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Phase 3a Jemima > Geriatrics > Flashcards

Geriatrics Flashcards

1
Q

what is benign paroxysmal positional vertigo

A

it is a common cause of recurrent vertigo episodes triggered by head movement

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2
Q

is BPPV a central or peripheral cause of vertigo

A

it is a peripheral cause - problem is in the inner ear rather than the brain

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3
Q

how does BPPV present

A

it presents with head movements that cause vertigo - turning over in bed for example
symptoms settle after 20-60 seconds
asymptomatic between attacks
doesnt cause hearing loss or tinnitus

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4
Q

what is the cause of BPPV

A

it is caused by calcium carbonate crystals called otoconia that become displaces into the semicircular canals
the crystals disrupt the normal flow of endolymph through the canals thus confusing the vestibular system
head movement creates flow of endolymph in the canals triggering episodes of vertigo

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5
Q

what semicircular canal do the calcium carbonate crystals in BPPV most commonly get displaced into

A

the posterior semicircular canal

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6
Q

what can cause disruption of the calcium carbonate crystals in BPPV

A

idiopathic - no known cause
viral illness
head trauma
aging

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7
Q

what manoeuvre is used to diagnose BPPV

A

the Dix-Hallpike manoeuvre

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8
Q

how is the Dix-Hallpike manoeuvre used to diagnose BPPV

A

it involves moving the patients head in a certain way that it moves the endolymph through the semicircular canals and triggers vertigo
- will trigger rotational nystagmus and symptoms of vertigo

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9
Q

what is the Epley manoeuvre

A

it can be used to treat BPPV
- moves crystals into a position that it doesnt disrupt endolymph flow

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10
Q

what are Brandt-daroff exercises

A

these are exercises that the patient can perform at home to improve the symptoms of BPPV

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11
Q

what do the Brandt-dartoff exercises involve

A

sitting on the end of a bed and lying sideways, rolling from one side to the other, while rotating the head slightly to face the ceiling

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12
Q

what are causes of BPPV

A

mostly idiopathic
head injury
post viral illness
labyrinthitis
complications of surgery

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13
Q

what are risk factors of BPPV

A

older age (40-60)
female
manières disease
patients with migraines or anxiety disorders

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14
Q

how do you treat BPPV

A

normally self limiting
repositioning techniques
anti-emetics: prochlorperazine/cyclizine
vestibular seditives: cinnarizine/betahistine
surgery in patients with incurable symptoms - denervate or obliterate the semicircular canal

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15
Q

what is chronic heart failure

A

it is the clinical features of impaired heart function of the left ventricle to pump blood out of the heart and round the body

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16
Q

what are the results of impaired left ventricular function

A

-chronic backing up of blood
- left atrium, pulmonary veins and lungs experience increased volume and pressure of blood
-this causes fluid to leak and it cant be reabsorbed
-this leads to pulmonary oedema

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17
Q

what is ejection fraction

A

it is the percentage of blood in the left ventricle ejected with each ventricular contraction

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18
Q

what ejection fraction is considered normal

A

anything above 50%

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19
Q

what is heart failure with reduced ejection fraction

A

this is when the ejection fraction is less than 50% - due to left ventricular disfunction

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20
Q

what is heart failure with preserved ejection fraction

A

it is when someone has the clinical features of heart failure but an ejection fraction greater than 50%
- this is due to diastolic dysfunction (issue with left ventricle filling)

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21
Q

what are causes of chronic heart failure

A

ischaemic heart disease
valvular heart disease - aortic stenosis
hypertension
arrhythmias - atrial fibrillation
cardiomyopathy

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22
Q

what are symptoms of chronic heart failure

A

breathlessness - worse on exertion
cough - frothy white/pink sputum
orthopnoea - breathlessness when lying flat
paroxysmal nocturnal dyspnoea - sudden waking at night with severe SOB, cough, wheeze
peripheral oedema - bilateral
fatigue

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23
Q

what are signs of chronic heart failure on examination

A

tachycardia
tachypnoea
hypertension
murmurs
3rd heart sound
bilateral basal crackles
raised JVP - backlog of right side of heart
peripheral oedema - bilateral

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24
Q

what causes paroxysmal nocturnal dyspnoea

A
  1. fluid settles across a large area of the lungs when lying down causing breathlessness
  2. during sleep the resp. centre of the brain becomes less responsive allowing for more significant pulmonary congestion and hypoxia
  3. less adrenalin when asleep meaning the myocardium is more relaxed, reducing co
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25
Q

what investigations should be done for someone with suspected heart failure

A

clinical assessment - history and exam
N-terminal pro-B-type natriuretic peptide (NT-proBNP) blood test
ECG
ECHO
bloods - FBC, U+E, TFT, LFT, lipids, blood glucose
CXR and lung function tests

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26
Q

what is the new york heart association classification

A

it is a system used to grade the severity of symptoms related to heart failure

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27
Q

what are the different grades in the new york heard association classification

A

class 1 - no limitation on activity
class 2 - comfortable at rest but symptomatic with ordinary activities
class 3 - comfortable at rest but symptomatic with any activity
class 4 - symptomatic at rest

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28
Q

what are the five principles of management for someone with heart failure (RAMPS)

A

Refer to cardiology
Advise them on the condition
Medication
Procedural or surgical interventions
Specialist heart failure MDT

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29
Q

what are the guidelines on when to refer depending on the NT-proBNP result

A

400-2000 ng/L should be seen and have an echo within 6 weeks
above 2000 ng/L should be seen and have an echo within 2 weeks

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30
Q

what lifestyle management can you advise someone who has heart failure

A

flu, covid and pneumococcal vaccinations
stop smoking
cardiac rehabilitation - personalised exercise programme

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31
Q

what is the medical treatment for heart failure (ABAL)

A

ACE inhibitor - ramipril
Beta blocker - bisoprolol
Aldosterone antagonist - spironolactone
Loop diuretics - furosemide/bumetanide

angiotensin receptor blockers (candesartan) can be used instead of ACE inhibitor if its not well tolerated

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32
Q

what needs to be carefully monitored in patients on diuretics, ACE inhibitors and aldosterone antagonists

A

U+E as all three of these medications can cause electrolyte imbalances
- hyperkalaemia !!

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33
Q

other than ABAL management plan what other medications may be used in heart failure

A

SGLT2 inhibitor - dapagliflozin
sacubitril with valsartan
ivabradine
hydralazine with a nitrate
digoxin

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34
Q

what surgical interventions are done in the management of heart failure

A
  1. implantable cardioverter defibrillators - continually monitor HR and apply a shock if it identifies a shockable arrhythmia
  2. cardiac resynchronisation therapy - used in severe heart failure (EJ less than 35%), and involves biventricular pacemakers which aims to synchronise heart chamber contractions
  3. heart transplant
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35
Q

what are common symptoms of constipation

A

two or more of the following related to over 25% of bowel movements
- straining
- lumpy hard stool
- sense of incomplete emptying
- need for manual maneuvers
- fewer than 3 bowel movements in a week

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36
Q

what is considered normal stool on the bristol stool chart

A

4

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37
Q

what other sensations can constipation be associated with

A

feeling of fullness
bloating
stomach pain
reduced appetite

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38
Q

what can prolonged constipation lead to

A

fecal impaction

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39
Q

what is fecal impaction

A

this is a mass of hard stool in the rectum or colon
it is very uncomfortable and associated with pain, diarrhoea/incontinence

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40
Q

what shouldnt be given in fecal impaction

A

laxatives as it can make it worse by creating more pressure and movement upstream of the blockage

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41
Q

what are common causes of constipation in the elderly

A

multifactorial
medication side effects
insufficient fibre/water
electrolyte imbalance - calcium, potassium and magnesium
endocrine disorders
chronic nerve dysfunction
IBS
pelvic floor dysfunction
anxiety
depression
reduced physical activity
mechanical obstruction

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42
Q

what medications can cause constipation

A

anticholinergics - antihistamines, medication for overactive bladder, muscle relaxants
opiates
diuretics
calcium and iron supplements

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43
Q

what are red flags of constipation

A

blood in stool
new weight loss
new/rapidly worsening symptoms

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44
Q

how do you treat constipation

A

identify and reduce constipating medication is possible
increase dietary fibre and water
encourage regular exercise
laxatives

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45
Q

what laxatives are good for constipation in the elderly

A

osmotic agents - lactulose/sorbitol/miralax
stimulant agents - senna/bisacodyl
bulking agents - methylcellulose

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46
Q

how is fecal impaction treated

A

enemas
suppositories

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47
Q

what type of enemas should be used in fecal impaction

A

use warm tap water or mineral oil enemas

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48
Q

what type of laxatives should be avoided long term due to toxicity

A

magnesium based laxatives

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49
Q

what laxatives should be avoided in fecal impaction (especially)

A

bulking agents

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50
Q

what is delirium

A

acute, transient and reversible state of confusion usually as a result of organic processes

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51
Q

how common is it for elderly patients to get delirium

A

one in five elderly patients on medical or surgical wards are affected by delirium

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52
Q

what are the clinical features of delirium

A

there are hyperactive and hypoactive states which the patients often fluctuate between

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53
Q

what are the clinical features of hyperactive delirium

A

typical delirium presentation
- agitation
- delusions
- hallucinations
- wandering
- aggression

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54
Q

what are the clinical features of hypoactive delirium

A

lethargy
slowness with everyday tasks
excessive sleeping
inattention

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55
Q

what are common causes of delirium

A

CHIMPS PHONED
constipation
hypoxia
infection
metabolic disturbance
pain
sleeplessness
prescriptions
hypothermia/pyrexia
organ dysfunction - hepatic/renal issues
nutrition
environmental changes
drugs

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56
Q

what assessment scores can be used to assess delirium

A

abbreviated mental test score
mini mental state exam
ACE III

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57
Q

what bloods should be performed on someone with delirium

A

FBC
U+E
LFT
coagulation/INR
TFTs
calcium
B12 and folate/haematinics
glucose
blood cultures

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58
Q

what should be included in a confusion screen

A

urinalysis
bloods
imaging - CT head, CXR

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59
Q

what is the general supportive management for delirium

A
  • keep consistent nursing and medical team, re-orientation, calm and consistent care
  • clear and concise communication
  • ensure the patient has access to aids such as glasses, hearing aids, walking sticks
  • enable the patient to do what they can for themselves
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60
Q

what environmental adaption management strategies can be used to help someone with delirium

A
  • ensure there is access to a clock and other orientation reminders for day/date/time
  • have familiar objects where possible
  • involve the family/friends and or/carers in the care of the patient
  • control the level of noise around the patient
  • ensure lighting and temperature is okay
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61
Q

what medication can be used in delirium

A

haloperidol is usually the first line medication option - 0.5mg
if benzodiazepines are used lorazepam is first line (0.5mg)

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62
Q

what can you do to prevent episodes of delirium

A

avoid drugs known to precipitate delirium - opiates and benzodiazepines
identify patients at higher risk of developing delirium
assess other factors which may induce or exacerbate delirium (pain control, drugs etc)
employ supportive/environmental management

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63
Q

what are precipitating factors of delirium

A

new illness
recent discharge from hospital
falls
acute or chronic pain
poor oral intake
recent changes in environment
comorbidities
current medication
alcohol use
sensory impairment

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64
Q

what is the 4As test (4AT)

A

it is a short four item tool to assess delirium
- alertness
- cognition (test of orientation)
- attention (recitation of months backwards)
- presence of acute change or fluctuating course

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65
Q

what is dementia

A

it is an irreversible, progressive decline and impairment of more than one aspect of higher brain function

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66
Q

what are the different types of dementia

A

alzheimers
fronto-temporal
lewy body
vascular

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67
Q

what is the cause of alzeimers dementia

A

amyloid plaques (beta amyloid) and neurofibrillary tangles (tau) build up within the brain, leading to reduction in information transmission and eventually the death of brain cells

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68
Q

what are the clinical features of alzheimers dementia

A

normally develops after the age of 60
can affect all areas of the brain
most common presenting symptom is memory loss with varying changes in planning, reasoning, speech and orientation

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69
Q

what areas of the brain are affected by alzheimers disease

A

entorhinal cortex and the hippocampus
- later affects areas in cerebral cortex responsible for language, reasoning and social behaviour

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70
Q

what causes vascular dementia

A

micro-infarcts within the brain

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71
Q

what is the progression of vascular dementia like

A

it is a stepwise progression, often showing periods of stability at one level of functioning before an acute decline progression

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72
Q

what are the most commonly affected areas in vascular dementia

A

white matter of both cerebral hemispheres, grey nuclei, thalamus and striatum

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73
Q

what are risk factors for developing vascular dementia

A

hypertension - major rf
smoking
diabetes
hyperlipidaemia
obesity
hypertension

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74
Q

what are the clinical features of vascular dementia

A

mood disturbances and disorders are common in vascular dementia
psychosis, delusions, hallucination and paranoia can often be seen in later disease
emotional lability can be prominent

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75
Q

what is disease progression like in lewy body dementia

A

it is very rapid - death most commonly occurs in the first 7 years post diagnosis

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76
Q

what causes lewy body dementia

A

spherical lewy body proteins (alpha syncluein) are deposited within the brain

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77
Q

what are the clinical features of lewy body dementia

A

Visual hallucinations and parkinson like symptoms
problem multitasking
problems performing complex cognitive actions
sleep disorders and fluctuation

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78
Q

what causes frontotemporal dementia

A

neuron damage and death in the frontal and temporal lobes
- atrophy due to deposition of abnormal proteins (tau) within the lobes

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79
Q

what behavioural presentations can be seen in frontotemporal dementia

A

altered emotional responsiveness, apathy, disinhibition, impulsivity
progressive decline noted in interpersonal skills
changes in food preference - more childlike
obsessions and rituals may be noted

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80
Q

what semantic presentations can be seen in frontotemporal dementia

A

progressive decline in the understanding of word meanings
speech may still be fluent but there is difficulty in name retrieval and use of less precise terms
are unable to determine the meanings of common words when asked
tens to develop into the inability to recognise objects, or familiar faces

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81
Q

what non fluent presentations can be seen in frontotemporal dementia

A

progressive breakdown in the output of language
the speech takes effort and is not fluent
speech apraxia or disorders of speech sound
there also tends to be impaired comprehension of sentences and an impact on literacy skills

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82
Q

what are ddx of dementia

A

prion protein disease
HIV related cognitive impairment/decline
normal pressure hydrocephalus
severe depression
mild cognitive imapairment

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83
Q

what are the man ways in treating alzheimers

A

Acetylcholinesterase inhibitors - donepezil (more severe) , rivastigmine, galantamine (mild-moderate)
memantine - severe

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84
Q

what are side effects of memantine

A

headaches
dizziness
constipation

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85
Q

what non medication treatments are used in dementia

A

cognitive stimulation therapy - memory, problem solving, language ability
cognitive rehabilitation
reminiscence and life story work

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86
Q

what is the risk of someone over 65 falling at least once per year

A

30%

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87
Q

what is the risk of someone over 80 falling at least once per year

A

50%

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88
Q

what questions are important to ask in a falls history

A

when did they fall
who saw them fall/were they alone
where did they fall
was there any warning/dizziness/chest pain
was there any incontinence/tongue biting
was there loss of consciousness
did they injure themselves
what happened after
could they get up off the floor after the fall
any weakness after the fall
why do they think they fell
how many times has this happened

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89
Q

what symptoms are important to ask about in a falls history

A

chest pain
dizziness
palpitations
shortness of breath
cough
loss of consciousness
seizures
sensory or motor disturbance
abdo pain - diarrhoea or constipation
joint pain
muscle weakness

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90
Q

what types of medications can commonly cause falls

A

beta blockers
diabetic medications (hypoglycaemia)
antihypertensives (hypotension)
benzodiazepines (drowsiness)
antibiotics

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91
Q

what investigations should be done in someone who has had a fall

A

vitals - BP, HR, O2, temp
lying and standing BP
urine dipstick
ECG, ECHO
blood glucose
cognitive screening
FBC, U+E, LFT
bone profile
CXR, CT head

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92
Q

what is assessed in a patient when completing a complete falls risk assessment

A
  • gait
  • visual problems
  • hearing problems
  • medication review
  • alcohol intake
  • postural hypotension
  • cognitive decline
  • foot wear
  • continence
  • environmental hazards
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93
Q

what is the 30 day mortality of a hip fracture

A

5-10 %

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94
Q

what are major risk factors for getting a hip fracture

A

increased age and osteoporosis

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95
Q

what are the two types of hip fracture

A

intra capsular
extra capsular

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96
Q

how quickly should surgery be performed after a hip fracture

A

within 48 hours ideally

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97
Q

what are the anatomical parts of the top of the femur

A

head
neck
greater trochanter (lateral)
lesser trochanter (medial)
intertrochanteric line
shaft

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98
Q

what is the anatomical structure of the hip joint

A

the capsule of the hip (strong fibrous structure) attaches to the rim of the acetabulum on the pelvis and the intertrochanteric line on the femur, and surrounds the head and neck of the femur

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99
Q

what is the blood supply of the femur

A

it is a retrograde blood supply
- medial and lateral circumflex femoral artery

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100
Q

what is an intracapsular neck of femur fracture

A

this is when the break in the femoral neck occurs within the capsule of the joint
- proximal to the intertrochanteric line

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101
Q

what are the risks of an intracapsular neck of femur fracture

A

commonly affects the blood supply and can cause avascular necrosis of the bone

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102
Q

what is the Garden classification of intracapsular NOF fractures

A

class I: incomplete fracture and non displaced
class II: complete fracture and non displaced
class III: partial displacement
class IV: total displacement

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103
Q

what classifications of intracapsular NOF fractures will have a disrupted blood supply

A

displaced fractures
- non displaced fractures may still have an intact blood supply

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104
Q

what is a hemiarthroplasty

A

this is when the head of the femur is replaced but the acetabulum is not.
Cement is used to hold the stem of the prosthesis in the shaft of the femur

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105
Q

what is a total hip replacement

A

this is when both the head of the femur and the acetabulum is replaced

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106
Q

what are types of extracapsular hip fractures

A

intertrochanteric fracture
subtrochanteric fracture

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107
Q

what is an intertrochanteric fracture

A

this is when the fracture occurs between the greater and lesser trochanter

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108
Q

how is a intertrochanteric fracture surgically treated

A

with a dynamic hip screw

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109
Q

what is a subtrochanteric fracture

A

this is a fracture that is below the lesser trochanter and proximal to the shaft of the femur

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110
Q

how is a subtrochanteric fracture treated surgically

A

with an intramedullary nail

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111
Q

how does a hip fracture present

A

with pain in the groin or hip which may radiate to the knee, often unable to weight bare
- Shortened, abducted and externally rotated leg

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112
Q

what investigations should be done for a suspected hip fracture

A

x-ray - anterior-posterior and lateral views
MRI/CT if the X ray is negative but fracture is suspected

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113
Q

how is a hip fracture treated

A

analgesia
VTE risk assessment and prophylaxis
surgery

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114
Q

what is frailty

A

health state related to the aging process in which multiple body systems gradually lose their built in reserves
- increase risk of adverse outcomes such as falls, delirium and disability

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115
Q

what is the pathophysiology of aging

A

there is an accelerated decline in physiological reserve and normal mechanisms begin failing

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116
Q

what is the issue with frailty in the elderly

A

it increases the potential for serious adverse outcomes after seemingly minor stressor events

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117
Q

when should frailty in the elderly be assessed

A

routine outpatient appointments
social services assessment for care and support
review by community care teams after referral
primary care review of older people
home carers in the community
ambulance crews

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118
Q

what is the phenotype model of frailty

A

describes a group of characteristics - unintentional weight loss, reduced muscle strength, reduced gait speed, self reported exhaustion and low energy expenditure.
- generally individuals with three or more are said to have frailty

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119
Q

what is the cumulative deficit model of frailty

A

it assumes an accumulation of deficits (loss of hearing, low mood, tremor, dementia etc) which can occur with increasing age and which combine to increase the frailty index

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120
Q

what is a central clinical feature of frailty

A

loss of skeletal muscle function

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121
Q

how can you help prevent frailty

A

physical activity - resistance exercise
sufficient diet
reduction in smoking

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122
Q

what is acute malnutrition

A

this is a brief period of inadequate nutrition that is most commonly due to an acute illness with a high inflammatory state, such as pneumonia
results in muscle wasting and rapid weight loss

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123
Q

what is malnutrition

A

it is the sudden/chronic decrease in the intake of sufficient nutrition

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124
Q

what is chronic malnutrition

A

this is inadequate nutrition which lasts longer than three months
often secondary to social, behavioural and economic factors

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125
Q

what parameters are measured in the Malnutrition Universal Screening Tool (MUST)

A

weight
height
BMI
% unplanned weight loss
acute illness score - patient is acutely unwell and there has been no/likely to have been no nutritional intake for >5 days

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126
Q

what are the three main reasons why someone might become malnourished

A

inadequate amounts of nutrients
difficulty absorbing nutrients
increased nutritional needs

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127
Q

what are risk factors for malnutrition

A

being hospitalised for extended periods of time
problems with dentition, taste or smell
polypharmacy
social isolation and loneliness
mental health issues
cognitive issues - confusion

128
Q

what clinical features of malnutrition are seen in adults

A

high susceptibility or long durations of infections
slow or poor wound healing
altered vital signs including bradycardia, hypotension, hypothermia
depleted subcutaneous fat stores
low skeletal muscle mass

129
Q

what are important areas to cover in the history when querying malnutrition

A

weight history - current, recent changes to weight, changed to clothing fit
meal history
protein intake
hydration

130
Q

how is malnutrition treated

A

involve dieticians
oral nutrition should be used as long as possible - can use things like forticepts to help nutrition
if the patient is unable to swallow safely or unable to take sufficient calories then nasogastric feeding should be considered
for long germ feeding a gastrostomy (PEG/RIG) or jejunostomy should be considered

131
Q

what is re-feeding syndrome

A

this is a condition caused by a rapid re-introduction of normal nutrition to a patient who was chronically malnourished
- key electrolytes such as potassium and phosphate are depleted
- when there is normal levels of nutrition these electrolytes with shift from extracellular to intracellular due to large insulin response
- this can cause hypokalaemia and hypophosphataemia

132
Q

what can re feeding syndrome lead to

A

cardiac complications - arrhythmias
seizures

133
Q

what are complications of malnutrition

A

impaired immunity
poor wound healing
growth restriction in children
unintentional weight loss - muscle mass
multi organ failure
death

134
Q

what is an advanced directive

A

it is a statement explaining what medical treatment the individual would not want in the future should they lack capacity
this is a legally binding document - written with a lawyer present

135
Q

what are the advantages of an advanced directive

A

it enables an individual to think about what they would like to happen to them in the event they lose capacity.

136
Q

what are limitations of an advance directive

A

an advance directive cannot be used to
- ask for specific medical treatment
- request something illegal
- choose someone to make decisions for you unless that person is given lasting power of attorney
- refuse treatment for a mental health condition

137
Q

when might a doctor not follow an advanced directive

A
  • the individual makes changes which invalidates the directive
  • there have been advances in treatment which may have affected the initial treatment
  • there is ambiguity in the working of the directive
138
Q

what is advanced care planning

A

it is a voluntary process
it is a discussion between an individual and their care providers about their preferences and priorities for their future care, while they have mental capacity

139
Q

what is an advanced statement

A

it is wishes, preferences and priorities of a patient and may include nomination of a names spokes person
- not legally binding

140
Q

what is is a lasting power of attorney

A

this is someone who has been nominated to make decisions up to or including life sustaining treatment on behalf of someone who no longer has mental capacity
- this is legally binding
- this is LPA for health and welfare

141
Q

who might benefit from ACP conversations

A

people facing the prospect of deteriorating health due to long term conditions
people with declining functional status
people facing key transitions in their health and care needs
people facing major surgery or high risk tx
people facing acute life threatening conditions

142
Q

what is osteoporosis

A

this is a progressive, systemic skeletal disorder characterised by reduced bone density

143
Q

what is the precursor to osteoporosis

A

osteopenia

144
Q

is the pathophysiology of osteoporosis

A

when there is a mismatch between activity of osteoclasts and osteoblasts causing high bone resorption - either through increased osteoclast activity or decreased osteoblast activity
this eventually leads to lower bone density

145
Q

what are general risk factors for osteoporosis

A

increased age
female sex
post menopause - early menopause
reduced mobility and activity
low BMI
smoking
alcohol intake over 3 units per day
parental history of hip fracture
previous fragility fracture

146
Q

what are medical conditions which increase the risk of osteoporosis

A

rheumatoid arthritis
primary hyperparathyroidism
chronic kidney disease
gastrointestinal disease - IBD, coeliac
hyperthyroidism
chronic liver disease

147
Q

what medications increase the risk of osteoporosis

A

corticosteroids - any dose orally for over three months, and doses above 7.5mg/day
SSRI
PPI
anti-epileptics
anti-oestrogens

148
Q

what is a fragility fracture

A

it is a low impact fracture from standing height or less

149
Q

what are the most common sites for fragility fracture

A

vertebral
hip - proximal femur
wrist - distal radius

150
Q

how do you assess fracture risk

A

FRAX tool - calculates the 10 year fracture probability

151
Q

what factors does the FRAX score take into account

A

age
sex
BMI
previous fracture
parental hip fracture
smoking status
alcohol consumption
glucocorticoid use
rheumatoid arthritis
secondary osteoporosis

152
Q

when should you start assessing someones fracture risk

A

all women over 65
all men over 75
women under 65 and men under 75 with risk factors

153
Q

what would the management plan for someone who is at low risk of fracture in the next 10 yrs

A

no need to measure bone marrow density (DEXA)
give lifestyle advise and reassurance
monitor risk factors

154
Q

what would management be for someone who is at intermediate risk for fracture in the next 10 yrs

A

arrange a DEXA scan and recalculate the risk score with BMD taken into account
monitor risk factors

155
Q

what would the management be for someone who is at high risk of fracture in the next 10 years

A

offer treatment
arrange DEXA scan to help guide treatment

156
Q

what populations may the risk assessment tools underestimate the fracture risk in

A

patients over 80
multiple previous fragility fractures
patients taking oral glucocorticoids - >7.5mg prednisolone for 3 months or more

157
Q

what two regions are typically used for a DXA scan

A

the femoral neck and the spine

158
Q

what is the T score for a DXA scan

A

it is the number of standard deviations the patients bone density is from the mean bone density of a normal 30 yr old adult

159
Q

what is the z score for a DXA scan

A

it is the number of standard deviations the patients bone density is from the mean bone density of age and gender matched control

160
Q

what other investigations may be done for someone with suspected osteoporosis

A

bone profile
U+E
vitamin D
PTH
thyroid function tests
testosterone

161
Q

what T score indicates osteopenia

A

-1 to -2.5

162
Q

what T score indicates osteoporosis

A

< -2.5

163
Q

what T score indicates severe osteoporosis

A

< -2.5 AND previous fracture

164
Q

what lifestyle advice should be given to someone with osteoporosis

A

regular exercise - strength based and weight baring exercise
stop smoking
reduce alcohol intake
adequate dietary calcium intake (minimum 700mg/day)
adequate vitamin D intake
maintaining a healthy weight

165
Q

what should patients with vitamin D below 50nmol/L be offered

A

rapid correction: 300,000 IU vitamin D3 over 6-10 weeks
maintenance 800-2,000 IU vitamin D3/day

166
Q

what is the first line treatment for patients with osteoporosis

A

bisphosphonates
- alendronic acid: 10mg daily or 70mg weekly
- ibandronic acid
- risendronate sodium: 5mg daily, 53mg weekly
- zoledronic acid: 5mg IV once per year

167
Q

what advice needs to be given about taking oral bisphosphonates

A

should always be taken on an empty stomach
tablets should be swallowed whole with a glass of water in an upright position
remain upright for 30 minutes after taking the medication

168
Q

what are the potential side effects of bisphosphonates

A

gastrointestinal upset - dyspepsia and reflux
atypical fractures
osteonecrosis of the jaw - swelling, pain, erythema

169
Q

what non bisphosphonate treatment can be given to help osteoporosis

A

Denosumab - monoclonal antibody which binds RANKL and reduces osteoclast activity
Teriparatide - synthetic parathyroid hormone
Raloxifene - selective oestrogen receptor modulator (also reduced risk of oestrogen receptor positive breast cancer but does increase VTE risk)
Hormone replacement therapy
Romosozumab - increases new bone formation and decreases bone resorption

170
Q

how long is the typical course of bisphosphonates

A

normally a five year oral course or three year IV course, then the patient should be reassessed
if the patient falls below the treatment threshold then they can come off the drugs with a review in 2 years. If not then they should continue treatment for up to 10 yrs oral and 6 yrs IV

171
Q

what are complications of osteoporosis

A

hip fractures
rib fractures
wrist fractures
vertebral fractures
chronic pain

172
Q

what is Parkinsons disease

A

it is a disease causing progressive reduction in dopamine in the basal ganglia, leading to movement disorder

173
Q

are the symptoms of parkinsons symmetrical or asymmetrical

A

asymmetrical

174
Q

what is the classic triad of parkinsons disease

A

Resting tremor
Rigidity
Bradykinesia

175
Q

what is the pathophysiology of parkinsons

A

The basal ganglia is responsible for coordinating habitual movements such as walking, controlling voluntary movements and learning specific movement patters. Dopamine plays an essential role in its function (from nigrostriatal pathway) and in parkinsons there is a slow but progressive drop in dopamine production

176
Q

what are the features of a parkinsons tremor

A

worse on one side
4-6hz frequency
pill rolling
noticeable at rest
gets better with movement
performing a task with the other hand exaggerates the tremor

177
Q

what are the features of parkinsons rigidity

A

there will be tension - resistance to passive movement
when passively moving a limb there will be tension in it that gives way to movement in small increments - cogwheel rigidity

178
Q

what are features of parkinsons bradykinesia

A

handwriting gets smaller
small steps when walking - shuffling gait
rapid frequency of steps to compensate for the small steps and to avoid falling over
difficulty initiating movement
difficulty turning around when standing
reduced facial movement and expressions

179
Q

what are other symptoms of parkinsons other than the core three sx

A

depression
sleep disturbance and insomnia
loss of the sense of smell
postural instability
cognitive impairment and memory issues

179
Q

what are the features of benign essential tremor

A

symmetrical
6-12hz
improves at rest
worse with intentional movement
improves with alcohol

180
Q

what are examples of parkinson plus syndromes

A

multiple system atrophy
dementia with lewy bodies
progressive supranuclear palsy
corticobasal degeneration

181
Q

what is multiple system atrophy

A

it is a rare condition where the neurones of various systems in the brain degenerate which includes the basal ganglia
it also leads to autonomic dysfunction and cerebellar dysfunction

182
Q

how is parkinsons diagnosed

A

clinically diagnosed on the history and exam
NICE guidelines recommend the UK parkinsons disease society brain bank clinical diagnostic criteria

183
Q

what are the treatments for parkinsons

A

Levodopa combined with peripheral decarboxylase inhibitors
COMT inhibitors
dopamine agonists
monoamine oxidase B inhibitors

184
Q

How does levodopa work in parkinsons

A

it is a synthetic dopamine and is the most effective treatment for symptoms but becomes less effective over time

185
Q

what is levodopa often combined with

A

it is usually combined with a peripheral decarboxylase inhibitor which stops it being metabolised in the body before it reaches the brain

186
Q

what is the main side effect of levodopa

A

dyskinesia - abnormal movements associated with excessive motor activity

187
Q

what are examples of dyskinesia side effects you can get from levodopa

A

Dystonia
chorea
athetosis

188
Q

what is dystonia

A

where excessive muscle contraction leads to abnormal postures or exaggerated movements

189
Q

what is chorea

A

it is abnormal involuntary movements that can be jerking and random

190
Q

what is athetosis

A

it is involuntary twisting or writhing movements usually in the fingers, hands or feet

191
Q

what can be used to manage dyskinesia associated with levodopa

A

amantadine - glutamate antagonist

192
Q

what are COMT inhibitors

A

they are inhibitors of catechol-o-methyltransferase, which metabolises levodopa in the body and brain
they are often taken with levodopa to slow its breakdown and extend its duration

193
Q

what is an example of a COMT inhibitor

A

entacapone

194
Q

what are examples of dopamine agonists

A

bromocriptine
pergolide
cabergoline

195
Q

what is a side effect of prolonged use of dopamine agonists

A

pulmonary fibrosis

196
Q

what are monoamine oxidase B inhibitors

A

they block the action of monoamine oxidase B enzymes which break down dopamine, serotonin and adrenaline thus increasing circulating dopamine.
they are are typically used to delay the use of levodopa

197
Q

what are examples of monoamine oxidase B inhibitors

A

selegiline
rasagiline

198
Q

what are symptoms can be caused polypharmacy

A

tiredness
sleepiness
decreased alertness
confusion
falls
depression
weakness
tremors
visual or auditory hallucinations
anxiety
dizziness

199
Q

what can polypharmacy lead to in the elderly

A

adverse drug reactions
decreased medication compliance
poor quality of life
unnecessary drug expenses

200
Q

what can be done to reduce the incidence and adverse effects of polypharmacy in the elderly

A

regular evaluations of medications - monthly
a single drug should be prescribed instead of multiple to treat a single condition
medications should be started with a lower dosage where possible
drugs taken once/twice a day should be prescribed over those you have to take more frequently
if a drug has no therapeutic benefit it should be stopped

201
Q

what are pressure ulcers

A

they are areas of damage to skin and the tissue underneath due extended periods of pressure on one area of the body

202
Q

where do pressure ulcers usually form

A

bony parts of the body such as heels, elbows, hips and tailbone

203
Q

what are symptoms of pressure ulcers

A

discoloured patches of skin that do not change colour when pressed
a patch of skin tat feels warm, spongy or hard
pain or itchiness in the affected area
blister/open wounds in the area

204
Q

what are causes of pressure sores

A

mobility issues
previous pressure ulcer
in intensive care or recent surgery
underweight
swollen, sweaty or broken skin
poor circulation or fragile skin
have problems feeling sensation/pain

205
Q

how do pressure ulcers develop

A

they develop when a large amount of pressure is applied to an area over a short period of time/less pressure applied over a longer period. This pressure disrupts the flow of blood through the skin, causing the skin to become starved of oxygen and nutrients, leading to skin break down

206
Q

how many people admitted to hospital with a sudden illness will get a pressure ulcer

A

around 1 in 20

207
Q

what is the treatment for pressure ulcers

A

use of dressings
creams/gels to help the healing process and relieve pressure
surgery recommended for the most serious cases

208
Q

how can you prevent pressure ulcers

A

regularly changing the persons position
using equipment to protect vulnerable parts of the body - mattresses and cushions

209
Q

what is a grade 1 pressure ulcer

A

most superficial
affected area of skin appears discoloured
dont turn white when pressure is put on them
skin intact but they may hurt or itch
can feel warms, spongy or hard

210
Q

what is a grade 2 pressure ulcer

A

there is some epidermis or dermis damage leading to skin loss
the ulcer looks like an open wound/blister

211
Q

what is a grade three pressure ulcer

A

skin loss occurs through out the entire thickness of the skin
the underlying tissue is also damaged although underlying muscle and bone are not
ulcer appears as a deep cavity like wound

212
Q

what is a grade 4 pressure ulcer

A

most severe type of ulcer
the skin is severely damaged and there is tissue necrosis
the underlying muscles or bone may be damaged
high risk of life threatening infection

213
Q

who is at increased risk of developing pressure ulcers

A

those with mobility problems
poor nutrition
underlying health condition that disrupts blood supply or makes skin vulnerable to damage
being over 70
urinary or bowel incontinence
serious mental health conditions

214
Q

what health conditions increase risk of pressure ulcers

A

type 1 and type 2 diabetes
peripheral arterial disease
heart failure
kidney failure
COPD

215
Q

what care team will be involved in pressure ulcer management

A

tissue viability nurse
social worker
physiotherapist
occupational therapist
dietician
surgeons if bad enough

216
Q

what dressings are used for pressure ulcers

A

hydrocolloid dressings
alginate dressings

217
Q

what are complications of pressure ulcers

A

cellulitis
blood poisoning + sepsis
bone and joint infection
necrotising fasciitis
gas gangrene

218
Q

what is the pathophysiology of squamous cell carcinoma

A

cancerous mutations occur in squamous keratinocytes in the epidermis which lie within the stratum spinosum

219
Q

what are the five layers of the epidermis

A

stratum corneum
stratum lucidum
stratum granulosum
stratum spinosum
stratum basale

220
Q

what is the main cause of squamous cell carcinoma

A

ultraviolet exposure - UVB

221
Q

what are risk factors for squamous cell carcinoma

A

ultraviolet radiation
immunosuppression
Fitzpatrick skin types I and II
solid organ transplant recipients
increasing age
male sex
ionising radiation
sites of chronic inflammation

222
Q

what is the morphology of a squamous cell lesion like

A

firm to palpate - may be nodular/plaque like
may ulcerate and bleed
may be tender/painful
may have a crust top with a nodular base
size is variable

223
Q

what is Bowens disease

A

it is also known as SCC in situ and it occurs when the cancerous cells are confined to the epidermis

224
Q

what is actinic keratosis

A

involves the formation of precancerous scaly lesions on the skin - about a 10% risk of developing into SCC

225
Q

how is SCC investigated

A

punch or incisional biopsy
ultrasound of lymph nodes and CT/MRI for staging or if metastasis is suspected

226
Q

what classification systems exist for SCC

A

histopathological
clinicopathological
borders classification

227
Q

what staging system is used for SCC

A

the American joint commission on cancer TNM system and are broadly catagorised as either low or high risk

228
Q

what are high risk features for scc

A

size > 2mm deep
> 20mm wide
site: face, ear, genitals, hands, feet
recurrence
immunosuppressed individual
poor differentiation
perineural invasion
high tumour budding

229
Q

what is the treatment for a squamous cell carcinoma in situ

A

destructive therapies - cryotherapy
topical therapies - 5 fluorouracil (chemotherapeutic agent)

230
Q

what is the treatment for invasive SCC

A

conventional surgical excision with minimum 4mm margins

231
Q

what is the treatment for metastatic SCC

A

surgical excision
radiotherapy
chemotherapy

232
Q

what are complications of surgical management of SCC

A

bleeding
post operative bleeding
pain
scarring - keloid
nerve damage
physical deformities

233
Q

how quickly should a potential SCC be seen in a clinic

A

NICE suggests a 2 week wait

234
Q

what is a stroke

A

it is an acute neurological deficit attributed to an acute focal injury of the brain, spinal cord or retina by either a vascular occlusion or haemorrhage

235
Q

what is more common ischaemic or haemorrhagic stroke

A

ischaemic

236
Q

what are types of ischaemic stroke

A

large vessel atherosclerosis
small vessel occlusion
cardioembolic ischaemic stroke

237
Q

what is a large vessel atherosclerosis stroke

A

it is a common cause of ischaemic stroke. It is caused by the buildup and rupture of atherosclerotic plaques leading to the occlusion of blood supply

238
Q

in western populations where is the most common site of atherosclerosis in ischaemic stroke

A

internal carotid artery
- circle of willis, vertebral arteries and aortic arch may also be sources

239
Q

what are the small vessels of the brain

A

the small vessels are penetrating arteries that branch off larger ones of the circle of willis to supply deep subcortical and brainstem structures

240
Q

what are small vessel occlusion ischaemic strokes caused by

A

this is when the small vessels of the brain lose blood supply due to lipohyalinosis (narrowing due to being exposed to a high blood pressure) or due to atheroma

241
Q

what do small vessel occlusions in the brain lead to

A

lacunar strokes

242
Q

what is a cardioembolic stroke

A

this is when a piece of debris from the heart shoots off into the cerebral vasculature

243
Q

what is cardioembolic ischaemic stroke common in

A

atrial fibrillation

244
Q

what are causes of cardioembolic ischaemic stroke

A

atrial fibrillation
endocarditis
venous clots via patient foramen ovale
thrombus
atrial dissection
non atherosclerotic arterial wall disease
non inflammatory vasculopathy
haematological disorders
cryptogenic - no cause

245
Q

what is a haemorrhagic stroke

A

this is when there is bleeding into the brain itself

246
Q

what are the most common causes of haemorrhagic stroke

A

hypertension
cerebral amyloid angiopathy - amyloid deposition round blood vessels leads to weakening and rupture

247
Q

what are causes of haemorrhagic stroke

A

hypertension
cerebral amyloid angiopathy
bleeding disorders
drugs - anticoagulants, cocaine
vascular malformations

248
Q

what are causes of subarachnoid haemorrhage

A

traumatic injury - road traffic collisions for example
spontaneous - aneurysm, arteriovenous malformation, SAH of unknown aetiology, rare disease

249
Q

what are risk factors for subarachnoid haemorrhage

A

hypertension
smoking
family history
autosomal dominant polycystic kidney disease
aged over 50
female sex

250
Q

what are the clinical features of a subarachnoid haemorrhage

A

sudden onset severe headache
nausea and vomiting
photophobia

251
Q

what would you see in clinical examination in subarachnoid haemorrhage

A

reduced level of consciousness
neck stiffness
Kernigs sign - inability to extend knee due to pain when the patient is supine and hip and knee are flexed to 90o

252
Q

when would you do a lumbar puncture in a suspected subarachnoid haemorrhage

A

you would do it 12 hours after symptom onset if a SAH was suspected but the CT head didnt show any evidence of bleeding

253
Q

what would you expect the CSF in someone who has had a subarachnoid haemorrhage to look like

A

yellow stained - xanthochromia

254
Q

how is a subarachnoid haemorrhage managed

A

emergency - ABDCE!!!
then discuss urgently with neurosurgical team

255
Q

what surgical intervention can be done in subarachnoid haemorrhage

A

obliteration of the ruptured aneurysm done via clipping, insertion of wire coil or other endovascular treatments
balloon angioplasty in cerebral vasospasm
ventricular drainage in secondary hydrocephalus

256
Q

what are complications of subarachnoid haemorrhage

A

obstructive hydrocephalus - blood pooling
arterial vasospasm - give nimodipine
re-bleeding of aneurysms
neurological deficits

257
Q

what are risk factors for developing a stroke

A

high BMI
high fasting glucose
high blood pressure
high LDL cholesterol
kidney dysfunction
smoking
low physical activity
poor diet
alcohol consumption
environmental - air pollution, lead exposure etc

258
Q

what history would indicate a stroke

A
  1. a focal neurological deficit
  2. a persistent neurological deficit
  3. a deficit that has come on acutely
  4. no history of head trauma
259
Q

what key features are used to establish if someone is eligible for thrombolysis

A
  1. time from onset of symptoms
  2. the time the patient was last known to be unaffected
  3. if the patient was asleep did they wake up with a deficit
  4. do they take any regular medications
260
Q

what is the criteria for a total anterior circulation stroke

A

all three o the following
1. unilateral weakness and/or sensory deficit of the face, arm and leg
2. homonymous hemianopia
3. higher cerebral dysfunction (dysphasia, visuospatial disorder)

261
Q

what is the criteria for a partial anterior circulation stroke

A

two if the following
1. unilateral weakness and/or sensory deficit of the face, arm and leg
2. homonymous hemianopia
3. high cerebral dysfunction

262
Q

what is the criteria for lacunar syndrome (lacunar stroke)

A

one of the following
- pre sensory stroke
- pure motor stroke
- sensory motor stroke
- ataxic hemiparesis

263
Q

what is the criteria for posterior circulation syndrome

A

one of the following
- cranial nerve palsy and a contralateral motor/sensory deficit
- bilateral motor/sensory deficit
- conjugate eye movement disorder
- cerebellar dysfunction
- isolated homonymous hemianopia or cortical blindness

264
Q

what are differential diagnosis for stroke

A

Todds paresis
hypoglycaemia
old stroke - new insult caused by reappearance
hemiplegic migraine/migraine aura
brain tumours or other space occupying lesions
hypertensive encephalopathy
functional neurological disorder
central nervous system infection
Wernicke’s encephalopathy

265
Q

what investigations are dine for potential stroke

A

Blood sugar
CT head
CT angiogram and perfusion Chest X ray
ECG
bloods
24 hour ECG
carotid dopplers
MRI
Lumbar puncture
Echo

266
Q

what investigations should be done in a younger person with a stroke (<50)

A

vasculitis screen - ANA and ANCA
haematological studies
HIV and syphilis

267
Q

what is the management of ischaemic stroke

A

thrombolysis - tissue plasminogen activator such as alteplase which is given WITHIN 4.5 hours or up to 9 hours after the stroke
thrombectomy - up to 24 hours post stroke
aspirin - 300mg immediately
decompressive hemicraniectomy - with large area of infarction to prevent raised ICP

268
Q

how is a haemorrhagic stroke managed

A

anticoagulant reversal if required - vitamin K , prothrombin complex concentrate
blood pressure control - if elevated should be lowered to 130-140mmHg
neurosurgical intervention

269
Q

what should be considered for people who are inpatients with an ischaemic stroke

A

endarterectomy if a carotid vessel is occluded by >50% on the side where a stroke has happened
cardiological or surgical intervention if there is evidence that a cardiac lesion is the cause of the stroke

270
Q

what long term care should be put in place after someone has had a stroke

A

blood pressure management - bp <130
lipids - high intensity statins, 80mg atorvastatin
antiplatelets - 75mg clopidogrel OD long term
anticoagulation - DOAC after initial aspirin if patient suspected to have AF
lifestyle factors - smoking, diet, alcohol

271
Q

what are complications of stroke

A

aspiration events
long term neurological deficit
seizures
cerebral oedema
obstructive hydrocephalus
ischaemic stroke can undergo haemorrhagic transformation
further stroke

272
Q

what are the two types of urinary incontinence

A

urge
stress

273
Q

what is the cause of urge incontinence

A

overactivity of the detrusor muscle of the bladder

274
Q

what are the symptoms of urge incontinence

A

suddenly feeling the urge to pass urine
having to rush to the bathroom
key in door incontinence

275
Q

what is the cause of stress incontinence

A

weakening of the pelvic floor muscles and sphincter muscles which then allows urine to leak at times of increased pressure on the bladder

276
Q

what are symptoms of stress incontinence

A

urinary leakage when laughing, coughing, surprised etc

277
Q

what is mixed incontinence

A

it is a combination of urge and stress incontinence

278
Q

what is overflow incontinence

A

can occur when there is a chronic urinary retention due to an obstruction to the outflow of urine resulting in an overflow of urine
- incontinence occurs without the need to pass urine

279
Q

what can cause overflow incontinence

A

anticholinergic medication
fibroids
pelvic tumours
neurological conditions such as ms, diabetic neuropathy and spinal cord injuries

280
Q

is overflow incontinence more common in men or women

A

it is more common in men, and rare in women

281
Q

what are risk factors for urinary incontinence

A

increased age
postmenopausal status
increased BMI
previous pregnancies and vaginal deliveries
pelvic organ prolapse
pelvic floor surgery
neurological conditions - ms
cognitive impairment and dementia

282
Q

what modifiable lifestyle factors can contribute to incontinence symptoms

A

caffeine consumption
alcohol consumption
medications
BMI

283
Q

what can be asked to assess severity of incontinence

A

frequency of incontinence
frequency of urination
nighttime urination
use of pads and changing of clothes

284
Q

what should be examined when investigating incontinence

A

pelvic organ prolapse
atrophic vaginitis
urethral diverticulum
pelvic masses
during exam ask the patient to cough and watch for leakage
strength of pelvic muscle contraction can be assessed during a bimanual

285
Q

What is the modified oxford grading system used for pelvic muscle contraction

A

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 and drawing inwards

286
Q

what investigations should be done for incontinence

A

a bladder diary
urine dipstick testing
post void residual bladder volume
urodynamic testing

287
Q

what urodynamic tests can be done for incontinence testing

A

cystomety - measures detrusor muscle contraction and pressure
uroflowmetry - measures flow rate
leak point pressure
post void residual bladder volume
video urodynamic testing - filling the bladder with contrast and taking X rays as the bladder is emptied

288
Q

what management can be done for stress incontinence

A

avoid caffeine, diuretic and overfilling of bladder
avoid excessive or restricted fluid intake
weight loss
supervised pelvic floor exercises
surgery
duloxetine

289
Q

what surgical options can be offered for stress incontinence

A

tension free vaginal tape = mesh sling looped under urethra and behind pubic symphysis to abdo wall
autologous sling procedures = strip of fascia from patients abdomen used as sling
colposuspension = stitches connecting the anterior vaginal wall and the pubic symphysis round the urethra
intramural urethral bulking - injections round urethra to reduce diameter and add support

290
Q

how is urge incontinence managed

A

bladder retraining
anticholinergic medication - oxybutynin
mirabegron
invasive procedures

291
Q

what are side effects of anticholinergic medications

A

dry mouth, dry eyes, urinary retention, constipation, postural hypotension
can lead to cognitive decline, memory issues and worsening dementia

292
Q

what is mirabegron

A

it works as a beta 3 agonist and stimulates the sympathetic nervous system to reduce symptoms of urge incontinence

293
Q

what condition is mirabegron contraindicated in

A

uncontrolled hypertension as it can lead to a hypertensive crisis and increase the risk of TIA and stroke

294
Q

what invasive options are there for urge incontinence

A

botulinum toxin type A injection
percutaneous sacral nerve stimulation
augmentation cystoplasty
urinary diversion

295
Q

what is labyrinthitis

A

inflammation of the bony labyrinth of the inner ear, including the semicircular canals, vestibule (middle section) and cochlea

296
Q

what is labyrinthitis normally caused by

A

upper respiratory tract infection

297
Q

what is the presentation of labyrinthitis

A

Labyrinthitis presents with acute onset vertigo, similarly to vestibular neuronitis.
Unlike vestibular neuronitis, labyrinthitis can also be associated with:
Hearing loss
Tinnitus
Patients may have symptoms associated with the causative virus, such as a cough, sore throat and blocked nose.

298
Q

How is labyrinthitis diagnosed

A

A clinical diagnosis is based on history and examination findings. It is important to exclude a central cause of the vertigo.
The head impulse test can be used to diagnose peripheral causes of vertigo, resulting from problems with the vestibular system (e.g., vestibular neuronitis or labyrinthitis).

299
Q

how is labyrinthitis treated

A

Management is the same as with vestibular neuronitis, with supportive care and short-term use (up to 3 days) of medication to suppress the symptoms. Options for managing symptoms are:
Prochlorperazine
Antihistamines (e.g., cyclizine, cinnarizine and promethazine)

300
Q

how is bacterial labyrinthitis treated

A

Antibiotics are used to treat bacterial labyrinthitis. The underlying infection (e.g., otitis media or meningitis) needs appropriate treatment.

301
Q

can patients have lasting symptoms of labyrinthitis

A

Patients rarely have lasting symptoms, including permanent hearing impairment. This is more common after bacterial labyrinthitis, particularly associated with meningitis.

302
Q

what is vestibular neuronitis

A

Vestibular neuronitis describes inflammation of the vestibular nerve. This is usually attributed to a viral infection.

303
Q

what is the pathophysiology of vestibular neuritis

A

Vestibular neuronitis refers to inflammation of the vestibular nerve. A viral infection may trigger this inflammation. It distorts the signals travelling from the vestibular system to the brain, confusing the signal required to sense movements of the head. This results in episodes of vertigo, where the brain thinks the head is moving when it is not.

304
Q

what is the presentation of vestibular neuritis

A

Acute onset vertigo
recent history of viral illness
Symptoms are most severe for the first few days. Initially, vertigo may be constant, after which it is triggered or worsened by head movement. It is often associated with:
Nausea and vomiting (may be severe)
Balance problems

Need to differentiate between peripheral and central cause with vertigo. If they have any neuro sx then may be central - urgent management

305
Q

what is the difference between labyrinthitis and vestibular neuritis

A

Labyrinthitis – Loss of hearing
Neuronitis – No loss of hearing

306
Q

what is the head impulse test

A

The head impulse test can be used to diagnose peripheral causes of vertigo, resulting from problems with the vestibular system (e.g., vestibular neuronitis or labyrinthitis).

307
Q

how does the head impulse test work

A

The head impulse test involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner holds the patient’s head and rapidly jerks it 10-20 degrees in one direction while the patient continues looking at the examiner’s nose. The head is slowly moved back to the centre before repeating in the opposite direction. Ensure they have no neck pain or pathology before performing the test.

A patient with a normally functioning vestibular system will keep their eyes fixed on the examiner’s nose.

308
Q

what will the head impulse test show if someone has a problem with their vestibular system

A

In a patient with an abnormally functioning vestibular system (e.g., vestibular neuronitis or labyrinthitis), the eyes will saccade (rapidly move back and forth) as they eventually fix back on the examiner.

309
Q

what will the head impulse test show if someone has a central cause of vertigo

A

nothing, the test will be normal

310
Q

what is the management of vestibular neuritis

A

Patients may need admission if they are becoming dehydrated due to severe nausea and vomiting.
For peripheral vertigo, short-term options for managing symptoms include:
Prochlorperazine
Antihistamines (e.g., cyclizine, cinnarizine and promethazine)
NICE advise that symptomatic treatment can be used for up to 3 days. More extended use may slow down the recovery.
NICE also recommend referral if the symptoms do not improve after 1 week or resolve after 6 weeks, as they may require further investigation or vestibular rehabilitation therapy (VRT).

311
Q

what is the prognosis of vestibular neuritis

A

Symptoms are most severe for the first few days, after which they gradually resolve over the following 2-6 weeks.

Benign paroxysmal positional vertigo (BPPV) may develop after vestibular neuronitis.

312
Q

what anti-emetics should be avoided in parkinsons

A

metoclopramide
prochlorperazine
- reduces dopamine, increases parkinsons symptoms

313
Q

what anti-emetics are used in parkinsons

A

domperidone - selectively inhibits dopamine in gut and has a lesser effect on systemic dopamine

314
Q

what is the mechanism of action of ondansetron

A

it is a 5-HT3 receptor antagonist

315
Q

when would you not use ondansetron

A

if someone had a prolonged QT - can cause prolongation and cause heart arrhythmias

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