Geriatrics Flashcards
Give the points of a Mini Mental State Exam
Orientation (time and place) - where they are, what date, time, month, year it is
Registration - 3 unrelated objects, get them to repeat
Attention and calculation - Do serial sum (keep subtracting 7 from 100), and/or spell word backwards
Recall - Say those 3 objects again
Language - Ask them to name an object, repeat phrase “no ifs, ands or buts”, give them a 3 stage command (take paper, fold it, throw it), read and do a command, writing a sentence, draw pentagons that intersect.
24-30 no impairment
18-23 mild
<18 severe impairment
What is osteoporosis
Low Bone Mineral Density (<2.5 SD from mean peak mass), causing fragile bones with increased risk of fracture
Risk factors for osteoporosis
SHATTERED
S - Steroid (glucocorticoids decrease Ca2+ absorption in gut)
H - Hyperthyroid, HyperPT, hypocalcaemia/Hypercalciuria
A - Alcohol/smoking
T - Thin (low BMI)
T - Testosterone decrease
E - Early menopause
R - Renal/liver failure
E - Erosive bone disease (myeloma, RA)
D - Dietary reduced Ca2+, malabsorption, diabetes
Also, older age, female, previous fragility fracture, physical inactivity
Conditions that cause secondary osteoporosis
- Hyperthyroid
- Hyperparathyroid
- Alcohol abuse
- Immobilisation
- Cushings
- Turner syndrome
What are the most common fractures in osteoporotic patients
- Vertebral crush
- Distal radius (Colles fracture) (wrist)
- Proximul femur/ NOF
In vertebral crush patient will have hunched back (kyphosis) and height loss >4cm.
Why does menopause cause osteoporosis
Oestrogen inhibits bone resorption by decreasing osteoclast activity. When this decreases (menopause) resorption>formation.
How is osteoporosis classified
Femoral neck T score, measured using a DEXA scan
Normal >-1
Osteopenia -2.5 to -1
Osteoporosis <-2.5
Severe <-2.5 and fracture
T score is SDs below average healthy adult
Investigations in osteoporosis
FRAX tool screening (Anyone on steroids, anyone over 50 with risk factors, women over 65, men over 75)
DEXA scan (Dual Energy Xray Absorptiometry) - measures bone mineral density. Usually measured at hip
Provides 2 readings;
- Z score - number of SDs patients BMD falls below mean for their age
- T score - number of SDs patients BMD falls below mean for young healthy adult
Ca2+, phosphate and ALP should all be tested (and appear normal unless underlying cause)
Management of osteoporosis
Lifestyle
- Activity/exercise
- Maintain weight
- Adequate vitD/calcium
- Stop smoking/alcohol.
Managed with bisphosphonates (Alendronate)
How should bisphosphonates be taken? What are their side effects?
To be given on empty stomach, first thing in the morning with a full glass of water. Stay upright for 30 mins after taking and dont eat or drink for 30 mins after.
- Reflux/oesophagitis
- Osteonecrosis of jaw
- Osteonecrosis of external auditory canal
- Oesophageal ulcers
How is osteoporosis monitored
Follow up in 5 years if no treatment
On treatment, FRAX/DEXA in 3-5 years. Come off treatment if BMD improves (T>-2.5) with no fragility fracture
Delirium vs Dementia
Factors pointing to delirium as opposed to dementia
- Acute onset
- Impairment of consciousness
- Fluctuating symptoms (worse at night/ periods of normality)
- Abnormal perceptions
- Agitiation, fear, delusions
What is Delirium
An acute, fluctuating disturbance of consciousness and cognition, often with altered attention and perception
Reversible, and has an acute cause
Causes of Delirium
PINCHME
Pain
Infection
Nutrition (electrolyte imbalances + hyponatraemia MC, also hypercalcaemia and hypo/hyperkalaemia)
Constipation
Hydration
Medication (opiates and anticholinergics)
Environment change
Risk factors for delirium
Age>65
Pre-existing cognitive development
Polypharmacy
Hospitalisation
Sensory impairment
Comorbidities
Clinical features of delirium
Types:
Hyperactive: Agitated, restless, hallucinating
Hypoactive: Lethargic, reduced responsiveness
Can be mixed
Symptoms:
- Acute onset, fluctuating course
- Impaired attention and concentration
- Disorientation/memory impairment
- Drowsiness, disorientation, disorganised thought
- Lack of interest
Possible investigations of delirium
Clinical diagnosis using DSM-5 and short Confusion Assessment Method (Short-CAM) but can diagnose cause
-Basic labs (FBC, U&E, thyroid, glucose, LFT)
- Infection screen: Urinalysis, blood culture, CXR
- Mediation review
- Calcium
- B12/folate
- CT head
Tests used to diagnose delirium
DSM-5
Short-CAM (confusion, inattention, disorganised thought, altered consciousness)
4As
- Alertness
- Attention (Test attention by asking them to list months of the year backwards)
- Acute change/fluctuation
- AMT4 (abbreviated mental test) (age, DOB, place, current year)
Risks of delirium left untreated
- Risk of dementia
- Longer hospital stay
- Increased mortality
What is benign paroxysmal position vertigo (BPPV)
Sudden onset dizziness and vertigo (false spinning/ moving sensation - self or world around you) triggered by changes in head position.
Average age of onset is 55 years. Good prognosis, resolves in weeks-months, half will have recurrence 3-5 years after diagnosis
Pathophysiology of benign paroxysmal position vertigo (BPPV)
Crystals of calcium carbonate called otoconia that become displaced into the semicircular canals. Occurs most often in posterior semicircular canal.
May be displaced by viral infection, head trauma, ageing or without a known cause.
Crystals disrupt flow of endolymph, confusing the vestibular system. Head movement creates flow through canals, triggering vertigo
How does BPPV present and what examination can be done to confirm
- Vertigo triggered by a change in head position (could be rolling over in bed or looking up)
- Nausea
- 10-20 second episodes
Dix-Hallpike manoeuvre
- Patient sits with head turned to 45 and eyes wide open. Patient leans back to lying, with one ear pointed to the ground, let head go over the edge of the couch. (30-40 degrees).
- While in this position, check for nystagmus (involuntary eye movement) flickering towards affected side
- AKA Rotatory nystagmus, and repeat both sides
- (Triggers movement of endolymph through semicircular canals, triggering vertigo if they have BPPV)
How can BPPV be managed
Good prognosis, resolves spontaneously after weeks-months.
Epley manoeuvre (successful in 80% of cases)
- Follow steps of Dix Hallpike, until head turned 45, and dangling 30 off the edge of the bed
- Rotate 90 degrees past central position, and then have patient roll over, so head moves another 90 degrees.
- Have them sit up sideways off the edge of the couch and position head in central position (chin to chest).
- Support patients head for 30 seconds, until dizziness settles.
Can also teach exercises they can do alone (vestibular rehabilitation) - Brandt-Daroff exercises.
Betahistine can be used but “evidence limited” (so basically dont use but remember just in case for exam)
What 3 factors play into a normal gait
- Neurological system (basal ganglia and cortical basal ganglia loop)
- MSK (tone/strength)
- Effective processing of the senses (sight, sound, sensation)
Risk factors for falling
- Lower limb muscle weakness
- Vision problems
- Balance/gait disturbance (diabetes, rheumatoid arthritis, parkinsons)
- Incontinence
- Polypharmacy
- > 65yo
- Fear of falling
- Depression
- Postural hypotension
- Psychoactive drugs
Questions to ask about a fall
- Where were you/ what were you doing when you fell
- How fast/hard did they fall
- Did anyone witness it
- Any associated features before/after?
- Why do they think they fell?
Systems review!, PMH, Social history
What medications can cause postural hypotension
- Nitrates
- Diuretics
- Anticholinergics
- Antidepressants
- Beta blockers
- Ldopa
- ACEi/ARB
Other medications that cause falls due to other mechanisms
- Benzodiazepines
- Antipsychotics
- Opiates
- Anticonvulsants
- Codeine
- Digoxin
What tests should be done on Falls patients
Bedside - Basic obs, BP, Glucose, Urine dip, ECG
Bloods - FBC, U+E, LFT, bone profile
Imaging - X ray (chest/injured limbs), CT head, cardiac echo
Vit D, calcium, vision, hearing, neurological exam
What special tests can be done in a falls patient
Turn 180 (stand behind patient have them turn to face you, counting how many steps it takes. Healthy adult - 3 or fewer steps. 4 or more is a sign of poor balance, instability, decreased agility)
Timed up and Go test (Check balance and mobility by timing how long it takes them to stand, walk 3m and return)
What is squamous cell carcinoma and give its usual locations
2nd most common skin cancer. Most common cancer of the head and neck. Arises from the squamous cells of the mucosa.
- Nasal cavity
- Paranasal sinuses
- Mouth
- Salivary glands
- Pharynx
- Larynx
Head and neck cancers spread to lymph nodes first, so may be found as lymphadenopathy, with no clear original tumour
Risk factors for SCC
- Smoking
- Chewing tobacco and betel quid (south-east Asia habit)
- Alcohol
- HPV-16
- EBV
- Long standing leg ulcer (Marjolin ulcer)
*HPV also causes cervical cancer - HPV vaccine protects against strains 6,11,16,18
Red flags in SCC
- Lump in mouth or lip
- Unexplained mouth ulcer >3 weeks
- Persistent neck lump
- Unexplained thyroid lump
- Unexplained hoarse voice
- Erythroplakia or eryhtroleuoplakia
Management of SCC
MDT approach and TNM grading
- Chemotherapy
- Radiotherapy
- Surgery
Cetuximab is a monoclonal antibody used for SCC of the head and neck. Inhibits epidermal growth factor receptor
Skin SCC risk factors
- Excessive sunlight/ UVA therapy
- Actinic keratoses, Bowen’s disease
- Smoking
- Immunosuppression/HIV
- Long standing leg ulcer (E.g. Marjolin’s)
How does skin SCC present
- Typically on sun exposed sites (neck, dorsum of hands, face, arms)
- Rapidly expanding, painless, ulcerate nodules
- Cauliflower like appearance
- Areas of bleeding
Management of skin SCC
Surgical excision with margins
- 4mm if lesion <20mm in diameter
- 6mm margin if >20mm diameter
Mohs surgery if high risk or cosmetically important
Good vs bad prognosis - Skin SCC
Good
- Well differentiated, <20mm diameter, <2mm deep, no associations
Poor
- Poorly differentiated, >20mm diameter, >4mm deep, immunosuppression
What are pressure ulcers
Typically occur in patients with reduced mobility. Prolonged pressure on particular areas, e.g. sacrum whilst sitting, lead to skin breaking down.
Occurs due to a mix of reduced blood flow and local ischaemia, reduced lymph drainage, abnormal changes in shape of tissues under pressure.
What factors predispose to pressure ulcers
- Illness, paralysis, advancing age, causing increased pressure to certain areas
- Develop over bony prominences, such as sacrum or heel.
- Malnourishment
- Urinary/Faecal incontinence
- Lack of mobility
- Pain
What scoring system is used to screen for patients at risk of developing ulcers
Waterlow score
Some factors:
- BMI
- Nutritional status
- Skin type
- Mobility
- Continence
How are pressure ulcers graded
1 - Non blanching erythema of intact skin. Discolouration, warmth, oedema, induration, hardness.
2 - Partial thickness skin loss involving dermis/epidermis. Superficial, presents as an abrasion or blister. TREAT from here
3 - Full thickness skin loss involving damage to or necrosis of subcut tissue that may extend down to, but not through, underlying fascia.
4 - Extensive destruction, tissue necrosis, damage to muscle, bone or supporting structures, +- full thickness skin loss
Prevention of pressure ulcers
- Regular repositioning
- Supportive surfaces (pressure relieving mattresses, cushions, pads to distribute weight evenly)
- Nutrition and hydration
- Avoid friction and shear
- Education and training + regular skin checks
- Protective dressing and barrier creams
How are pressure ulcers managed
- Moist wound environment encouraging ulcer healing. Hydrocolloid dressings and hydrogels. Avoid soap - drying effect
- Wound swabs not routine, use systemic Abx on a clinic basis (e.g. if cellulitis)
- Surgical debridement may be needed
All patients need wound dressing, analgesia, nutritional assessment
What are neuropathic ulcers
Commonly occur over plantar surface of metatarsal head and plantar surface of hallux.
Plantar neuropathic ulcer is what most commonly leads to amputation in diabetic patients
Management includes cushioned shoes, to reduce callous formation
What is a Marjolins ulcer
Squamous cell carcinoma
Occurs at sites of chronic inflammation e.g. burns, osteomyelitis, after 10-20 years
Mainly occur on lower limbs
What are venous ulcers caused by
Predisposed by venous hypertension or chronic venous insufficiency.
Occur after a minor injury, due to leucocyte sequestration or capillary fibrin cuff
Features of venous ulcers
- Gaiter area (top of foot to bottom of calf - usually above medial malleolus), both medial and lateral aspects, usually painless
- May be associated varicose veins, PAD, deep venous insuffiency secondary to DVT.
- Oedema
- Brown pigmentation
- Lipodermatosclerosis
- Eczema
- Painless/less painful than arterial
How is Venous ulceration investigated
ABPI - 0.9-1.2.
- <0.9 indicates arterial disease.
- >1.3 may also indicate disease, in form of false negative results secondary to arterial calcification
Doppler USS to look for presence of reflux. Duplex USS to find anatomy/flow of vein.
Associations with venous ulcers
Deep venous insufficiency related to previous DVT.
Superficial venous insufficiency associated with varicose veins.
Management of venous ulcers
4 layer compression banding after exclusion of arterial disease or surgery
Skin grafting if >10cm or failure to heal after 12 weeks
How do arterial ulcers normally present
- Distal (toes, or dorsum of foot)
- PAD
- Distant absent pulses, pallor, intermittent claudication
- Smaller, deeper, better defined borders.
- Punched out appearance
- Less likely to bleed but more painful
- Pain worse when lying down. Pain worse on elevation, relieved on lowering
How do venous ulcers presetn
- Gaiter area
- Chronic changes e.g. hyperpigmentation, venous eczema, lipodermatosclerosis
- Occur after minor injury
- Larger, more superficial
- Irregular, gently sloping border
- More likely to bleed but less painful
- Pain relieved by elevation and worse when lowering
Investigations in ulcers
- ABPI
- FBC/CRP/Comorbidity investigation (FBC, HBA1c)
- Charcoal swab if infection
- Skin biopsy with 2 week wait if cancer suspected
How are arterial ulcers managed
- Urgent referral to vascular to consider surgical revascularisation.
- If underlying disease treated, ulcer should heal rapidly.
- Debridement and compression NOT used in arterial
How are venous ulcers managed
- Compression bandaging (usually 4 layer)
- Oral pentoxyfylline, peripheral vasodilator, improves healing
- Small evidence base supporting use of flavinoids
How should multimorbidity be assessed
Investigate treatment burden
Social circumstances
Pain management
PRISMA-7 questionnaire
