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Phase 3a > Geriatrics > Flashcards

Geriatrics Flashcards

1
Q

What is Benign paroxysmal positional vertigo?

A

Common peripheral cause of recurrent episodes of vertigo triggered by head movement because of problems in the inner ear. More common in older adults.

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2
Q

Describe the presentation of BPPV

A
  • Asymptomatic between attacks
  • Common trigger is turning over in bed
  • Symptoms usually last 20-60 seconds
  • Episodes can come and go
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3
Q

Describe the pathophysiology of BPPV

A
  • Crystals of calcium carbonate called otoconia become displaced into the semicircular canals most often in the posterior semicircular canal.
  • Cause can be viral infection, head trauma, ageing or idiopathic
  • Otoconia disrupt the normal flow of endolymph through canals confusing the vestibular system
  • Head movement creates flow of endolymph in canals triggering episodes of vertigo
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4
Q

Describe Dix-Hallpike Manoeuvre

A
  • Diagnostic for BPPV - moves head in a way that moves endolymph through semicircular canals and triggers vertigo
  • Patient sits upright head 45 degrees to one side, support head and rapidly lower patient so head hangs off bed 20-30 degrees
  • Watch eyes for 30-60 secs for rotational beats of nystagmus towards affected ear
  • Repeat on other side
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5
Q

What is the Epley Manoeuvre?

A

Treats BPPV - moves crystals into a positional that doesn’t disrupt endolymph flow

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6
Q

Describe Brandt-Daroff Exercises

A
  • Performed at home by patient to treat BPPV
  • Roll from side to side on the bed facing the ceiling
  • Repeat several times a day
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7
Q

State 5 causes of Cardiac Failure

A
  • IHD
  • Hypertension
  • Cardiomyopathy
  • VHD
  • CHD
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8
Q

Describe the types of cardiac failure

A
  • Systolic - failure to contract, ejection fraction <40%
  • Diastolic - inability to relax and fill, ejection fraction >50%
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9
Q

Describe the pathology of cardiac failure

A

Compensatory changes - sympathetic stimulation |(increases HR), increased RAAS (due to fall in CO, leads to increased water retention and oedema), cardiac changes (ventricular dilation and myocyte hypertrophy)

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10
Q

Describe left cardiac failure and symptoms

A
  • Reduced ejection fraction (systolic)
  • Symptoms - pulmonary oedema, tachycardia, pleural effusion
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11
Q

Describe right cardiac failure and symptoms

A
  • Can be caused by left ventricular failure
  • Symptoms - pitting oedema, ascites, weight gain (fluids)
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12
Q

State 3 investigations for cardiac failure

A
  • ECG - may show underlying causes
  • Bloods - Brain Natriuretic Peptide (released by ventricles with mycocardial wall stress)
  • Cardiac enzymes - creatinine kinase, Troponin I, Troponin T, Myoglobulin
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13
Q

State the management for cardiac failure

A
  • Lifestyle changes
  • ACE inhibitors - dilates blood vessels
  • Beta blockers
  • Diuretics
  • Heart transplant
  • Oxygen (acute)
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14
Q

Describe the presentation of delirium

A
  • Acute onset
  • Fluctuating course
  • Inattention
  • Altered level of consciousness
  • Usually reversible
  • Associated with underlying medical cause
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15
Q

State the causes of delirium

A

Drug use (introduction, dose adjustments)

Electrolyte and physiological abnormalities

Lack of drug (withdrawal)

Infection

Reduced sensory input (deaf, blind, changing environment)

Intracranial problems (stroke, post-ictal, meningitis, subdural haematoma)

Urinary retention and faecal impaction

Myocardial (MI, Arrhythmias, HF)

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16
Q

Describe the treatment for delirium

A
  • Treat the cause - meds review, infection, pain relief, low dose haloperidol/lorazepam
  • Manage the environment - soft lighting, clocks and calendars, sleep hygiene, avoid room/ward moves, minimise provocation
  • Capacity assessment - MHA, MCA
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17
Q

Describe the types of delirium

A
  • Hyperactive - agitation, inappropriate behaviour, hallucinations
  • Hypoactive - lethargy, reduced concentration
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18
Q

How would you assess delirium?

A
  • History - collateral, cognitive screening, previous level of function, social circumstances, risk factors
  • Bedside tests - 02 sats, bp, temp, ABG/VBG
  • Investigations - FBC, LFT, U&E, CRP/ESR Sputum culture, Folate, B12, HbA1c, TFT, CXR, ECG, urinalysis
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19
Q

State some delirium differentials

A
  • Depression
  • Dementia
  • Mental illness
  • Anxiety
  • Thyroid disease
  • Temporal lobe epilepsy
  • Charles Bonnet syndrome
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20
Q

Dementia Investigations

A

Mini-Mental State Examination - out of 30. 25-30 normal. 21-24 mild. 10-20 moderate. <10 severe

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21
Q

Dementia management

A
  • Healthier lifestyle
  • Social support
  • ACh inhibitor - rivastigmine
  • Control CV risk factors
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22
Q

Differences between delirium and dementia

A

Delirium - acute onset, fluctuating course, lasts hours to weeks, altered consciousness
Dementia - insidious onset, progressive course, lasts months to years, normal consciousness unless severe

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23
Q

Describe Alzheimer’s history, symptoms and pathology

A

History - gradual onset
Symptoms - aphasia, agnosia, apraxia, amnesia
Pathology - degeneration of cerebral cortex with cortical atrophy

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24
Q

Describe vascular dementia history, symptoms and pathology

A

History - abrupt or gradual onset
Symptoms - stepwise deterioration with short periods of stability, raise BP
Pathology - brain damage from cerebrovascular disease

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25
Q

Describe Lewy-Body dementia history, symptoms and pathology

A

History - Insidious onset
Symptoms - fluctuating cognition, impairment with visuospatial ability
Pathology - deposition of abnormal proteins, associated with Parkinsons

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26
Q

Describe fronto-temporal dementia history, symptoms and pathology

A

History - insidious onset with rapid progression
Symptoms - behavioural and personality changes
Pathology - atrophy of fronto-temporal lobes

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27
Q

Malnutrition causes

A
  • Decreased nutrient intake (starvation)
  • Increased nutrient requirements (sepsis or injury)
  • Inability to utilise ingested nutrients (malabsorption)
  • Or combination of above
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28
Q

Risks for developing malnutrition

A
  • Eaten little or nothing for >5 days
  • Poor absorptive capacity
  • High nutrient losses
  • Increased nutritional needs from causes such as catabolism
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29
Q

How to diagnose malnutrition

A
  • BMI <18.5kg/m2
  • Unintentional weight loss >10% last 3-6months
  • BMI <20 AND unintentional weight loss >5% within last 3-6 months
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30
Q

Consequences of malnutrition

A
    • Impaired immunity
    • Impaired wound healing
    • Muscle mass loss
    • Respiratory function loss
    • Cardiac function loss
    • Impaired skin integrity
    • Impaired recovery from illness
    • Worsening prognosis
    • Low quality of life
    • Prolonged hospital stay
    • More hospital admissions
    • Greater healthcare needs
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31
Q

Describe refeeding syndrome and pathology

A
  • Prolonged starvation followed by provision of nutritional supplementation from any route
  • Chronic malnutrition leads to decreased insulin levels, energy source switch, normal serum phsophate levels, low intracellular phosphate levels
  • Refeeding leads to insulin increase, movement of electrolytes into cell results in decreased serum electrolyte levels
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32
Q

Refeeding syndrome clinical features

A
  • CVS: arrhythmia, HT, CHF
  • GI: abdo pain, constipation, vomiting, anorexia
  • MUSC: weakness, myalgias, rhabdomyolysis, osteomalacia
  • NEURO: weakness, paraesthesia, ataxia
  • METABOLIC: infections, thrombocytopaenia, haemolysis, anaemia
  • OTHER: ATN, wernicke’s encephalopathy, liver failure
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33
Q

Refeeding syndrome investigations

A

Bloods:

  • Hypophosphataemia
  • Hypokalaemia
  • Hypomagnesaemia
  • Hyperglycaemia
  • Thiamine deficiency
  • Trace elements deficiencies
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34
Q

Refeeding syndrome management

A
  • Recognise patients at risk
  • Replace electrolytes
  • Supportive care
  • Monitor glucose and Na levels
  • Feeds, vitamins (B6, B12), folate
  • Refer to nutritional support team/dietician
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35
Q

What does a patient need to be able to do to have capacity

A
  • Understand the information relevant to the decision
  • Retain the information
  • Weigh up the information
  • Communicate the decision
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36
Q

Things to consider with Mental Capacity Act

A
  • Assume capacity - until proven otherwise
  • Maximise decision making capacity - all support to help person make a decision should be given
  • Freedom to make seemingly unwise decisions - unwise decisions do not prove incapacity
  • Best interests - all decisions taken on behalf of the person must be in their best interests
  • Least restrictive option - care that achieves the necessary goal and interferes the least with the person’s rights and freedom of action must be chosen
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37
Q

Describe different types of Mental Health Acts

A
  • Section 2 - 28 days for assessment, not renewable, done by an Approved Mental Health Professional and 2 Drs.
  • Section 3 - Treatment for up to 6 months, can be renewed
  • Section 4 - 72 hour assessment order, used in emergency when section 2 would cause delay
  • Section 5(2) - a voluntary patient in hospital detained by a doctor for 72 hours
  • Section 5(4) - a voluntary patient in hospital detained by a nurse for 6 hours
  • Section 135 - a court order obtained allows police to break into property to remove a person to a Place of Safety
  • Section 136 - someone found in a public place with mental disorder taken by police to a Place of Safety
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38
Q

Things to consider with best interests

A

Consider:

  • Whether the person is likely to regain capacity and can the decision wait
  • How to encourage and optimise the participation of the person in the decision
  • The past and present wishes, feelings, beliefs, values of the person and any other relevant factors
  • Views of other relevant people
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39
Q

Describe advanced directives

A
  • Can state treatment wishes in advance e.g.
    • authorise or request specific procedures
    • Refuse treatment in a predefined future situation
  • Advance refusals of treatment are legally binding if:
    • The person is an adult
    • Was competent and fully informed when making the decision
    • The decision is clearly applicable to current circumstances
    • There is no reason to believe that they have since changed their mind
  • Advance requests for treatment don’t have same legal binding status but should be considered when assessing best interests
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40
Q

Describe DoLs

A

Deprivation of Liberty

Occurs when a person does not consent to care or treatment, for example, a person with dementia who is not free to leave a care home and lacks capacity to consent to this

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41
Q

Describe LPAs

A

Lasting power of attorney

A document which a person can nominate someone else to make certain decisions on their behalf e.g. finances, health, personal welfare when they are unable to do so themselves.

To be valid it needs to be registered with the Office of the public Guardian

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42
Q

Describe IMCAs

A

Independent mental capacity advocate

- Commissioned from independent organisations by the NHS and local authorities to ensure that MCA is being followed
- Role: to support and represent people who lack capacity and they do not have anyone else to represent them in decisions about changes in long-term accomadation or serious medical treamtent. They can also be present for decisions regarding care reviews or adult protection.
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43
Q

Osteoporosis description

A

A systemic skeletal disease characterised by low bone mass and microarchitectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture

44
Q

Osteopenia description

A

Precursor to osteoporosis characterised by low bone density. Defined as bone mineral density 1-2.5 SD below mean

45
Q

Osteomalacia description

A

Poor bone mineralisation leading to soft bones due to lack of calcium (adult form of rickets)

46
Q

Osteoporosis causes

A
  • Primary - post-menopausal
  • Secondary - SHATTERED
    • Steroid use
    • Hyperthyroidism/hyperparathyroidism
    • Alcohol
    • Thin (low BMI)
    • Testosterone low
    • Early menopause
    • Renal or liver failure
    • Erosive/inflammatory bone disease
    • Dietary calcium low
47
Q

Osteoporosis risk factors

A
  • Patient - old, female, low BMI, diet, athletes
  • Disease - RA, SLE, Hyperthyroidism, Hyperparathyroidism, Cushing’s, Hypogonadism, Renal disease
  • Medication - Corticosteroids, Hormonal (depo-provera, androgen deprivation, aromatase inhibitors, GnRH analogues)
48
Q

Osteoporosis patholgy

A
  • Increased resorption by oesteoclasts and decreased formation by osteoblasts → inadequate peak bone mass
  • With ageing comes decrease in trabecular thickness + decrease in connections between horizontal trabeculae = decrease in trabecular strength and increased susceptibility to fracture
  • Oestrogen deficiency → loss of restraining effects of oestrogen on bone turnover → cancellous bone loss and microarchitectual disruption
  • Eular buckling theory says that trabeculae make bones stronger
49
Q

Osteoporosis symptoms

A
  • Asymptomatic until fracture
  • Hip - neck of femure after fall on side or back
  • Wrist - distal radius (Colle/Smith’s fracture from fall on outstretched arm)
  • Vertebra - shorter and stooping posture, can lead to kyphosis (curvature of spine)
50
Q

Osteoporosis investigations

A
  • DEXA BMD (Dual Energy XR and Absoptiometry) - T score (standard deviation). < -2.5 = OP, -1—2.5 = Osteopenia, > -1 = normal
  • FRAX (fracture risk assessment) - age, sex, BMI, previous fractures, steroids
51
Q

Osteoporosis treatment

A
  • Lifestyle - smoking, alcohol, Vit D supplements
  • Alendronate daily (1st line) - oral bisphosphonate, inhibits bone resorption through inhibition of Farnesyl Prophosphate synthase (in cholesterol pathway) which reduces osteoclast activity by removing their ruffled border
  • Different Bisphosphonate (2nd line) - e.g. Risedronate (daily), Idandronate (weekly)
  • Strontium ranelate (3rd line) - reduces fracture rate
  • Recombinant human parathyroid peptide (3rd line) - e.g. Teriparatide. Increases osteoblast activity and bone formation
52
Q

Osteoporosis primary prevention

A
  • Adcak D3 - Vit D + Calcium
  • HRT - menopausal women
  • Corticosteroids
  • Smoking and alcohol cessation
  • DEXA scans
53
Q

Bisphosphonates clinical uses

A
  • Prevention and treatment of osteoporosis
  • Hypercalcaemia
  • Paget’s disease
  • Pain from bone metastases
54
Q

Bisphosphonates adverse effects

A
  • Oesophageal reactions: oesophagitis, oesophageal ulcers
  • Osteonecrosis of the jaw
  • Increased risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate
55
Q

When should you stop taking bisphosphonates

A

After 5 years if the patient is:
- <75
- Femoral neck T-store of > -2.5
- Low risk according to FRAX/NOGG

56
Q

Parkinson’s epidemiology

A

More common in men

Mean age of diagnosis is 65 years

57
Q

Parkinson’s pathology

A
  • Neurodegenerative loss of dopamine secreting cells from the pars compacta of the substantia nigra that project to the striatum → reduced striatal dopamine levels
  • Less dopamine inhibits thalamus → decreased movement
  • Under microscopy there are Lewy bodies (intracytoplasmic intrusion bodies in remaining neurones)
58
Q

Parkinson’s diagnostic criteria

A
  • 4 diagnostic criteria:
  • Bradykinesia - slowness or absence of movement
  • Resting tremor - may be unilateral
  • Rigidity - pain, increased tone in limbs and trunk
  • Postural instability - impaired balance
  • Gait - small shuffling steps, reduced arm swing, slow start
  • Mental health - Depression (20-40%), dementia
59
Q

Parkinson’s differentials

A
  • If incontinence, dementia, symmetry, early falls, tremor in action are present in early stages think:
  • Normal pressure hydrocephalus - increase CSF → enlarged ventricles. Magnetic gait, incontinence, dementia. Treat with surgical correction
  • Essential tremor - very common. No rest tremor, no increased tone, better after alcohol. Treat with deep brain stimulation or beta blockers (primidone)
60
Q

Parkinson’s investigations

A
  • DaTSCAN - imaging of dopaminergic terminals of nigrostriatal neurons in striatum, shows reduced dopamine supply
  • CT/MRI shows substantia nigra atrophy
  • Microscopy shows Lewy bodies
  • Diagnosis mostly made off history and exam
61
Q

Describe bradykinesia

A
    • Poverty of movement also seen (hypokinesia)
    • Slow, shuffling steps
    • Reduced arm swinging
    • Difficulty in intiating movement
62
Q

Describe parkinson’s tremor

A
  • Most marked at rest, reduced on movement
  • Worse when stressed or tired
  • Typically pill-rolling, asymmetrical
63
Q

Describe Parkinson’s rigidity

A
  • Lead-pipe - hypertonic in limb throughout the range of movements of a joint
  • Cogwheel - muscular stiffness through the range of passive movement due to superimposed tremor
64
Q

Dopamine receptor agonists side effects

A
  • Ergot-derived dopamine receptor agonists (bromocriptine, cabergoline) have been associated with pulmonary, retroperitoneal and cardiac fibrosis - do ECG, ESR, creatinine and chest X-ray prior to treatment and close monitoring
  • Can cause impulse control disorders and excessive daytime sleepiness
  • More likely than levodopa to cause hallucinations in older patients
  • Nasal congestion and postural hypotension are also seen in some patients
65
Q

Describe levodopa and side effects

A
  • Usually combined with a decarboxylase inhibitor (carbidopa or benserazide) to prevent peripheral metabolism of levodopa to dopamine
  • Reduced effectiveness with time (2 years)
  • Unwanted effects: dyskinesia (writhing movements), on-off effect, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drowsiness
66
Q

Medications other than Levodopa used for Parkinson’s

A
  • MAO-B inhibitors - inhibits dopamine breakdown
  • COMT inhibitors - inhibits dopamine breakdwon, adjunct to Levodopa
  • Antimuscarinins - help with tremor and rigidity
  • Amantidine - thought to increase dopamine release and prevent reuptake at synapses
67
Q

Describe stroke types

A
  • TIA - if symptoms and signs last less than 24 hours
  • Thrombotic stroke - thrombosis from large vessels e.g. carotid
  • Embolic stroke - usually a blood clot but fat, air or clumps of bacteria may act as an embolus. AF is an important cause of emboli forming in the heart
  • Cerebral hemisphere infarcts - contralateral hemiplegia: initially flaccid then spastic, contralateral sensory loss, homonymous hemianopia, dysphasia
  • Brainstem infarction - may result in more severe symptoms including quadriplegia and lock-in-syndrome
  • Lacunar infarcts - small infarcts around the basal ganglia, internal capsule, thalamus and pons. May result in pure motor, pure sensory, mixed motor and sensory signs or ataxia
68
Q

Features of stroke

A
  • Motor weakness
  • Speech problems
  • Swallowing problems
  • Visual field defects - homonymous hemianopia
  • Balance problems
69
Q

Describe the acute stroke management

A
  • ABCDE assessment
  • Urgent neuroimaging to rule out haemorrhagic stroke
  • Thrombolysis (alteplase) - withing 4,5h of symptom onset, not had a previous intracranial haemorrhage, uncontrolled hypertension, pregnant
  • Aspiring 300mg - ASAP and antiplatelet therapy should be continued
70
Q

What is the management for a TIA with ABCD2 score >= 4

A
  • Aspirin - 300mg daily, started immediately
  • Specialist referral within 24 hours of onset of symptoms
  • Secondary prevention measures
71
Q

What is the management for a TIA with ABCD2 score <= 3

A
  • Specialist referral withing 1 week of symptom onset, including decision on brain imaging
  • If vascular territory or pathology is uncertain, refer for brain imaging
  • Crescendo TIAs (two or more episodes in a week) should be treated as being at high risk, regardless of ABCD2 score.
72
Q

Stroke differentials

A
  • Hypoglycaemia
  • Migrainous aura
  • Mass lesions
  • Syncope due to arrhythmia
  • Simple partial seizures
73
Q

What questions should you ask patient/ witness presenting with syncope

A
  • Precipitating factors?
  • Activity the patient was involved in before the event?
  • Position the patient was in when the event occurred? (i.e. detailed account by eyewitnesses)
  • Was loss of consciousness complete?
  • Was loss of consciousness with rapid onset and short duration?
  • Was recovery spontaneous, complete, and without sequelae?
  • Were there seizures? If so, describe it.
  • Was postural tone lost?
  • Patient’s medical history, esp cardiac disease.
  • Family history of cardiac disease?
74
Q

Red flags with syncope

A
  • Exertional onset
  • Chest pain
  • Dyspnoea
  • Low back pain
  • Palpitations
  • Severe headache
  • Focal neurological deficits, diplopia, ataxia or dysarthia
75
Q

How might constipation present in history and exam?

A
  • Less than 3 stools a week
  • Hard stools that are difficult to pass
  • Rabbit dropping stools
  • Straining and painful passages
  • Abdo pain
  • Abnormal posture (retentive posturing)
  • Rectal bleeding
  • Faecal impaction causing overflow soiling incontinence of loose smelly stools
  • Hard stool may be palpable in abdo
  • Loss of the sensation of the need to open bowels (desensitisation)
76
Q

What is Encopresis?

A

Faecal incontinence usually a sign of chronic constipation where rectum becomes stretched and looses sensation. Large hard stools remain in rectum and only loose stools are able to bypass blockage and leak out.

77
Q

What lifestyle factors can cause constipation?

A
  • Habitually not opening bowels
  • Low fibre diet
  • Poor fluid intake and dehydration
  • Sedentary lifestyle
  • Psychosocial problems
78
Q

What are some secondary causes for constipation?

A
  • Hirschsprung’s disease
  • Cystic fibrosis
  • Hypothyroidism
  • Spinal cord lesions
  • Sexual abuse
  • Intestinal obstruction
  • Anal stenosis
  • Cows milk intolerance
79
Q

Constipation red flags

A
  • Vomiting - intestinal obstruction of Hirschsprung’s disease
  • Ribbon stool - anal stenosis
  • Abnormal anus - anal stenosis, IBD or sexual abuse
  • Abnormal lower back or buttocks - spina bifida, spinal cord lesion or sacral agenesis
  • Acute severe abdo pain and bloating - obstruction or intussusception.
80
Q

Constipation complications

A
  • Pain
    • Reduced sensation
    • Anal fissures
    • Haemorrhoids
    • Overflow and soiling
    • Psychosocial morbidity
81
Q

Constipation management

A

Idiopathic constipation - rule out other diagnosis

  • Correct any reversible contributing factors
  • Start laxatives (movicol is first line)
  • Faecal impaction may require disimpaction regimen with high doses of laxatives at first
82
Q

What are the types of fractures?

A

Compound - skin is broken and broken bone is exposed to the air

Stable - the sections of bone remain in alignment at the fracture

Pathological - when a bone breaks due to an abnormality within the bone

83
Q

What terms can describe the way a bone breaks

A
  • Transverse
  • Oblique
  • Spiral
  • Segmental
  • Comminuted (breaking into multiple fragments)
  • Compression fractures (affecting the vertebrae in spine)
  • Greenstick (typically in children)
  • Buckle (torus)
  • Salter-Harris (growth plate fracture)
84
Q

Describe the types of wrist fractures

A

Colle’s fracture - transverse fracture of the distal radius near the wrist causing the distal portion to displace posteriorly (dinner fork deformity) usually caused by fall onto an outstretched hand.

Scaphoid fracture - tenderness in the anatomical snuffbox. Scaphoid has a retrograde blood supply so fracture can cut off blood resulting in avascular necrosis and non-union

85
Q

Describe the types of ankle fractures

A

Weber classification - describes fractures of lateral malleolus in relation to distal syndesmosis between the tibia and fibula.

  • Type A - below the ankle joint - will leave the sundesmosis intact
  • Type B - at the level of the ankle joint - the syndesmosis will be intact or partially torn
  • Type C - above the ankle joint - the syndesmosis will be disrupted
86
Q

Describe pelvic ring fractures

A

When one part of the ring fractures another will also fracture. Often leads to intra-abdominal bleeding which can lead to shock and death - needs emergency resuscitation and trauma management

87
Q

Describe a pathological fracture

A

Occur due to an underlying disease of the bone such as a tumour, osteoporosis or Paget’s disease. May occur with minor trauma or spontaneously. Common sites are femur and vertebral bodies.

88
Q

Describe the correlation between frailty and fractures

A

Occur due to weakness in the bone, usually osteoporosis, with minor trauma.

Risk of a fragility fracture over the next 10 years can be predicted using FAX score.

First line treatments to reduce risk are calcium and vitamin D and bisphosphonates.

89
Q

Fracture management

A

1st line - pain management

Straightforward fractures can be managed with closed reduction (manipulation of the limb), a plaster cast and follow-up in fracture clinic

Comples fractures requiring surgery (open reduction) refer to trauma and orthopaedics, make nil by mouth.

90
Q

Early fracture complications

A

Early complications:

  • Damage to local structures (tendons, muscles, arteries, nerves, skin)
  • Haemorrhage leading to shock
  • Compartment syndrome
  • Fat embolism
  • Venous thromboembolism due to immobility
91
Q

Longer term fracture complications

A

Longer-term complications:

  • Delayed union
  • Malunion
  • Non-union
  • Avascular necrosis
  • Infection
  • Joint instability
  • Joint stifness
  • Contractures
  • Arthritis
  • Chronic pain
  • Complex regional pain syndrome
92
Q

Describe fat embolism in fractures

A

Can occur after fracture of long bones e.g. femur. Fat globules are released into circulation following fracture and can become lodged in blood vessels and cause blood flow obstruction and systemic inflammatory response resulting in fat embolism syndrome.

Typically presents 24-72 hours after fracture.

93
Q

What is Gurds criteria for fat embolsim diagnosis

A

Major criteria:

  • Respiratory distress
  • Petechial rash
  • Cerebral involvement

Minor criteria includes:

  • Jaundice
  • Thrombocytopenia
  • Fever
  • Tachycardia
94
Q

Describe urge incontinence

A

Caused by overactivity or the detrusor muscle.

Suddenly feeling the urge to pass urine, having to rush. Can impact quality of life through anxiety of no toilet access.

95
Q

Describe stress incontinence

A

Pelvic floor is a sling of muscles to support pelvic contents with three canals running through: urethral, vaginal and rectal canals. Weak pelvic floor muscles means organs are poorly supported.

Stress incontinence is due to weakness of the pelvic floor and sphincter muscles which allows urine to leak at times of increased pressure on bladder e.g. laughing or coughing.

96
Q

Describe overflow incontinence

A

Occurs with chronic urinary retention due to obstruction to the outflow of urine. Results in an overflow of urine with no urge to pass urine.

More common in women

97
Q

Overflow incontinence causes

A
  • Anticholinergic medications
  • Fibroids
  • Pelvic tumours
  • Neurological conditions e.g. MS, diabetic neuropathy and spinal cord injuries.
98
Q

Incontinence risk factors

A
  • Increased age
  • Postmenopausal
  • Increase BMI
  • Previous pregnancies and vaginal deliveries
  • Pelvic organ prolapse
  • Pelvic floor surgery
  • Neurological conditions e.g. MS
  • Cognitive impairment and dementia
99
Q

Describe history taking for urinary incontinence

A

Medical history - distinguish between stress and urge incontinence

Modifiable lifestyle factors - caffiene consumption, alcohol consumption, medications, BMI

Severity - frequency of urination, frequency of incontinence, nighttime urination, use of pads and changes of clothing

100
Q

Describe examination for urinary incontinence

A

Examination - pelvic tone, pelvic organ prolapse, atrophic vaginitis, urethral diverticulum, pelvic masses

Bimanual examination to test pelvic muscles using the modified oxford grading system:

  • 0 - no contraction
  • 1 - faint contraction
  • 2 - weak contraction
  • 3 - moderate contraction with some resistance
  • 4 - good contraction with resistance
  • 5 - strong contraction, a firm squeeze drawing inwards
101
Q

Urinary incontinence investigations

A

bladder diary - track fluid intake and episodes of urination and incontinence over at least 3 days

Urine dipstick test - assess for infection, microscopic haematuria and other pathology

Post-void residual bladder volume - measured using bladder scan to assess for incomplete emptying

Urodynamic testing - when there is no response to first-line medical treatments,

102
Q

Describe urodynamic tests and types

A

Thin catheter inserted into bladder and rectum to measure pressure, bladder is filled with liquid.

  • Cystometry - measures detrusor muscle contraction
  • Uroflowmetry - measures flow rate
  • Leak point pressure - the point at which the bladder pressure results in leakage of urine including whilst coughing or jumping
  • Video urodynamic testing - filling bladder with contrast and taking eray images as the bladder is emptied (not routine)
103
Q

Non surgical management of stress incontinence

A
  • Avoid caffeine, diuretics and overfilling bladder
  • Avoid excessive or restricted fluid intake
  • Weight loss
  • Surgery
  • Supervised pelvic floor exercises - with specialist nurse or physiotherapist. Eight contractions three times daily
104
Q

Surgical management of stress incontinence

A
  • Tension-free vaginal tape (TVT) - mesh sling looped under urethra and up behind the pubic symphysis to the abdo wall
  • Autologous sling procedures - strip of fascia used rather than mesh in TVT
  • Colposuspension - stitches connecting anterior vaginal wall and pubic symphysis around urethra pulling vaginal wall forwards and adding support to urethra
  • Intramural urethral bulking - injections around urethra to reduce the diameter and add support.
105
Q

Non surgical management of urge incontinence

A
  • Bladder retraining - first line, increase time between bvoiding for at least 6 weeks
  • Anticholinergic medication - e.g. oxybutynin, tolterodine and solifenacin (S/E dry mouth, dry eyes, urinary retention, constipation, postural hypotension, cognitive decline)
  • Mirabegron - alternative to anticholinergic meds (contraindicated in uncontrolled hypertension, BP monitored regularly)
106
Q

Invasive procedures to manage urge incontinence

A
  • Botulinum toxin type A - injection into bladder wall
  • Percutaneous sacral nerve stimulation - implanting a device in the back that stimulates sacral nerves
  • Augmentation cystoplasty - using bowel tissue to enlarge bladder
  • Urinary diversion - redirecting urinary flow to a urostomy on the abdomen.
107
Q
A

Phase 3a (12 decks)

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