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Phase 3a Medicine > Geriatrics > Flashcards

Geriatrics Flashcards

1
Q

Benign paroxysmal positional vertigo

A

Recurrent episodes of vertigo triggered by head movement

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2
Q

What causes benign paroxysmal positional vertigo?

A

Crystals of calcium carbonate (otoconia) become displaced into the semicircular canals of the inner ear, disrupting the normal flow of endolymph through the canals, confusing the vestibular system

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3
Q

Risk factors for benign paroxysmal positional vertigo

A
  • Viral infection
  • Head trauma
  • Ageing
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4
Q

Presentation of benign paroxysmal positional vertigo

A

Sudden onset of dizziness and vertigo triggered by changes in head position, commonly turning over in bed or gazing upwards
Symptoms settle after 20-60 seconds

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5
Q

How is benign paroxysmal positional vertigo diagnosed?

A

Dix-Hallpike manoeuvre (move their head and trigger vertigo)

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6
Q

What investigation is used to exclude differential diagnoses of benign paroxysmal positional vertigo?

A

MRI/CT head (brainstem stroke, vestibular schwannoma)

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7
Q

Management of benign paroxysmal positional vertigo

A
  • Epley manoeuvre
  • Brandt-Daroff exercises
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8
Q

What are some medical causes of falls?

A
  • Cognitive impairment
  • Arthritis
  • Muscle weakness
  • Disorders of balance and gait (Parkinson’s, ataxia, stroke)
  • Visual impairment
  • Postural hypotension and syncope
  • Vestibular disorders
  • Polypharmacy
  • Alcohol excess
  • Peripheral neuropathy
  • Effects of ageing on strength/postural stability/reaction time
  • Use of walking aid
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9
Q

What external environmental causes are there for falls?

A
  • Rugs
  • Stairs
  • Footwear
  • Poor lighting
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10
Q

What drugs can increase your risk of falls?

A
  • Benzodiazepine
  • Antipsychotics
  • Opiates
  • Anticonvulsants
  • Codeine
  • Digoxin
  • Antihypertensives
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11
Q

What are complications of a fall without a long lie?

A
  • Pain
  • Loss of confidence
  • Loss of independence
  • Hospital admission
  • Serious injury, e.g. hip fracture, head injury
  • Death
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12
Q

Management of falls

A
  • Treat medical risk factors where possible (medication review)
  • Modify environmental hazards in home
  • Patient education and training
  • Mitigation of complications: treat osteoporosis, use hip protectors, walking frames, personal alarms
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13
Q

What should be assessed in a falls patient?

A
  • Injuries/deformities
  • Osteoporosis risk
  • Cognition and dementia screen
  • Neurological examination, including gait, muscle strength, balance and vision
  • Cardiovascular examination
  • Turn 180 test
  • Timed up and go test
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14
Q

Hypothermia

A

Core temperature < 32
Whole-body cooling

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15
Q

What happens to the pulse, BP, cardiac output, cerebral blood flow and respiration in hypothermia?

A

Pulse rate falls
Systemic BP falls
Cardiac output falls
Cerebral blood flow falls
Respiration becomes shallow and slow

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16
Q

What happens to muscles and reflexes in hypothermia?

A

Muscle stiffness
Tendon reflexes become sluggish and then absent
As coma ensues, pupillary and other brainstem reflexes are lost

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17
Q

What ECG changes are seen in hypothermia?

A

Bradycardia with J waves (pathognomic), prolongation of PR and QT intervals and QRS complex

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18
Q

Which way does the oxygen dissociation curve move in hypothermia?

A

Left

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19
Q

Medical risk factors for hypothermia

A
  • Impaired thermoregulation - pneumonia, MI, heart failure
  • Reduced metabolism - immobility, hypothyroidism, DM
  • Autonomic neuropathy - DM, Parkinson’s
  • Excess heat loss - psoriasis, widespread dermatological disease
  • Decreased cold awareness - dementia, confusion
  • Increased exposure to cold - falls
  • Depressant drugs - hypnotics, alcohol, tranquilisers, antidepressants, diuretics
  • Elderly (reduced ability to sense cold, little insulating fat)
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20
Q

Environmental risk factors for hypothermia

A
  • Poor heating - poverty, poor housing
  • Inadequate clothing
  • Poor nutrition
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21
Q

Clinical manifestation of mild and severe hypothermia

A

Mild
* Shivering
* Intense discomfort

Severe
* Impaired judgement, including lack of awareness of cold
* Drowsiness and coma
* Death (from ventricular fibrillation)

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22
Q

What investigations should be done in someone with hypothermia?

A
  • U&E
  • Glucose
  • Amylase
  • TFT
  • FBC
  • Blood cultures
  • ECG
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23
Q

Management of hypothermia

A
  • Keep them horizontal or slightly head down
  • Rewarm gradually: remove wet clothing, direct heat from electric blanket, warm humidified oxygen, warm IV infusion or warm fluids orally
  • Treat underlying conditions, e.g. sepsis, sedative drugs, hypothyroidism
  • Correct metabolic abnormalities
  • Diagnose and treat arrhythmias
  • Consider antibiotics to prevent pneumonia
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24
Q

Complications of hypothermia

A
  • Arrhythmias
  • Pneumonia
  • Pancreatitis
  • AKI
  • DIC
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25
Q

Constipation

A
  • Infrequent passage of stool (< 3 spontaneous bowel motions per week)
  • Difficulty passing stool
  • Sensation of incomplete emptying
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26
Q

Causes of constipation

A
  • Poor diet with lack of fibre
  • Lack of exerise
  • Dehydration
  • Colorectal carcinoma
  • Strictures, e.g. Crohn’s
  • Hypercalcaemia
  • Hypothyroidism
  • Opiates, iron and calcium channel blockers
  • Spinal injury
  • Diabetic neuropathy
  • Parkinson’s disease
  • MS
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27
Q

What score on the Bristol stool chart is constipation?

A

1-2

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28
Q

What criteria assesses for constipation?

A

Rome IV criteria

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29
Q

What is the Rome IV criteria?

A

To diagnose chronic idiopathic constipation, 2 or more of the following for the last 3 months with symptoms onset at least 6 months prior to diagnosis:
* Straining during more than 25% of defecations
* Lumpy or hard stools more than 25% of defecations
* Sensation of incomplete evacuation more than 25% of defecations
* Sensation of anorectal obstruction/blockage more than 25% of defecations
* Manual manoeuvres to facilitate more than 25% of defecations, e.g. digital evacuation
* Fewer than 3 spontaneous bowel movements per week
* Loose stools are rarely present without the use of laxatives
* Insufficient criteria for IBS

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30
Q

What investigations should be used to rule out secondary causes of constipation?

A
  • Faecal calprotectin (IBD, colorectal cancer)
  • Quantitative faecal immunochemical test (IBD, colorectal cancer)
  • TFT (hypothyroidism)
  • HbA1c (DM)
  • CT abdomen and pelvis (diverticular stricture, malignancy)
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31
Q

When does constipation need urgent assessment?

A

New change in bowel habit or other concerning ‘red flag’ symptoms:
* Weight loss
* Rectal bleeding
* Family history of colorectal cancer
* Abdominal pain
* Iron deficiency anaemia

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32
Q

Lifestyle modifications for constipation

A
  • Healthy diet, high in whole grains, fruit and vegetable
  • Good fluid intake
  • Regular exercise
  • Regular, unhurried toilet routine
  • Respond immediately to sensation to defecate
  • Ensure appropriate access to toilets and privacy
  • Provide supported seating if unsteady on toilet
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33
Q

Medications for constipation

A
  • Bulk-forming laxatives: dietary fibre, methylcellulose, mucilaginous gums, mucilaginous seeds and seed coats (ispaghula husk)
  • Stimulant laxatives: phenolphthalein, bisacodyl, anthraquinones (senna, dantron), docusate sodium, methylnaltrexone (for opioid-induced constipation), lubiprostone, prucalopride, linaclotide, sodium picosulfate
  • Osmotic laxatives: magnesium sulphate, lactulose, macrogols
  • Suppositories: bisacodyl, glycerol
  • Enemas: arachis oil, sodium docusate, hypertonic phosphate, sodium citrate
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34
Q

Other, more rogue, management options for constipation

A
  • Biofeedback for defecatory disorders
  • Prokinetics (Prucalopride), secretagogues (Linaclotide, Lubiprostone)
  • Interventional treatments
  • Surgery
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35
Q

Pressure ulcer

A

Skin ischaemia from sustained pressure over a bony prominence, most commonly the heel and sacrum

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36
Q

Risk factors for pressure ulcers

A
  • Prolonged immobility - paraplegia, operation, severe physical disease
  • Decreased sensation - diabetes mellitus, neurological disease, coma
  • Vascular disease - diabetes mellitus, atherosclerosis, vasculitis
  • Poor nutrition - anaemia, hypoalbuminaemia, vitamin C or zinc deficiency
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37
Q

What are the grades of pressure ulcer?

A
  • 1: non-blanching erythema of intact skin
  • 2: partial thickness loss involving the epidermis, dermis or both
  • 3: full thickness skin loss involving damage/necrosis of subcutaneous tissue
  • 4: extensive loss, destruction/necrosis of muscle, bone or support structures
  • Unstageable: depth unknown, base of ulcer covered by debris
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38
Q

How do you assess risk of pressure ulcer?

A

Waterlow pressure ulcer risk assessment

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39
Q

Prevention of pressure ulcers

A
  • Detect at risk patients (tissue viability nurses)
  • Barrier creams
  • Pressure redistribution - bed rest with pillows and fleeces to keep pressure off bony areas and prevent friction, air-filled cushions for those in wheelchairs and special pressure-relieving mattresses
  • Repositioning - regular turning
  • Regular skin assessment
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40
Q

Treatment of pressure ulcers

A
  • As for prevention
  • Adequate nutrition
  • Non-irritant occlusive moist dressings, e.g. hydrocolloid dressings and hydrogels
  • Adequate analgesia (may need opiates)
  • Plastic surgery (debridement and grafting)
  • Antibiotics if infection
  • Treatment of underlying condition
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41
Q

Polypharmacy

A

Taking 5 or more medications

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42
Q

STOPP-START

A

Polypharmacy toolkit
* STOPP tool asses which drugs can be potentially discontinued in elderly patients
* START tool suggests medications that may provide additional benefits

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43
Q

Malnutrition

A

State in which a deficiency of energy, protein and/or other nutrients causes measurable adverse effects on the body’s form, composition, function and clinical outcome

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44
Q

Cause of malnutrition

A
  1. Reduced nutritional intake
  2. Increased nutritional requirements
  3. Inability to utilise nutrients ingested
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45
Q

What happens physiologically to the body in the first 24 hours of starvation and as it continues? What happens when the insulin levels fall?

A

Body relies on energy from the breakdown of hepatic glycogen to glucose and gluconeogenesis mainly from pyruvate, lactate, glyerol and amino acids (muscle loss)

As starvation continues: insulin levels fall which results in lipolysis and subsequent gluconeogenesis (glycerol) and use of non-esterified fatty acids directly as fuel or oxidised to form ketone bodies

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46
Q

What adaptions does the body make during prolonged starvation?

A
  • Decrease in metabolic rate and total body energy expenditure
  • CNS starts using ketone bodies instead of glucose
  • Gluconeogenesis in liver decreases
  • Protein breakdown in muscle decreases due to increase in ketone bodies
  • Most energy comes from adipose tissue with some gluconeogenesis from amino acids
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47
Q

What medical reasons are there for reduced nutrient intake?

A
  • NBM
  • Dysphagia
  • Cognitive impairment (dementia)
  • Muscle weakness and incoordination
  • Sensory deficits
  • Severe arthritis
  • Very ill
  • Malignancy
  • Nausea
  • Painful mouth
  • Alcohol and drugs
  • Sedation and coma
  • Anorexia nervosa
  • Depression
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48
Q

What social reasons are there for reduced nutrient intake?

A
  • Poverty
  • Social isolation
  • Nobody to assist with eating
  • Unappetising food
  • Lost dentures
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49
Q

What are causes of increased nutrient requirements?

A
  • Sepsis
  • Burns
  • Trauma
  • Surgery
  • Very ill
  • Severe chronic inflammatory diseases
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50
Q

What are causes of inability to utilise nutrients ingested?

A
  • GI disease, particularly involving small bowel
  • Diarrhoea
  • Vomiting
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51
Q

What are the 3 aspects of the MUST score?

A
  1. BMI
  2. Weight loss
  3. Acute disease affect score (pt acutely ill and there has been or is likely to be no nutritional intake for > 5 days)
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52
Q

How is malnutrition screened?

A

Malnutrition Universal Screening Tool (MUST)

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53
Q

What BMI scores points on MUST score?

A

<18.5 = 2
18.5-20 = 1

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54
Q

What unplanned weight loss in past 3-6 months scores points on MUST?

A

> 10% = 2
5-10% = 1

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55
Q

How many points does acute disease effect score on MUST?

A

2

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56
Q

What does a MUST score of 0 indicate?

A

Low risk of malnutrition
Routine clinical care
Repeat screening (weekly in hospital, monthly in care homes and annually in community)

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57
Q

What does a MUST score of 1 indicate?

A

Medium risk
Observe
Document dietary intake for 3 days if in hospital or care home
* If adequate: repeat screening as for low risk
* If inadequate: follow local policy, set goals, improve and increase overall nutritional intake, monitor and review care plan regularly

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58
Q

What does a MUST score of 2 or more indicate?

A

High risk
Treat
* Refer to dietitian, nutritional support team or implement local policy
* Set goals, improve and increase overall nutritional intake
* Monitor and review care plan weekly in hospital, monthly in care home/community

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59
Q

What are the steps of managing malnutrition?

A
  1. Food - snacks, nourishing drinks, food fortification
  2. Oral nutritional supplements
  3. Enteral nutrition - NG tube (stomach), nasojejunal tube (jejunum), PEG (stomach) or post-pyloric/surgical PEJ
  4. Parenteral feeding (IV)
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60
Q

Indications for a PEG tube

A
  • Dysphagia (stroke, head and neck surgery, neurological conditions)
  • Cystic fibrosis
  • Inadequate oral nutritional intake likely to be long term
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61
Q

Indications for post-pyeloric/surgical percutaneous endoscopic jejunostomy

A
  • Delayed gastric emptying
  • Upper GI/pancreatic surgery
  • High risk of aspiration
  • Severe acute pancreatitis
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61
Q

When is parenteral nutrition needed?

A

Gut is inaccessible or unable to absorb sufficient nutrients
* Inadequate absorption (short bowel syndrome)
* GI fistula
* Bowel obstruction
* Prolonged bowel rest
* Severe malnutrition
* Significant weight loss
* Hypoproteinaemia when enteral therapy is not possible

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62
Q

How long can an NG tube, NJ tube and PEG tube be kept in?

A

NG tube: 30 days
NJ tube: 60 days
PEG: long term

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63
Q

Complications of malnutrition

A
  • Infection
  • Reduced muscle strength - falls, chest infections, reduced mobility and inactivity
  • Poor wound healing
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64
Q

Refeeding syndrome

A

Group of clinical symptoms and signs that can occur in the malnourished/starved patient when reintroducing nutrition, due to a shift in the use of energy stores from fat metabolism to carbohydrate metabolism, which initiates insulin release and cellular uptake of potassium, phosphate and magnesium, and shifts in fluids and electrolytes

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65
Q

Complications of refeeding syndrome

A
  • Fluid retention
  • Cardiac arrhythmias and heart failure
  • Respiratory insufficiency
  • Convulsions
  • Coma and death
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66
Q

Management of refeeding syndrome

A
  • Slow reintroduction of nutrition
  • Daily monitoring of refeeding bloods (U&Es, phosphate, magnesium)
  • IV pabrinex or thiamine + vitamin B, prior to feeding and for first 10 days
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67
Q

Risk factors for squamous cell carcinoma

A
  • Chronic UV damage
  • Arsenic ingestion in early life
  • Immunosuppression, e.g. renal transplant patients (HPV)
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68
Q

Presentation of squamous cell carcinoma

A

Nodule
* Keratotic (hard)
* Raised, ill-defined edges
* Ulcerated
* Sun-exposed sites
* Can grow rapidly

May be found on solar keratoses, Bowen’s disease, areas of chronic inflammation, on the lips of smokers or in long-standing ulcers

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69
Q

What must be examined in a patient with squamous cell carcinoma?

A

Regional lymph nodes

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70
Q

Differential diagnosis of squamous cell carcinoma

A

Keratoacanthoma (fast-growing, benign, self-limiting papule plugged with keratin)

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71
Q

Management of squamous cell carcinoma

A
  • Surgical excision with a minimum margin of 5mm
  • Radiotherapy to treat recurrence/affected nodes
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72
Q

Complications of squamous cell carcinoma

A

Local destruction
(Metastasis rare)

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73
Q

Which is worse - basal cell carcinoma or squamous cell carcinoma?

A

Squamous cell carcinoma
Higher metastatic potential

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74
Q

What is the commonest cause of transient loss of consciousness?

A

Syncope

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75
Q

Most common causes of syncope in older adults

A
  • Vasovagal (faints)
  • Carotid sinus hypersensitivity
  • Cardiac - arrhythmias, valvular disease, conduction abnormalities
  • Orthostatic hypotension
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76
Q

Why are older people particularly at risk of depression?

A
  • Physical co-morbidities, e.g. stroke, Parkinson’s, dementia, infection (neurosyphilis), hypothyroidism, vitamin B12 and folate deficiency, hypercalcaemia, potassium/sodium imbalance, anaemia
  • Chronic health problems, e.g. DM, COPD, CCF, chronic pain syndromes
  • Polypharmacy - antihypertensives (beta blockers, nifedipine, clonidine), opioids, antipsychotics, benzodiazepines, levodopa, digoxin, corticosteroids
  • Negative thoughts about the future (part of Beck’s triad)
  • More likely to lose loved ones
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77
Q

Why is depression under-recognised and under-diagnosed in the elderly?

A
  • “Depression without sadness” - lethargy, apathy, physical complaints
  • Biological symptoms thouht of as a physical illness
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78
Q

What management of depression is more commonly used in the elderly?

A

ECT

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79
Q

Poor prognostic factors for depression

A
  • Elderly
  • Comorbidity
  • Lack of social supports
  • Insidious onset
  • Low self-confidence
80
Q

Which group of antidepressants is safest in the elderly?

81
Q

Delirium

A

Acute state of change in consciousness, often shown as confusion, difficulties with understanding and memory or personality changes

82
Q

PINCH MEEE

Causes of delirium

A
  • Pain
  • Infection - UTI, pneumonia
  • Nutrition - malnutrition and vitamin deficiencies (thiamine, vitamin B12 and folate)
  • Constipation and faecal impaction
  • Hypoxia - respiratory failure, MI, cardiac failure, PE
  • Medication - benzodiazepines, opioids, steroids, anticholinergics, tricyclic antidepressants
  • Environment
  • Endocrine - thyroid disorder, hyperparathyroidism, Cushing’s, Addison’s, DM
  • Electrolyte imbalance (hypercalcaemia, hyponatraemia) dehydration, CKD
  • Alcohol
  • Intracranial events - stroke, space-occupying lesion, head trauma, epilepsy
  • Sensory deprivation
  • Sleep deprivation
  • Post-operation
  • Urinary retention
83
Q

Presentation of delirium

A

Fluctuating, impaired consciousness with onset over hours to days, or a rapid deterioration in pre-existing cognitive function with associated behavioural changes
* Global disturbance of cognition - perceptual distortions, impaired abstract thinking and comprehension, memory impairment, disorientation, thought disorder, impaired language
* Psychomotor disturbance (hypoactive or hyperactive)
* Impairment of consciousness and attention
* Disturbance of sleep-wake cycle
* Emotional dysregulation

84
Q

What are the 3 types of delirium and how are they different?

A
  • Hypoactive (40%) - lethargy, slowness with everyday tasks, excessive sleeping, inattention
  • Hyperactive (25%) - agitation, aggression, wandering, hallucinations, delusions
  • Mixed (35%)
85
Q

3 cognitive assessments and score to diagnose delirium

A
  • Abbreviated mental test (AMT)
  • Short confusion assessment method (short-CAM)
  • 4 As test (4AT)
86
Q

How is delirium diagnosed?

A

Clinically
Cognitive assessment based on DSM-5 criteria:
* Disturbance in awareness and attention
* Acute onset, acute change from baseline and fluctuant
* Disturbance in cognition
* Not better explained by pre-existing, established or evolving neurocognitive disorder and absence of severely reduced GCS
* Evidence of organic cause

87
Q

Confusion screen bloods

A
  • FBC
  • U&E
  • LFT
  • Coagulation/INR
  • TFT
  • Calcium
  • B12 and folate
  • Glucose
  • Blood cultures
  • CRP/ESR
88
Q

Routine investigations for delirium

A
  • Confusion screen bloods
  • Urinalysis
  • ECG
89
Q

Delirium investigations to be considered based on history/examination

A
  • CT head
  • Chest x-ray
  • ABG
  • Lumbar puncture
  • EEG
  • Sputum culture
90
Q

Differences between delirium and dementia

A
  • Onset
  • Fluctuations
  • Duration
  • Cause
  • Conscious level and arousal
  • Attention
  • Hallucinations
  • Psychomotor activity
  • Sleep-wake cycle
  • Autonomic features
91
Q

U R SAFE

Management of delirium

A
  • Underlying cause - investigate and treat
  • Reassure and reorientate to time, place, day and date
  • Sleep - healthy sleep patterns (turn off lights at night, minimise noise)
  • Antipsychotics
  • Family and friends
  • Environment - quiet, well-lit side room; consistent care and staff; orientation aids
92
Q

Managing disturbed, violent or distressed behaviour in delirium patients

A
  • Address underlying cause of behaviour, e.g. thirst, need for toilet, pain
  • Use non-verbal and verbal de-escalation techniques, e.g. redirection, active listening
  • Involve relatives or carers
  • Sedation if a risk to themselves or others (oral/IM): low-dose haloperdol or olanzapine (antipsychotic) or lorazepam (benzodiazepine)
  • Refer to specialist elderly care psychiatrists or geriatricians
  • Consider involvement of local delirium and dementia team
93
Q

Legal aspects of caring for a patient with delirium

A
  • Mental capacity assessment (people with delirium usually lack capacity so need to act in their best interest)
  • If least restrictive option deprives them of their liberty (mittens, hospital bed rails, not allownig them to leave hospital): deprivation of liberty safeguarding (DoLS)
94
Q

Complications of delirium

A
  • Dementia
  • Institutionalisation
  • Death
  • Slower recovery and longer hospital stays
  • Anxiety and distress
  • Morbidity - pressure areas, dehydration, malnutrition, falls
95
Q

What is dementia?

A
  • An acquired state characterised by impairment of 2 or more cognitive domains
  • Persisting for more than 6 months
  • Severe enough to impact on ability to function
  • Not primarily attributable to another mental disorder
96
Q

Neurodegenerative causes of dementia

A
  • Alzheimer’s disease
  • Frontotemporal dementia (Pick’s disease)
  • Lewy body dementia
  • Parkinson’s disease
  • Huntington’s disease
  • MS
  • Corticobasal degeneration
  • MND
  • Wilson’s disease
97
Q

Cause of rapid onset dementia

A

Creutzfeldt-Jakob disease (CJD)

98
Q

What toxins can cause dementia?

A
  • Alcohol (Korsakoff dementia)
  • Heavy metal
  • Barbiturates
  • Benzodiazepines
99
Q

2nd most common cause of dementia

A

Vascular dementia

100
Q

Reversible causes of dementia

A
  • Normal pressure hydrocephalus
  • Space occupying lesion
  • Seizures
  • Vitamin deficiencies (B12, folate, thiamine)
  • Hypothyroidism
  • Cushing’s syndrome
  • Uraemia
  • Depression
  • Infection (HIV, HSV, encephalitis, PML)
101
Q

Risk factors for dementia

A
  • Advancing age
  • Family history
  • Genetics (presenilin, amyloid precursor protein)
  • Down’s syndrome (Alzheimer’s)
  • Low IQ
  • Cerebrovascular disease (vascular)
  • Vascular risk factors (vascular)
102
Q

Cognitive domains

A
  • Memory
  • Visuospatial
  • Language
  • Executive function
  • Social cognition/behavioural
  • Attention
103
Q

Examples of memory impairment

A
  • Repetitive in conversation
  • Struggles to follow plot on serialised TV shows
  • Forgets appointments
  • Relies on partner (head-turning sign)
  • Limited knowledge of current affairs
  • Poor retention of address
  • Can’t remember breakfast
  • Can’t name pictures
104
Q

Examples of visuospatial impairment

A
  • Difficulty reading unusual fonts
  • Optician visits
  • Bumping/scratching cars and loss of confidence driving, particularly at night
  • Misperceptions and hallucinations
  • Unable to perceive fragmented letters
  • Unable to draw clock face and intersecting pentagons
  • Unable to describe simple/complex pictures
  • Simultanagnosia (unable to perceive more than one object at once)
  • Prospagnosia (unable to recognise faces)
105
Q

Examples of language impairment

A
  • Forgetting words and incorrect word use
  • Stumbling over words and clumsy articulation
  • Vague descriptions and loss of specificity
  • Asking what things are or mean
  • Unable to name things
  • Unable to repeat difficult words and phrases
  • Unable to follow complex commands
  • Unable to read unusual words
  • Unable to demonstrate use of object
106
Q

Examples of impaired executive function

A
  • Disorganised
  • Unable to multitask
  • Frequently distracted
  • Lacking initiative
  • Odd decisions
  • Poor abstraction
  • Impaired letter fluency
  • Poor performance on stroop task (naming colour of writing, not word)
  • Concrete interpretation of sayings
  • Poor estimates
107
Q

Examples of behavioural impairment

A
  • Loss of empathy
  • Apathy
  • Humourless
  • Inappropriate behaviour
  • Callous
  • Self-obsessed
  • Disinhibited
  • Preference for sweet food
108
Q

Examples of behavioural and psychological symptoms of dementia

A
  • Agitation and emotional lability
  • Depression and anxiety
  • Sleep cycle disturbance
  • Disinhibition
  • Withdrawal
  • Apathy
  • Wandering
  • Psychosis
109
Q

Examples of how dementia affects ADLs

A
  • Personal and domestic activities
  • Managing finances
  • Work
  • Basic personal care - washing, eating, toileting
  • Motor function - walking, transferring
110
Q

Presentation of dementia

A
  • Cognitive impairment (memory, visuospatial, language, executive function, behavioural and attention)
  • Behavioural and psychological symptoms
  • Struggling with ADLs
111
Q

Typical presentation of Alzheimer’s

A

4As: amnesia, aphasia, agnosia and apraxia
* Early episodic memory impairment
* Early aphasia

112
Q

Typical presentation of frontotemporal dementia

A
  • Stereotypical, repetitive and compulsive behaviour
  • Emotional blunting
  • Personality changes
  • Disinhibition
  • Apathy
  • Restlessness
  • Abnormal eating
  • Language problems - forgetting words, asking what things are
  • Memory relatively well preserved in early stages
113
Q

Typical presentation of vascular dementia

A
  • Confusion
  • Cardiovascular disease elsewhere
  • Memory impairment
  • Stepwise progression
114
Q

Typical presentation of Lewy body dementia

A
  • Parkinsonian features within 12 months of dementia
  • Visual hallucinations
  • Fluctuating cognition
  • Depression
  • Problems with REM sleep
  • Dysautonomia (BP, HR)
115
Q

What is Parkinson’s dementia?

A

Parkinsonian symptoms with dementia developing after 12 months

116
Q

Dementia in Huntington’s

A
  • Abnormal choreiform movements of face, hands and shoulders
  • Gait abnormalities
  • Dementia presents later
117
Q

Dementia and normal pressure hydrocephalus

A
  • Prominent frontal lobe dysfunction
  • Urinary incontinence
  • Wide gait
118
Q

What is Creutzfeldt-Jakob disease?

A
  • Disintegration of higher cerebral functions
  • Rapid progression with death within 2 years
119
Q

4 cognitive tests for dementia

A
  • Abbreviated mental test (AMT)
  • Addenbrooke’s cognitive examination (ACE) (82/100)
  • Montreal cognitive assessment (MoCA)
  • 6CIT
120
Q

Frontal lobe tests

A
  • Recall as many words as possible in 1 minute starting with the letter ‘S’
  • What is the age of the oldest person in the country?
  • Draw a cock face, put in the numbers and make the clock show 10 past 5
  • How are 2 objects (banana and orange) related?
  • Show them a series of hand movements and ask them to repeat
121
Q

Imaging for dementia

A
  • CT head
  • MRI head
  • Radionuclide scans (AD)
  • DaT/SPECT (Lewy body, AD, vascular, FTD)
122
Q

Investigations for younger people with dementia presentation

A
  • EEG
  • Genetic tests (Huntington’s, familial AD, FTD)
  • Voltage-gated potassium channel antibodies
  • Antineuronal antibodies (paraneoplastic limbic encephalitis)
  • HIV and syphilis serology
  • Metabolic tests
123
Q

What is mild cognitive impairment?

A

Impairment of 1 or more cognitive domains, not severe enough to impact on ability to function

124
Q

What is pseudodementia?

A

Cognitive impairment secondary to mental illness, most commonly depression

125
Q

Non-pharmacological management of dementia

A
  • Cognitive stimulation
  • Socialising (befriending services, day centres)
  • Psychological support
  • Aromatherapy, massage, music, dance, animal-assisted therapy
  • OT - home safety evaluation, motor sensors (wandering)
  • Assistance with personal care and ADLs - family, carers, assisted living, care home
  • Respite care for carers
126
Q

Legal aspects to dementia

A
  • Advanced care planning prior to deterioration - advance statements/decisions, lasting power of attorney, preferred place of care, financial matters
  • Obliged to contact DVLA
  • In later stages, may require Mental Capacity Act and Deprivation of Liberty Safeguarding
127
Q

In which type of dementia should risperidone not be given for psychosis?

A

Lewy body dementia

128
Q

Most common cause of dementia

A

Alzheimer’s disease

129
Q

Pathophysiology of Alzheimer’s disease

A
  • Acetylcholine deficiency damages forebrain
  • Senile plaques trigger formation of neurofibrillary tangles, disrupts neuronal signalling, trigger inflamation and weakens blood vessel walls increasing risk of haemorrhage
  • Neurofibrillary tangles promote neuronal cell death, leading to cortical atrophy, widened sulci and enlarged ventricles
130
Q

Cause of acetylcholine deficiency in Alzheimer’s

A

Degeneration of cholinergic neurones in the nucelus basalis of Meynert

131
Q

Cause of senile plaques in Alzheimer’s disease

A

Amyloid precursor protein (APP) helps neurones grow and repair after injury. After APP is used up, it is broken down by alpha and gamma secretase into soluble fragments. However, if beta secretase breaks down APP, it forms insoluble beta-amyloid, which forms beta-amyloid plaques. These build up in the neural cortex (neuritic plaques) and vessel walls (amyloid angiopathy).

132
Q

Cause of neurofibrillary tangles in Alzheimer’s disease

A

Tau protein ensures that microtubules of the cytoskeleton stay together. Beta amyloid plaques trigger pathways that lead to phosphorylation of tau proteins. This causes them to change shape, so they no longer support the microtubules and instead they clump together with other tau proteins to form NFT.

133
Q

Risk factors for Alzheimer’s disease

A
  • Increasing age
  • Female
  • Family history
  • Genetics (amyloid precursor protein, apolipoprotein E4, presenilin, trisomy 21)
  • Smoking
  • DM
  • Depression
  • Low educational attainment
  • Low social engagement
  • Head trauma
  • Learning difficulties
134
Q

Early stages of Alzheimer’s disease

A
  • Memory lapses - unable to recall new information
  • Difficulty finding words
  • Forgetting names of people and places
  • Problems with managing finances and difficulties at work
135
Q

Middle stages of Alzheimer’s disease

A
  • Language problems - decreased vocabulary, perseveration, global aphasia
  • Difficulty with executive thinking - problem solving, abstract thinking, reasoning, decision making, judgement, planning, organisation, processing
  • Decline in visuospatial abilities - getting lost, impaired driving, copying figures
  • Apraxia
  • Agnosia
136
Q

Later stages of Alzheimer’s disease

A
  • Disorientation to time and place
  • Incontinence
  • Eating problems
  • Wandering
  • Aggression, restlessness and agitation
  • Withdrawal
  • Apathy
  • Emotional lability
  • Depression and anxiety
  • Psychosis - hallucinations and delusions
  • Sleep cycle disturbance
  • Disinhibition
  • Problems with basic personal care - washing, eating, toileting
  • Problems with walking and transferring
137
Q

What does an MRI show in Alzheimer’s dementia?

A
  • Medial temporal lobe atrophy, including hippocampi
  • Cerebral atrophy
138
Q

Investigations for Alzheimer’s

A
  • MRI brain
  • Radionuclide scans (bind to amyloid)
  • DaT/SPECT (brain function, reduced dopmine transporter uptake)
  • CSF examination (tau raised and A-beta 42 reduced)
139
Q

What 2 syndromes do 10% of frontotemporal dementias have overlap with?

A
  • MND
  • Parkinsonian disorders
140
Q

Medications for Alzheimer’s disease

A
  • Acetylcholinesterase inhibitors: donepezil, rivastigmine, galantamine
  • Memantine (NMDA receptor antagonist, anti-glutamate)
141
Q

Cause of frontotemporal dementia

A

3R isoforms of the tau protein get hyperphosphorylated and change shape, so they are unable to tie together tubulin in the cytoskeleton and start clumping together, forming tangles of tau proteins (Pick’s bodies)
Neurones Pick’s bodies and non-functioning microtubules get damaged and undergo apoptosis, and as more and more neurones die, the brain atrophies (sulci widen) and ventricles expand

142
Q

Risk factors for frontotemporal dementia

A
  • Family history
  • Genetics: microtubule associated protein tau (MAPT), granulin precursor, hexanucleotide repeat expansion in C9ORF72 gene
143
Q

Symptoms of behavioural variant FTD

A

Frontal
* Personality changes
* Emotional blunting
* Loss of empathy
* Apathy
* Disinhibition
* Carelessness
* Behavioural change - compulsive behaviour
* Abnormal eating

144
Q

Symptoms of temporal lobe change in FTD

A

Language problems
* Effortful speech
* Halting speech
* Speech sound errors
* Speech apraxia
* Word finding difficulty
* Mispronouncing difficult words

145
Q

Different types of temporal FTD

A
  • Primary progressive aphasia: progressive impairment of language
  • Semantia dementia: fluent speech relatively lacking in meaningful content and progressive difficulty with comprehension of meaning or words
  • Primary non-fluent aphasia: loss of verbal fluency and increasingly telegrammatic speech
146
Q

Investigations for frontotemporal dementia

A
  • MRI: asymmetric frontal lobe and temporal lobe atrophy
  • DaT/SPECT (brain function, reduced dopamine transporter uptake)
  • Postmortem brain biopsy: Pick’s bodies (aggregated tau proteins)
147
Q

What tests would you do in someone < 65 presenting with frontotemporal dementia?

A
  • EEG
  • Genetic tests (FTD genes)
148
Q

Medications for symptoms of frontotemporal dementia
* Compulsions
* Distractibility/perseveration
* Euphoria, excitability, mania, impulsivity, irritability, persistent restlessness/agitation/aggression
* Abnormal eating

A

Compulsions: SSRI
Distractibility: amantadine
Euphoria: valproate semisodium, topiramate
Abnormal eating: topiramate

149
Q

Risk factors for Lewy body dementia

A
  • Increasing age
  • Male
  • Family history
150
Q

Pathophysiology of Lewy body dementia

A

Alpha-synuclein protein misfolds and aggregated to form Lewy bodies, which deposit inside neurones, particularly in the brainstem, substantia nigra and cortex
Lewy bodies lead to reduced levels of acetylcholine and dopamine
As the disease progresses, more and more neurones accumulate Lewy bodies and die

151
Q

Early symptoms of Lewy body dementia

A
  • Difficulty focusing
  • Poor memory
  • Visual hallucinations (people, animals, sense of presence)
  • Disorganised speech
  • Depression
152
Q

Later symptoms of Lewy body dementia

A

Mild Parkinsonian features
* Resting tremor
* Rigidity
* Bradykinesia
* Reduced facial expression

153
Q

Investigations for Lewy body dementia

A
  • Brain biopsy after autopsy: Lewy bodies (inclusions containing aggregations of alpha-synuclein) in cortex
  • DaT/SPECT (brain function, reduced dopamine transporter uptake)
154
Q

Medications for Lewy body dementia

A
  • Acetylcholinesterase inhibitors: rivastigmine and donepezil
  • Memantine (NMDA receptor antagonist)
155
Q

Medications for REM sleep behavioural disorder

A
  • Clonazepam
  • Melatonin
156
Q

Pathophysiology of vascular dementia

A

Vascular brain injury/dysfunction due to chronic ischaemia of the brain causing permanent tissue damage, death and liquefactive necrosis:
* Ischaemic stroke (AF with emboli, carotid artery disease)
* Small vessel disease (cerebral amyloid, atherosclerosis)
* Intracerebral or subarachnoid haemorrhage

157
Q

Risk factors for vascular dementia

A
  • Stroke and TIA
  • AF
  • Carotid artery disease
  • HTN
  • DM
  • Hypercholesterolaemia
  • Smoking
  • Ischaemic heart disease
  • Peripheral vascular disease
158
Q

Non-cognitive symptoms of vascular dementia

A
  • Apraxic gait disorder
  • Pyramidal signs: hyperreflexia, weakness, spasticity, positive Babinski sign
  • Urinary incontinence
  • Cardiovascular disease elsewhere
159
Q

Investigations for vascular dementia

A
  • MRI: multiple cortical and subcortical infarcts and changes (atrophy of brain cortex)
  • DaT/SPECT (brain function, reduced dopamine transporter uptake)
160
Q

Management of vascular dementia

A

Manage vascular risk factors
* Physical activity
* Healthy diet
* Healthy weight
* Stop smoking
* Drink alcohol moderately
* Optimise glycaemic control in DM
* Statin therapy for hypercholesterolaemia
* Control HTN
* Antiplatelet therapy in atherosclerosis
* Anticoagulation or antiplatelet therapy in cardioembolic disease
* Carotid endarterectomy or carotid angioplasty and stenting in carotid stenosis

161
Q

How is capacity assessed?

A
  1. Able to understand the information relevant to the decision
  2. Able to retain the information
  3. Able to weigh up the information
  4. Able to communicate the decision
162
Q

Key aspects of the mental capacity act

A
  • Person assumed to have capacity until proven otherwise
  • Maximise decision-making capacity - all practical support to help a person make a decision should be given
  • Freedom to make seemingly unwise decisions
  • All decisions taken on behalf of the person must be in their best interests
  • Least restricitve option - when making a decision on another person’s behalf, the alternative that achieves the necessary goal and interferes least with the person’s rights and freedom of action must be chosen
163
Q

Define frailty

A

State of increased vulnerability resulting from age-associated decline in functional reserve across multiple physiological systems, resulting in compromised ability to cope with every day or acute stressors

164
Q

Is frailty the same as old age?

A

No
Although increasing age is a risk factor for frailty

165
Q

Frailty syndromes that should raise suspicion of frailty

A
  • Falls
  • Immobility
  • Delirium
  • Incontinence
  • Susceptibility to side effects of medication
166
Q

Screening for frailty

A
  • PRISMA-7 questionnaire
  • Self-reported health status
167
Q

Assessments for frailty

A
  • Gait speed (>5s to walk 4m)
  • Timed up and go test (TUGT) (>10s to stand up from standard chair, walk 3m, turn, walk back to chair and sit down)
168
Q

What is the phenotype model of frailty?

A

Fried criteria (3 or more of):
* Unintentional weight loss
* Self-reported exhaustion
* Weakness (grip strength)
* Slow walking speed
* Low physical activity

169
Q

2 ways of assessing cumulative deficit in frailty

A
  • Rockwood clinical frailty scale
  • Electronic frailty index
170
Q

What tool measures severity of frailty after a comprehensive geriatric assessment?

A

Rockwood clinical frailty scale

171
Q

What are the different scores on the clinical frailty scale?

A
  1. Very fit
  2. Well (active occasionally)
  3. Managing well (medical problems well controlled)
  4. Vulnerable (not dependent, symptoms limit activities)
  5. Mildly frail (more evident slowing, need help with high order ADLs)
  6. Moderately frail (need help with all outside activities and keeping house, stairs, bathing)
  7. Severely frail (completely dependent ror personal care, not at high risk of dying)
  8. Very severely frail (approaching end of life, could not recover from minor illness)
  9. Terminally ill (life expectancy <6 months)
172
Q

When should frailty prompt discussions around end of life care?

A

Irreversible frailty/decline

173
Q

What is advance care planning?

A

Discussions about goals of care and means of setting on record preferenecs for care of patients who may lose capacity or communicating ability in the future

174
Q

Examples of things discussed in advance care planning

A
  • Legal aspects (advanced decision to refuse treatment, lasting power of attorney)
  • Preferred place of care
  • Treatment options acceptable to and suitable for patient
  • DNACPR
  • Specific plans for complex scenarios
175
Q

Advantages of advance care planning

A
  • Allows for uncertainty
  • Personalised care (stating preferences)
  • Avoids futile disease-oriented treatment
  • Patient-centred goals
  • Improves coordination of care (multiple agencies involved towards the end)
176
Q

What is palliative care?

A

Treatment that recognises the irreversible nature of the underlying disease process (holistic, symptom control)

177
Q

How does frailty affect how the body handles stressor events?

A

More likely to have adverse outcomes and decompensations, requiring hospitalisation or leading to death

178
Q

What is sarcopenia?

A

Loss of muscle mass or function (walking, speed, grip strength), usually due to disuse atrophy/deconditioning

179
Q

What is the management of sarcopenia?

A

Comprehensive geriatric assessment to optimise everything (balance, nutrition, home environment, vision, toileting needs, cognition, social situation)

180
Q

What campaign is trying to address deconditioning in hospital?

A

‘Sit up, get dressed, get moving’

181
Q

What bone is injured in hip fractures?

A

Proximal femur

182
Q

What are the 2 types of hip fractures?

A
  • Intra-capsular fracture: break in femoral neck proximal to the intertrochanteric line
  • Extra-capsular fracture: break in femoral neck distal to intertrochanteric line
183
Q

Grades of intra-capsular fracture

A

Grade 1: incomplete fracture and non-displaced
Grade 2: complete fracture and non-displaced
Grade 3: partial displacement (trabeculae are at an angle)
Grade 4: full displacement (trabeculae are parallel)

184
Q

Types of extra-capsular fracture

A

Intertrochanteric fractures: between greater and lesser trochanter
Subtrochanteric fractures: distal to lesser trochanter (although within 5cm) and to the proximal shaft of the femur

185
Q

Cause of hip fractures

A

Falls directly onto hip or twisting (foot planted and body rotates)

186
Q

Which type of hip fracture causes avascular necrosis and why?

A

Displaced intracapsular fractures (grade 3/4)
Damage the medial and lateral circumflex femoral arteries, removing blood supply to femoral head

187
Q

Risk factors for hip fractures

A
  • Increasing age
  • Osteoporosis and osteopenia
  • Female
  • Falls
  • Low muscle mass
  • Steroids
  • Smoking
  • Excess alcohol intake
  • Metastatic spread of cancer to bone
  • Increased risk of falls (MS)
188
Q

Presentation of hip fracture

A
  • Pain in groin or hip, which may radiate to the knee
  • Not able to weight bear
  • Shortened, abducted and externally rotated leg
  • Reduced range of motion
189
Q

Investigation for hip fracture and what it would show

A

X-ray
Disrupted Shenton’s line on anterior-posterior view

190
Q

Investigations for cause of fall

A
  • FBC (anaemia)
  • U&E (electrolyte imbalance)
  • ECG (arrhythmia)
  • Cardiac echo (heart failure)
  • ECG (MI)
  • Urine dipstick (UTI)
191
Q

Management of hip fracture

A
  • Analgesia (paracetamol, opioids)
  • VTE risk assessment and prophylaxis (LMWH, TED stockings, intermittent pneumatic compression)
  • Orthogeriatrics input (optime medical co-morbidities and complications)
  • Surgery within 48 hours
  • PT to start mobilisation and rehabilitation after operation
192
Q

Surgery for non-displaced intra-capsular fracture

A

Internal fixation, e.g. with screws

193
Q

Surgery for displaced intra-capsular fracture

A

Hemiarthroplasty (replace head of femur but leave acetabulum in place) or total hip replacement (head of femur and socket)

194
Q

Surgery for intertrochanteric extra-capsular fracture

A

Dynamic hip screw (through neck and into head of femur)

195
Q

Surgery for subtrochanteric extra-capsular fracture

A

Intramedullary nail (metal pole through greater trochanter into central cavity of shaft of femur)

197
Q

What are complications of a fall with a long lie?

A
  • Pressure ulcers
  • Dehydration
  • Rhabdomyolysis
  • Hypothermia

Phase 3a Medicine (7 decks)

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