additional dosing q 60 min, as required Assess for akathisia and extrapyramidal effects Avoid in older persons with parkinsonism Monitor for QT interval prolongation, torsade de pointes, neuroleptic malignant syndrome, withdrawal dyskinesias Oxygen supply Pain management Non-pharmacological measures: Environment: Light, sound, familiar objects Orientation: orienting stimuli (clocks, calendar, radio), simple Physiologic support: to, BP, Fluids/electrolytes, O2, nutrition, elimination, pain management Physical support: avoiding restraints and catheters, mobilizing pts, eyeglasses and hearing aids, sleep/wake habits Social support: family members,caretea 42. Vascular dementia. Definition, prevalence, risk factors, etiopathogenesis, clinical course, complications, diagnosis, treatment, prevention (L.5.10) Definition: gradual cognitive decline caused by small or large vessel disease. Prevalence: It is the second most common cause of dementia in the elderly (10-20% of cases); prevalence increases with age ranging from 1.2 to 4.2% of people over 65 years old Risk factors: (possible etiologies) Cerebrovascular disorders: 1. Large artery disease 2. Artery-to-artery embolism 3. Occlusion of an extra- or intracranial artery 4. Cardiac embolic events 5. Small vessel disease (lacunar infarcts; ischaemic white matter lesions) 6. Haemodynamic mechanisms 7. Specific arteriopathies 8. Haemorrhages (intracranial, subarachnoid) 9. Haematological factors 10. Venous diseases 11. Hereditary entities. Pathogenesis: The 3 most common mechanisms of vascular dementia: 1. multiple cortical infarcts, 2. a strategic single infarct 3. small vessel disease. Clinical Course: abrupt onset of cognitive impairment (Days to weeks) Often stepwise deterioration (some recovery after worsening) and fluctuating course of cognitive symptoms 20-40 % is insidious progression Complications: Future strokes Heart disease Loss of function Loss of independence Infections & pneumonia Pressure sores Diagnosis: Clinical neurological findings indicating focal brain lesion early in the course: (mild motor, sensory deficits, decreased coordination, brisk tendon reflexes, Babinski’s sign Bulbar signs including dysarthria and dysphagia Gait disorder: hemiplegic, apractic-atactic, small-stepped Unsteadiness and unprovoked falls Urinary frequency and urgency Psychomotor slowing, abnormal executive functioning Depression, anxiety, emotional lability Relatively preserved personality and insight in mild and moderate cases. Comorbid findings: History of cardiovascular diseases (not always present): arterial hypertension, coronary heart disease, atrial fibrillation Radiological findings: Computed tomography or magnetic resonance imaging: focal infarcts (70-90%), diffuse or patchy white matter lesions (70- 100%), often more extensive SPECT or PET: often patchy reduction of regional blood flow. Electroencephalography: if abnormal, more focal findings; Laboratory findings: No known specific tests; findings related to concomitant diseases, e.g. hyperlipidemia, diabetes mellitus, cardiac abnormality. Assessment of cognitive function: e.g. MMSE, Blessed dementia scale, Assessment of functional ability: eg. ADL, IADL, Barthel index Prevention & treatment of Vascular Dementia: 1. Control of risk factors of cerebrovascular disease; Control of hypertension: BP 135-150 mmHg To avoid nocturnal drop in BP Prevention of embolization: Anticoagulants (warfarin, INR 2,0-4,5) or Aspirin (up to 325 mg/d) Control of hypercholesterolemia and diabetes Nonsmoking 2. Improvement of cognitive functions; Acetylcholinesterase inhibitors (AChEIs) ( only for patient with mixed dementia) No strong evidence that drugs can improve cognitive functions in vascular dementia. 3. Management of non-cognitive functions (approach is the same as in other dementias, including Alzheimer type dementia) 41. Alzheimer disease. Definition, prevalence, risk factors, etiopathogenesis, clinical course, complications, diagnosis, treatment, prevention (L.5.10) Definition: Clinically AD is pure dementia syndrome without clinical evidence of another underlying specific disease relevant to the observed cognitive impairment AD is the most common cause of the dementia in the elderly Prevalence Alzheimer disease is the most frequent cause of dementia, and may contribute to 60 70% of cases. More prevalent in females The prevalence of Alzheimer's disease in Europe was estimated at 5.05% Risk factors: Age, lead poisoning, smoking, hypertension, cardiovascular diseases, lower education, lower socioeconomic class, family history down syndrome Etiopathogenesis: 1. Extracellular neuritic plaques in the grey matter of the brain Enzymatic cleavage Aβ peptide aggregation formation of insoluble plaques together with tau protein and microglia neurotoxic effect 2. Intracellular neurofibrillary tangles Increased phosphorylation hyperphosphorylation of tau formation of intracellular fibrils neurotoxic effect 3. Overall reduction of cholinergic function Clinical Course: Types of AD 1. Early onset, before 65 yrs of age (rare); 2. Late onset, after 65 yrs of age (more common). Key features: 1) short term memory impairment (later long term memory impaired as well); 2) progressing dependence 3) worsening motor function 4) behavioral problems. Cognitive and behavioural manifestations:- Memory loss Language impairment Difficulty getting around the neighbourhood or house. The loss of interest in the activities such as personal habits or community affairs. Depression Delusions and hallucinations Motor function usually remains intact until the final phase of illness. Diagnosis - AD criteria: 1. Causative AD genetic mutation OR 2. All of the following a. Memory and learning decline plus one other cognitive domain b. Steady gradual cognitive decline c. No evidence of mixed etiology (absence of other neurodegenerative or cerebrovascular disease or other condition contributing to cognitive decline) However, paradigm of diagnostics changes from exclusively clinical criteria towards diagnostic algorithms based on pathological changes and biomarkers (amyloid plaques, beta-amyloid deposits,neurofibril tangles, Tau proteins) found by modern diagnostic technologies (functional MRI, PET, cerebrospinal fluid (CSF) analysis) Complication: Bedbound, requires around the clock care Unable to speak Unable to walk or sit up without assistance Falls Problems with everyday activities bathing, dressing, eating Malnutrition and dehydration Withdrawal from social activities Management of AD: AD is not curable. The physician must treat medical problems, maintain the patient’s nutritient, and monitor drug use. Management includes: Simplification, definition, and familiarization of patient’s environment, while avoiding isolation and understimulation; Orientation therapy (e.g., familiarization with digital clocks and calendars), Exercise to reduce restlessness (physical therapy), Occupational and art therapy, Analysis of the environment for safety and security, Group therapy (reminiscence and socialization), and Family counselling services. Pharmacotherapy: 1- Cholinergic augmentation therapy ( Tacrine) Treatment with cholinesterase inhibitors can begin at any time after diagnosis, because their efficacy, though limited is established for patients with mild or moderate disease 2. N-methyl D-aspartate (NMDA) antagonist ( Memantine) Dosage: increase to mg day mg twice a day , mg day mg and mg as separate doses , and 20 mg/day (10 mg twice a day) at a minimum of one-week intervals if well tolerated. Prevention: Stop smoking, Cardiovascular health, Healthy balanced diet, Physical activity, avoid sedentary lifestyle 36. Dementia syndrome: definition, prevalence, causes. (L.5.10) Definition: Dementia is a neurocognitive disorder defined by the following: 1. Evidence of substantial cognitive decline from a previous level of performance in one or more domains (complex attention, executive ability, learning and memory, language, perceptual - motor - visual perception, praxis or social cognition) 2. The cognitive deficits interfere with independence (instrumental activities of daily living). 3. The cognitive deficits do not occur in the context of delirium. 4. The cognitive deficits are not attributable to another mental disorder Prevalence: Age group 60+ yrs prevalence is 5-7% 85+ yrs and older 1 out of 5 has dementia syndrome In Europe - 5 mln In the world appr. 50 mln (2017) Causes of dementia or chronic cognitive impairment: 37. Clinical course of dementia syndrome. (L.5.10) 2 types: 1. Early onset, before 65 yrs of age (rare); 2. Late onset, after 65 yrs of age (more common). Key features: short term memory impairment (later long term memory impaired as well); progressing dependence; worsening motor function; behavioral problems. S m om og e ion in Al heime di ea e There are 3 stages of Alzheimer's disease mild, moderate and severe with cognitive and functional decline stretching over 5 8 years. 1. The initial, mild stage: Usually lasts 2 3 years patients show short-term memory impairment often accompanied by symptoms of anxiety and depression. 2. During the moderate stage: The symptoms appear to abate as neuropsychiatric manifestations such as visual hallucinations, false beliefs and reversal of sleep patterns emerge. 3. Final, severe stage: Motor signs such as motor rigidity and prominent cognitive decline characterize the severe and final stage. Cognitive and functional decline tend to be linear throughout the 3 stages of the disease, whereas caregiver burden peaks with the onset of neuropsychiatric symptoms and declines somewhat during the, when the patient is more sedentary. 38. Investigation if dementia syndrome is suspected. (L.5.10) Evaluation by Neurologist, Psychiatric,Geriatrician 1. Comprehensive physical assessment 2. Lab tests: Peripheral blood count + ESR/ CRP Liver enzymes Renal function (creatinine, potassium) Thyroid gland (US+ check hormones level) According to need EEG, full comprehensive assessment, etc. Glucose Calcium Vitamin B12, folic acid Instrumental investigation: CT various abnormalities found cross sectionally (lateral ventricles, sulci, temporal lobe). Longitudinal assessment of some of these abnormalities might have higher diagnostic accuracy. MRI findings may correlate with degree of dementia. Specific diagnostic features not yet established. Regional cerebral blood flow (CBF) decreased cerebral flow found in AD, but there is significant overlap with normal aging. PET and SPECT temporoparietal deficit; (right) left asymmetry. Diagnostic value of abnormalities still being assessed. 3. Assessment of cognitive functions: Clock drawing test (CDT) Mini- Mental State Examination (MMSE) Blessed dementia scale 4. ADL, IADL 5. Comorbidities 6. Support to family 7. Neuropathology: Amyloid plaques Since the number of plaques increases with age, the number needed for diagnosis of AD is age dependent. Neurofibrillary tangles, amyloid angiopathy Loss of the choline acetyltransferase and acetylcholine in the cerebral cortex in AD. Neuritic plaques in the cerebral cortex (pathognomic microscopic feature), may be reactive astrocytes and microglia at the periphery. 39. Non-medicamental treatment of dementia syndrome. Enabling technologies. (L.5.10) Simplification and familiarization of the patient's environment, Avoid isolation, under stimulation and ensure safety (night lamp, gas cooker and bath monitor). Tools for orientation and support of memory (digital clocks, calendars, day planners, drug carousell, lost items locator, telephone with photos). Physical therapy to reduce restlessness. Occupational and art therapy. Group therapy and family counselling services. GERONTECHNOLOGY 40. Medicamental treatment of various types of dementia. (L.5.10) 1. Cholinergic augmentation therapy It works by increasing cholinergic synaptic transmission by inhibiting acetylcholinesterase in the synaptic cleft, thereby increasing the hydrolysis of acetylcholine released from presynaptic neurons. Drugs in this class differ from one another in the way they inhibit acetylcholinesterase. Treatment with cholinesterase inhibitors can begin at any time after diagnosis, because their efficacy, though limited, is established for patients with mild or moderate disease. 2. N-methyl D-aspartate (NMDA) antagonist: Memantine blocks the toxic effect associated with excess glutamate and regulates glutamate activation and is prescribed to treat symptoms of moderate to severe AD. 5 mg, once a day, available in tablet form. Dosage: increase to 10 mg/day (5 mg twice a day), 15 mg/day (5 mg and 10 mg as separate doses), and 20 mg/day (10 mg twice a day) at a minimum of one-week intervals if well tolerated.. Slowing the progression of Alzheimer’s disease not approved. Alpha-tocopherol (vitamin E), selegiline, propentofylline, Ginkgo biloba, Acetyl- L-Carnitine. 35. Syncope in older age: definition, prevalence, risk factors, etiopathogenesis, clinical course, complications, diagnostics, treatment, prevention. (L.5.9) Definition: Presyncope or a feeling of loss of consciousness (due to hypoperfusion in the brain, possible complaints I may faint“, I feel weak“ Syncope (S) or fainting is a sudden loss of consciousness associated with a lack of postural tone (the patient is unable to maintain body position and usually falls) Prevalence: In the elderly syncopes increase with age, especially from the age of 70 The prevalence among the elderly is 23% It is similar for men and women (women dominate slightly), for men it is more often due to cardiovascular diseases Risk factors: Cardiovascular disease is a major risk factor: patients with cardiovascular disease are twice as likely to experience syncope Cerebrovascular disorders: transient ischemic attack (TIA) or stroke Hypertension Low body mass index Alcohol consumption Diabetes mellitus or hyperglycaemia Etiopathogenesis: The main route is a drop in systemic blood pressure and a decrease in cerebral blood flow Manifestation alone or in combination reduction in systemic blood pressure dependent on cardiac output and total peripheral vascular resistance Types: Reflex: Vasovagal (related to psychiatric disorders or illnesses) Situational Carotid sinus syncope Orthostatic: Primary autonomic failure Secondary autonomic failure Drug-induced Caused by fluid loss Cardiovascular: Arrhythmia as the primary cause ○ Bradycardia ○ Tachycardia ○ Drug-induced bradycardias and tachyarrhythmias Structural heart disease Clinical course: Possible prodromal period (presyncope) with dizziness (up to 69%), nausea, sweating, weakness The duration of syncope is no longer than 20-30 seconds After syncope a person does not usually lose memory and orientation, but for the elderly a retrograde amnesia is possible Nausea may occur after syncope Complications: Recurrent syncope Injuries Admission to the Intensive Care Unit Hospitalisation sudden death as result of structural heart disease and primary arrhythmias and conduction disturbances Diagnostics: Careful collection of anamnesis 1) If the loss of consciousness meets the criteria for syncope: Was it a syncope or another event? Was it a transient reversible self-passing disorder of consciousness? Has the patient lost postural tone? 2) Number of episodes? 3) Prodrome: Prodrome symptoms related to convulsions Vasovagal vegetative symptoms Physical examination Blood pressure measurement (lying down and sitting), ECG record Treatment: No treatment: if syncope is rare and unlikely to recur It is important to train the patient: to know the cause of fainting, to avoid situations/other causal factors leading to loss of consciousness Additional treatment is needed: o If S episodes are common (this worsens the quality of life) o If S recurs without warning signs and there is a higher risk of injury o If a person passes out while performing risky actions (e.g. driving a car) S is treated according to the cause, such as: o Orthostatic elimination of orthostasis risk factors and treatment of causes o Caused by cardiovascular diseases (drugs, implantable pacemakers, cardioverter defibrillators) radiofrequency ablation is used. Pacemaker therapy may be effective in some but not all patients with syncope: pacemakers may correct cardiac arrhythmias but have no effect on decreasing blood pressure Prevention: Assessing risk factors Eliminating the causes of syncope Starting the treatment in time to reduce the risk of injury and death