Med C - Geriatrics Flashcards
What is Constipation classed as and what criteria do we use?
Constipation may involve any or all of the following (Rome IV criteria):
- Fewer than three bowel movements per week
- Hard stool in more than 25% of bowel movements
- Tenesmus (sense of incomplete evacuation) in more than 25% of bowel movements
- Excessive straining in more than 25% of bowel movements
- A need for manual evacuation of bowel movements
What are risk factors of Constipation
- Advanced age
- Inactivity
- Low calorie intake
- Low fibre diet
- Certain medications
- Female sex
Causes of constipation include:
- Dietary factors, such as inadequate fibre or fluid intake
- Behavioural factors, like inactivity or avoidance of defecation
- Electrolyte disturbances, like hypercalcaemia
- Certain drugs, particularly opiates, calcium channel blockers and some antipsychotics
- Neurological disorders, like spinal cord lesions, Parkinson’s disease, and diabetic neuropathy
- Endocrine disorders, such as hypothyroidism
- Colon diseases, like strictures or malignancies
- Anal diseases, like anal fissures or proctitis
Symptoms and signs of constipation include:
- Infrequent bowel movements (less than 3 per week)
- Difficulty passing bowel motions
- Tenesmus
- Excessive straining
- Abdominal distension
- Abdominal mass felt at the left or right lower quadrants (stool)
- Rectal bleeding
- Anal fissures
- Haemorrhoids
- Presence of hard stool or impaction on digital rectal examination
Alarm constipation features which may indicate gastrointestinal malignancy include:
Weight loss
Loss of appetite
Abdominal mass
Dark stool
The differential diagnosis for constipation includes:
- Irritable Bowel Syndrome (IBS) - characterized by abdominal pain, bloating, and alternating constipation and diarrhea
- Inflammatory Bowel Disease (IBD) - presents with abdominal pain, weight loss, and bloody diarrhea
- Anal fissures - characterized by severe anal pain during and after bowel movements, and bright red blood in the stool
- Hemorrhoids - symptoms include painless rectal bleeding, anal itching, and discomfort
- Colorectal cancer - symptoms include changes in bowel habits, rectal bleeding, and unintentional weight loss
Ix for Constipation
- Full blood count
- Electrolytes
- Thyroid function tests
- Blood glucose
- Abdominal x-ray if suspicious of a secondary cause of constipation
- Barium enema if suspicious of impaction or rectal mass
- Colonoscopy if suspicious of lower GI malignancy
Management for constipation?
- Exclusion of underlying causes including colorectal cancer
- Lifestyle modifications such as dietary improvements and increased exercise
- Enemas (e.g., sodium citrate) if impaction is present
- Suppositories such as glycerol
- Bulk laxatives such as ispaghula husk or methylcellulose
- Stool softeners like docusate sodium
- Osmotic laxatives like lactulose or macrogol
- Stimulant laxatives like senna or bisacodyl
If laxatives fail to resolve symptoms, referral to a specialist centre for evaluation of gut motility may be necessary.
What is delirium?
Delirium is an acute and fluctuating disturbance in attention and cognition, often accompanied by a change in consciousness. It is typically reversible and frequently seen in the elderly, particularly in inpatient settings.
What are the three subtypes of delirium?
- Hyperactive Delirium: Marked by increased psychomotor activity, restlessness, agitation, and hallucinations.
- Hypoactive Delirium: Characterised by lethargy, reduced responsiveness, and withdrawal.
- Mixed Delirium: Combines features of both hyperactive and hypoactive delirium.
The causes of delirium can be multifactorial and are remembered using the mnemonic DELIRIUMS:
- D: Drugs and Alcohol (Anti-cholinergics, opiates, anti-convulsants, recreational)
- E: Eyes, ears and emotional disturbances
- L: Low Output state (Myocardial Infarction, Acute Respiratory Distress Syndrome, Pulmonary Embolism, Congestive Heart Failure, Chronic Obstructive Pulmonary Disease)
- I: Infection
- R: Retention (of urine or stool)
- I: Ictal (related to seizure activity)
- U: Under-hydration/Under-nutrition
- M: Metabolic disorders (Electrolyte imbalance, thyroid disorders, Wernicke’s encephalopathy)
- (S): Subdural hematoma, Sleep deprivation
Delirium can present in a number of different ways, including:
- Disorientation
- Hallucinations - visual or auditory
- Inattention
- Memory problems
- Change in mood or personality. Sundowning is agitation and confusion worsening in the late afternoon or evening.
- Disturbed sleep
Patients may be hypoactive (sedated) or hyperactive (very agitated), and these presentations can fluctuate over time. Hyperactive delirium is easily seen due to the presentation, while hypoactive delirium can be easily missed as patients may appear more withdrawn.
Differentials for delirium?
- Dementia: Characterized by gradual onset, stable consciousness level, and progressive decline in cognitive function.
- Psychosis: May present with hallucinations and delusions, but usually with preserved orientation and memory.
- Depression: May exhibit poor concentration and slow cognition, but typically with a stable consciousness level and often accompanied by pervasive feelings of sadness or guilt.
- Stroke: Abrupt onset with focal neurologic signs and specific deficits in speech, motor, or sensory function.
What are common tools used for delirium?
4AT and CAM are commonly used tools for delirium assessment.
Ix for delirium?
- Bedside - bladder scan, review medications, ECG (arrhythmias, ischaemic changes that could cause hypoperfusion) urine MC&S - you should not perform urine dipstick if >65 as they are less sensitive in this age group.
- Bloods: FBC, urea and electrolyes, liver function tests, thyroid function tests, and blood cultures.
- Imaging: chest X-ray, or ultrasound of the abdomen. Neuroimaging with CT or MRI head is reserved for those without a clear identifiable cause
Management for delirium?
Management of delirium primarily focuses on treating the underlying cause. Non-pharmacological strategies should be the first line, which include:
- Providing an environment with good lighting
- Maintaining a regular sleep-wake cycle
- Regular orientation and reassurance
- Ensuring the patient’s glasses and hearing aids are used if needed
For patients who are extremely agitated and potentially a danger to themselves or others, pharmacological interventions such as small doses of haloperidol or lorazepam. Olanzapine may also be considered however, these should be used with caution, especially in the elderly, due to the risk of side effects.
What is another name for postural hypertension?
orthostatic hypotension
What is postural hypotension
Orthostatic hypotension is characterised by a decrease in systolic blood pressure of 20 mmHg or a decrease in diastolic blood pressure of 10 mmHg within three minutes of standing when compared with blood pressure from the sitting or supine position.
The causes of orthostatic hypotension include:
- Medications, particularly vasodilators, diuretics, negative inotropes, antidepressants, and opiates
- Chronic hypertension due to the loss of baroreceptor reflexes
- Dehydration
- Sepsis
- Autonomic nervous system dysfunction, such as Parkinson’s disease
- Adrenal insufficiency
Patients with orthostatic hypotension may present with:
- Dizziness
- Syncope
- Falls
- Fractures
- More frequent occurrences after meals or exercise
- More frequent occurrences in warm environments
- Sometimes precipitated by coughing or defecating
- Symptoms can occur several minutes after standing up
Differential Diagnosis of postural hypotension?
When diagnosing orthostatic hypotension, it is essential to rule out other conditions that may cause similar symptoms. These can include:
- Vertigo: Characterized by a spinning sensation and loss of balance
- Hypoglycemia: Presents with signs such as shakiness, hunger, confusion, and sweating
- Cardiac arrhythmias: Symptoms may include palpitations, chest pain, and shortness of breath
Ix for postural hypotension?
The diagnosis of orthostatic hypotension is confirmed by a significant fall of 20mmHg or more in systolic blood pressure, or a fall of 10mmHg or more in diastolic pressure upon standing.
Management of orthostatic hypotension depends on the underlying cause and may include:
- Ensuring adequate hydration
- Evaluating polypharmacy to identify medication-related causes
- Implementing strategies to reduce adverse outcomes from falls (e.g., fall alarm, soft flooring)
- Advising behavioral changes such as rising from sitting slowly, maintaining adequate hydration
- Recommending the use of compression stockings
- Employing pharmacotherapy, including fludrocortisone and midodrine, although the evidence base for fludrocortisone is weak
Risk factors for falling
- Lower limb muscle weakness
- Previous falls
- Vision problems
- Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson’s disease etc)
- Polypharmacy (4+ medications)
- Incontinence
- > 65
- Have a fear of falling
- Depression
- Postural hypotension
- Arthritis in lower limbs
- Psychoactive drugs
- Cognitive impairment
What is the risk assessmnet for falls?
Ideally, all patients should be screened for falls risk in order to establish the level of support they need, particularly when they are in a hospital or a home.
It is important to establish the following from the history:
* Where was the patient when they fell?
* When did they fall?
* Did anyone else see the patient fall? (collateral history)
* What happened? Were there any associated features before/during/after
* Why do they think they fell?
* Have they fallen before?
* Systems review
* Past medical history (especially issues related to balance/sight/gait)
* Social history
What are some medications that cause postural hypotension
Nitrates
Diuretics
Anticholinergic medication
Antidepressants
Beta-Blockers
L-Dopa
ACE inhibitors
Medications associated with falls due to other mechanisms
Benzo
Antipsychotics
Opiates
Anticonvulsants
Codeine
Digoxin
Other sedative agents
Ix for Falls
- A-E Approach
- Bedside: Basic observations, blood pressure, blood glucose, urine dip and ECG
- Bloods: Full Blood Count, Urea and Electrolytes, Liver function tests and bone profile
- Imaging: X-ray of chest/injured limbs, CT head and cardiac echo
Fall
Offer a multidisciplinary assessment by a qualified clinician to all patients over 65 with:
- > 2 falls in the last 12 months
- A fall that requires medical treatment
- Poor performance or failure to complete the ‘Turn 180° test’ or the ‘Timed up and Go test’
What is alzheimer’s disease?
Alzheimer’s disease is a chronic, neurodegenerative disorder characterized by the progressive accumulation of abnormal protein deposits, primarily amyloid plaques and tau tangles, in the brain. This leads to the deterioration of cognitive function, memory loss, and various behavioural and psychological symptoms.
Patho of Alzheimer’s Disease
Alzheimer’s disease is a complex and progressive neurodegenerative disorder characterized by distinct pathophysiological hallmarks. These hallmarks are responsible for the gradual decline in cognitive function and the characteristic clinical features observed in affected individuals.
Amyloid Plaques: The accumulation of beta-amyloid protein fragments outside nerve cells in the form of plaques is a hallmark feature. These abnormal protein deposits are believed to disrupt neuronal communication, trigger inflammation, and ultimately lead to cell death.
Tau Tangles: Inside nerve cells, abnormal tau protein accumulates, forming neurofibrillary tangles. These tangles interfere with the transport of essential nutrients within neurons, contributing to their dysfunction and eventual demise.
Neuronal Loss and Brain Atrophy: As the disease progresses, significant neuronal loss occurs, particularly in brain regions responsible for memory and cognitive function, such as the hippocampus and the cerebral cortex. This loss is associated with brain atrophy, visible on imaging studies.
Neurotransmitter Imbalance: Alzheimer’s disease disrupts the balance of neurotransmitters, particularly acetylcholine, which plays a crucial role in memory and learning. Reduced acetylcholine levels further contribute to cognitive decline.
Inflammatory Response: Chronic neuroinflammation, characterized by the activation of microglia and astrocytes, is a prominent feature in Alzheimer’s disease. Inflammation may exacerbate neuronal damage and contribute to the progression of the disease.
Several factors influence an individual’s risk of developing Alzheimer’s disease. These include:
Age: Advanced age is the most significant risk factor, with the incidence of Alzheimer’s disease increasing exponentially after the age of 65.
Genetic Predisposition: Mutations in specific genes, such as the apolipoprotein E (APOE) gene, increase the risk of developing Alzheimer’s disease. Additionally, individuals with Down’s syndrome are at a higher risk due to a triplication of chromosome 21, which carries the amyloid precursor protein (APP) gene.
Family History: Having a first-degree relative with Alzheimer’s disease can increase one’s susceptibility.
Cardiovascular Risk Factors: Conditions like hypertension, diabetes, obesity, and hypercholesterolemia have been associated with an elevated risk of Alzheimer’s disease.
Lifestyle Factors: Physical inactivity, smoking, and a diet high in saturated fats may contribute to increased risk.
Traumatic Brain Injury: A history of head injuries, particularly repeated concussions, has been linked to a higher risk of developing Alzheimer’s disease.
Low Educational Attainment: Lower levels of education may be associated with an increased risk.
What are the clinical features of Alzheimer’s Disease
- Memory Impairment: Early in the disease, individuals often experience difficulties in recalling recent events and conversations.
- Language Impairment: This may manifest as difficulty finding words, struggling to express oneself, and, in later stages, aphasia.
- Executive Dysfunction: Impaired ability to plan, organize, and carry out tasks, leading to difficulties in activities of daily living.
- Behavioural Changes: Individuals may exhibit agitation, aggression, or apathy, sometimes accompanied by mood swings and irritability.
- Psychological Symptoms: Hallucinations, delusions, and paranoia can occur, particularly in later stages of the disease.
- Disorientation: Affected individuals may become disoriented in familiar surroundings, unable to recognize places or people.
- Loss of Motor Skills: In advanced stages, motor skills decline, leading to difficulties with mobility and self-care.
Differential Diagnosis of Alzheimer’s disease
- Vascular Dementia: Cognitive impairment in vascular dementia often presents suddenly and is associated with a history of cerebrovascular events.
- Lewy Body Dementia: Visual hallucinations and fluctuating cognitive impairment are more common in Lewy body dementia.
- Frontotemporal Dementia: This condition typically presents with profound behavioural and personality changes, often affecting social conduct.
- Mild Cognitive Impairment (MCI): MCI is a transitional state between normal cognitive aging and dementia. Unlike Alzheimer’s, MCI may not significantly impact daily functioning.
- **Normal Age-Related Cognitive Decline: **Age-related cognitive changes are common but do not interfere significantly with daily activities.
Ix Alzheimer’s disease
History
Cognitive assessment
Examination
Blood Tests: BC, U&E, LFTs, CRP/ESR, Ca2+, TFTs, B12, folate, syphilis, HIV
CT/MRI/PET scan
CSF analysis
Management of Alzheimer’s disease?
Non-Pharmacological Approaches:
Support for Caregivers:
Patient-Centered Care:
Pharmacological Intervention
What are the non pharmaclogical methods for Alzheimer’s disease?
Psychological interventions, cognitive stimulation therapy, and occupational therapy can help manage behavioural and psychological symptoms.
Pharacologial interventions for Alzheimer’s disease
Medications, such as cholinesterase inhibitors (e.g. donepezil) and N-methyl-D-aspartate (NMDA) receptor antagonists (e.g. memantine), may be prescribed to manage cognitive symptoms.
- Pharmacological treatments may have modest benefits, and include the cholinesterase inhibitors rivastigamine, galantamine, and donpezil in mild-moderate dementia, and the NMDA inhibitor memantine in severe dementia (as classified using the MMSE score: severe: <10; moderate: 10-20; mild: 21-26/30.
- If there is evidence of behavioral and psychological symptoms of dementia (BPSD), low-dose risperidone may be started
What is Dementia with Lewy Body
Dementia with Lewy bodies (DLB) is a type of progressive dementia caused by deposits of an abnormal protein, alpha-synuclein, forming cytoplasmic inclusions known as Lewy bodies within brain cells. These aggregates disrupt normal cell functioning and eventually lead to neuronal death
Cause of Dementia with Lewy body
The primary pathological feature of DLB is the presence of Lewy bodies in the brain’s substantia nigra, paralimbic, and neocortical areas.
What is clinicl features of Dementia with Lewy Body
The clinical features of DLB include:
- Fluctuating cognition: Changes in attention and alertness may occur.
- Parkinsonism: Rigidity, bradykinesia, and postural instability are common.
- Visual hallucinations: Patients often experience complex and recurrent visual hallucinations.
- High sensitivity to neuroleptics: These drugs can induce or worsen parkinsonism.
A general rule of thumb that can help with distinguishing LBD form Parkinson’s disease (PD) is if cognitive impairment and parkinsonism develop <1 year of each other, it is likely LBD. If diagnosed with PD and dementia develops >1 year later this is Parkinson’s disease.
What ix would you do for suspected dementia with lewy body
Diagnosis is primarily clinical, involving a careful medical history and physical examination. However, some additional investigations may be useful, such as:
- Dopamine transporter (DaT) scan: This can help distinguish DLB from other types of dementia.
- Neuropsychological testing: To assess cognitive functioning and fluctuations.
- Electroencephalography (EEG): Although not diagnostic, a slowing background rhythm may be seen in DLB.
What is the management of Dementia with Lewy Body?
Non-pharmacological interventions: These include cognitive stimulation, physical therapy, and occupational therapy.
Supportive care: As DLB is a progressive disorder, palliative and end-of-life care considerations are essential.
Medications: Cholinesterase inhibitors can help manage cognitive symptoms. However, caution is required with antipsychotic medications due to neuroleptic sensitivity.
Definition of Parkinsons Disease?
Idiopathic Parkinson’s disease is the prototypical Parkinsonian syndrome. It is a sporadic disease, predominantly affecting adults over the age of 65 years. The disease is characterised by its presentation of asymmetric tremor, bradykinesia, and rigidity.
The core features of Parkinson’s disease include the triad of:
- Bradykinesia
- Asymmetric 3-5Hz “pill-rolling” tremor
- Lead pipe rigidity
Non-motor features of Parkinson’s disease are also common and include:
- Autonomic dysfunction, leading to constipation, symptomatic orthostasis (postural hypotension), and erectile dysfunction
- Olfactory loss
- Sleep disorders such as REM behavioural disorder
- Psychiatric features including depression, anxiety, and hallucinations
How do you decide what drug to start on with PD patients ?
Once a secure diagnosis of idiopathic Parkinson’s disease has been made, the choice of long term treatment is dependent primarily on the effect that the motor symptoms are having on the patient’s quality of life.
New data from the PD MED study has found that all patients with significant functional impairment should be started on levodopa.
For patients with clinical features of Parkinson’s disease, but in whom there is no functional impairment, the guidance is less clear and patients should be considered for either levodopa, dopamine agonists and monoamine oxidase inhibitors as directed by a specialist.
What are some peripheral and central side effects of levodopa
Peripheral side effects include:
- Postural hypotension
- Nausea & vomiting
Central side effects include:
- Hallucinations
- Confusion
- Dyskinesia
- Psychosis
examples of dopamne agonists used in PD
Ropinirole, rotigotine, Apomorphine
When is dopamine agonists used in patients with PD
Are often used in early disease in those without functional impairment, or late in disease when dyskinesias and motor fluctuations secondary to levodopa is a problem.
Examples of MAO-B Inhibitors used in PD
Selegiline, Rasagiline.
Complication of MAO-B Inhibitors
Can cause serotonin syndrome
Examples of COMT Inhibitors
Entacapone and tolcapone.
When is amantadine given in patients with PD
Can be used in those suffering from dyskinesia.
What is vascular dementia?
Vascular dementia is an umbrella term denoting a collection of cognitive impairment syndromes caused by cerebrovascular disease. The encompassed syndromes include stroke-related vascular disease, subcortical vascular dementia, and mixed dementia—a combination of Alzheimer’s disease and vascular dementia.
Signs and symptoms of vascular dementia
The hallmark of vascular dementia is a progressive, stepwise deterioration in cognition. This typically occurs over a span of several months to years. Patients may present with a history of strokes, which may be accompanied by stepwise cognitive decline or sudden changes in cognitive function, as well as stroke-like symptoms:
- Visual disturbance
- Sensory or motor symptoms
- Difficulty with attention and concentration
- Seizures
- Memory disturbance
- Gait/speech/emotional disturbance
To compare with Alzheimer’s dementia, there is less impairment in episodic memory and more in visual skills, semantic memory and executive functioning.
Ix for vascular dementia?
- Comprehensive history and examination.
- Formal cognition screening, such as MMSE (Mini-Mental State Examination) or MoCA (Montreal Cognitive Assessment).
- Medication review to exclude medication-induced cognitive impairment.
- Exclusion of reversible organic causes such as vitamin B12 or folic acid deficiency, hypothyroidism, or normal pressure hydrocephalus.
- Neuroimaging, preferably an MRI Head, to identify vascular changes, infarcts, or white matter hyperintensities indicative of cerebrovascular disease. The hallmark of vascular dementia is extensive white matter change and infarcts evident on MRI imaging.
The management of vascular dementia involves:
- Detection of and addressing cardiovascular risk factors such as hypertension, diabetes, hyperlipidemia, and smoking to slow disease progression.
- Cognitive stimulation programmes, music and art therapy, etc. to help with cognitive impairment.
- Symptomatic treatment, including cognitive enhancers such as cholinesterase inhibitors or memantine - if there is evidence of co-existent AD, Parkinson’s dementia, or dementia with Lewy bodies. Management of neuropsychiatric symptoms.
- Advanced care planning to prepare for progressive cognitive and physical decline.
