Geriatrics Flashcards
1
Q
what is benign paroxysmal positional vertigo
A
it is a common cause of recurrent vertigo episodes triggered by head movement
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
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
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
5
Q
what semicircular canal do the calcium carbonate crystals in BPPV most commonly get displaced into
A
the posterior semicircular canal
6
Q
what can cause disruption of the calcium carbonate crystals in BPPV
A
idiopathic - no known cause
viral illness
head trauma
aging
7
Q
what manoeuvre is used to diagnose BPPV
A
the Dix-Hallpike manoeuvre
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
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
10
Q
what are Brandt-daroff exercises
A
these are exercises that the patient can perform at home to improve the symptoms of BPPV
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
12
Q
what are causes of BPPV
A
mostly idiopathic
head injury
post viral illness
labyrinthitis
complications of surgery
13
Q
what are risk factors of BPPV
A
older age (40-60)
female
manières disease
patients with migraines or anxiety disorders
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
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
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
17
Q
what is ejection fraction
A
it is the percentage of blood in the left ventricle ejected with each ventricular contraction
18
Q
what ejection fraction is considered normal
A
anything above 50%
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
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)
21
Q
what are causes of chronic heart failure
A
ischaemic heart disease
valvular heart disease - aortic stenosis
hypertension
arrhythmias - atrial fibrillation
cardiomyopathy
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
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
24
Q
what causes paroxysmal nocturnal dyspnoea
A
- fluid settles across a large area of the lungs when lying down causing breathlessness
- during sleep the resp. centre of the brain becomes less responsive allowing for more significant pulmonary congestion and hypoxia
- less adrenalin when asleep meaning the myocardium is more relaxed, reducing co
25
what investigations should be done for someone with suspected heart failure
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
26
what is the new york heart association classification
it is a system used to grade the severity of symptoms related to heart failure
27
what are the different grades in the new york heard association classification
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
28
what are the five principles of management for someone with heart failure (RAMPS)
Refer to cardiology
Advise them on the condition
Medication
Procedural or surgical interventions
Specialist heart failure MDT
29
what are the guidelines on when to refer depending on the NT-proBNP result
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
30
what lifestyle management can you advise someone who has heart failure
flu, covid and pneumococcal vaccinations
stop smoking
cardiac rehabilitation - personalised exercise programme
31
what is the medical treatment for heart failure (ABAL)
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
32
what needs to be carefully monitored in patients on diuretics, ACE inhibitors and aldosterone antagonists
U+E as all three of these medications can cause electrolyte imbalances
- hyperkalaemia !!
33
other than ABAL management plan what other medications may be used in heart failure
SGLT2 inhibitor - dapagliflozin
sacubitril with valsartan
ivabradine
hydralazine with a nitrate
digoxin
34
what surgical interventions are done in the management of heart failure
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
35
what are common symptoms of constipation
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
36
what is considered normal stool on the bristol stool chart
4
37
what other sensations can constipation be associated with
feeling of fullness
bloating
stomach pain
reduced appetite
38
what can prolonged constipation lead to
fecal impaction
39
what is fecal impaction
this is a mass of hard stool in the rectum or colon
it is very uncomfortable and associated with pain, diarrhoea/incontinence
40
what shouldnt be given in fecal impaction
laxatives as it can make it worse by creating more pressure and movement upstream of the blockage
41
what are common causes of constipation in the elderly
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
42
what medications can cause constipation
anticholinergics - antihistamines, medication for overactive bladder, muscle relaxants
opiates
diuretics
calcium and iron supplements
43
what are red flags of constipation
blood in stool
new weight loss
new/rapidly worsening symptoms
44
how do you treat constipation
identify and reduce constipating medication is possible
increase dietary fibre and water
encourage regular exercise
laxatives
45
what laxatives are good for constipation in the elderly
osmotic agents - lactulose/sorbitol/miralax
stimulant agents - senna/bisacodyl
bulking agents - methylcellulose
46
how is fecal impaction treated
enemas
suppositories
47
what type of enemas should be used in fecal impaction
use warm tap water or mineral oil enemas
48
what type of laxatives should be avoided long term due to toxicity
magnesium based laxatives
49
what laxatives should be avoided in fecal impaction (especially)
bulking agents
50
what is delirium
acute, transient and reversible state of confusion usually as a result of organic processes
51
how common is it for elderly patients to get delirium
one in five elderly patients on medical or surgical wards are affected by delirium
52
what are the clinical features of delirium
there are hyperactive and hypoactive states which the patients often fluctuate between
53
what are the clinical features of hyperactive delirium
typical delirium presentation
- agitation
- delusions
- hallucinations
- wandering
- aggression
54
what are the clinical features of hypoactive delirium
lethargy
slowness with everyday tasks
excessive sleeping
inattention
55
what are common causes of delirium
CHIMPS PHONED
constipation
hypoxia
infection
metabolic disturbance
pain
sleeplessness
prescriptions
hypothermia/pyrexia
organ dysfunction - hepatic/renal issues
nutrition
environmental changes
drugs
56
what assessment scores can be used to assess delirium
abbreviated mental test score
mini mental state exam
ACE III
57
what bloods should be performed on someone with delirium
FBC
U+E
LFT
coagulation/INR
TFTs
calcium
B12 and folate/haematinics
glucose
blood cultures
58
what should be included in a confusion screen
urinalysis
bloods
imaging - CT head, CXR
59
what is the general supportive management for delirium
- 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
60
what environmental adaption management strategies can be used to help someone with delirium
- 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
61
what medication can be used in delirium
haloperidol is usually the first line medication option - 0.5mg
if benzodiazepines are used lorazepam is first line (0.5mg)
62
what can you do to prevent episodes of delirium
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
63
what are precipitating factors of delirium
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
64
what is the 4As test (4AT)
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
65
what is dementia
it is an irreversible, progressive decline and impairment of more than one aspect of higher brain function
66
what are the different types of dementia
alzheimers
fronto-temporal
lewy body
vascular
67
what is the cause of alzeimers dementia
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
68
what are the clinical features of alzheimers dementia
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
69
what areas of the brain are affected by alzheimers disease
entorhinal cortex and the hippocampus
- later affects areas in cerebral cortex responsible for language, reasoning and social behaviour
70
what causes vascular dementia
micro-infarcts within the brain
71
what is the progression of vascular dementia like
it is a stepwise progression, often showing periods of stability at one level of functioning before an acute decline progression
72
what are the most commonly affected areas in vascular dementia
white matter of both cerebral hemispheres, grey nuclei, thalamus and striatum
73
what are risk factors for developing vascular dementia
hypertension - major rf
smoking
diabetes
hyperlipidaemia
obesity
hypertension
74
what are the clinical features of vascular dementia
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
75
what is disease progression like in lewy body dementia
it is very rapid - death most commonly occurs in the first 7 years post diagnosis
76
what causes lewy body dementia
spherical lewy body proteins (alpha syncluein) are deposited within the brain
77
what are the clinical features of lewy body dementia
Visual hallucinations and parkinson like symptoms
problem multitasking
problems performing complex cognitive actions
sleep disorders and fluctuation
78
what causes frontotemporal dementia
neuron damage and death in the frontal and temporal lobes
- atrophy due to deposition of abnormal proteins (tau) within the lobes
79
what behavioural presentations can be seen in frontotemporal dementia
altered emotional responsiveness, apathy, disinhibition, impulsivity
progressive decline noted in interpersonal skills
changes in food preference - more childlike
obsessions and rituals may be noted
80
what semantic presentations can be seen in frontotemporal dementia
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
81
what non fluent presentations can be seen in frontotemporal dementia
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
82
what are ddx of dementia
prion protein disease
HIV related cognitive impairment/decline
normal pressure hydrocephalus
severe depression
mild cognitive imapairment
83
what are the man ways in treating alzheimers
Acetylcholinesterase inhibitors - donepezil (more severe) , rivastigmine, galantamine (mild-moderate)
memantine - severe
84
what are side effects of memantine
headaches
dizziness
constipation
85
what non medication treatments are used in dementia
cognitive stimulation therapy - memory, problem solving, language ability
cognitive rehabilitation
reminiscence and life story work
86
what is the risk of someone over 65 falling at least once per year
30%
87
what is the risk of someone over 80 falling at least once per year
50%
88
what questions are important to ask in a falls history
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
89
what symptoms are important to ask about in a falls history
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
90
what types of medications can commonly cause falls
beta blockers
diabetic medications (hypoglycaemia)
antihypertensives (hypotension)
benzodiazepines (drowsiness)
antibiotics
91
what investigations should be done in someone who has had a fall
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
92
what is assessed in a patient when completing a complete falls risk assessment
- gait
- visual problems
- hearing problems
- medication review
- alcohol intake
- postural hypotension
- cognitive decline
- foot wear
- continence
- environmental hazards
93
what is the 30 day mortality of a hip fracture
5-10 %
94
what are major risk factors for getting a hip fracture
increased age and osteoporosis
95
what are the two types of hip fracture
intra capsular
extra capsular
96
how quickly should surgery be performed after a hip fracture
within 48 hours ideally
97
what are the anatomical parts of the top of the femur
head
neck
greater trochanter (lateral)
lesser trochanter (medial)
intertrochanteric line
shaft
98
what is the anatomical structure of the hip joint
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
99
what is the blood supply of the femur
it is a retrograde blood supply
- medial and lateral circumflex femoral artery
100
what is an intracapsular neck of femur fracture
this is when the break in the femoral neck occurs within the capsule of the joint
- proximal to the intertrochanteric line
101
what are the risks of an intracapsular neck of femur fracture
commonly affects the blood supply and can cause avascular necrosis of the bone
102
what is the Garden classification of intracapsular NOF fractures
class I: incomplete fracture and non displaced
class II: complete fracture and non displaced
class III: partial displacement
class IV: total displacement
103
what classifications of intracapsular NOF fractures will have a disrupted blood supply
displaced fractures
- non displaced fractures may still have an intact blood supply
104
what is a hemiarthroplasty
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
105
what is a total hip replacement
this is when both the head of the femur and the acetabulum is replaced
106
what are types of extracapsular hip fractures
intertrochanteric fracture
subtrochanteric fracture
107
what is an intertrochanteric fracture
this is when the fracture occurs between the greater and lesser trochanter
108
how is a intertrochanteric fracture surgically treated
with a dynamic hip screw
109
what is a subtrochanteric fracture
this is a fracture that is below the lesser trochanter and proximal to the shaft of the femur
110
how is a subtrochanteric fracture treated surgically
with an intramedullary nail
111
how does a hip fracture present
with pain in the groin or hip which may radiate to the knee, often unable to weight bare
- Shortened, abducted and externally rotated leg
112
what investigations should be done for a suspected hip fracture
x-ray - anterior-posterior and lateral views
MRI/CT if the X ray is negative but fracture is suspected
113
how is a hip fracture treated
analgesia
VTE risk assessment and prophylaxis
surgery
114
what is frailty
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
115
what is the pathophysiology of aging
there is an accelerated decline in physiological reserve and normal mechanisms begin failing
116
what is the issue with frailty in the elderly
it increases the potential for serious adverse outcomes after seemingly minor stressor events
117
when should frailty in the elderly be assessed
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
118
what is the phenotype model of frailty
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
119
what is the cumulative deficit model of frailty
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
120
what is a central clinical feature of frailty
loss of skeletal muscle function
121
how can you help prevent frailty
physical activity - resistance exercise
sufficient diet
reduction in smoking
122
what is acute malnutrition
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
123
what is malnutrition
it is the sudden/chronic decrease in the intake of sufficient nutrition
124
what is chronic malnutrition
this is inadequate nutrition which lasts longer than three months
often secondary to social, behavioural and economic factors
125
what parameters are measured in the Malnutrition Universal Screening Tool (MUST)
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
126
what are the three main reasons why someone might become malnourished
inadequate amounts of nutrients
difficulty absorbing nutrients
increased nutritional needs
127
what are risk factors for malnutrition
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
what clinical features of malnutrition are seen in adults
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
what are important areas to cover in the history when querying malnutrition
weight history - current, recent changes to weight, changed to clothing fit
meal history
protein intake
hydration
130
how is malnutrition treated
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
what is re-feeding syndrome
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
what can re feeding syndrome lead to
cardiac complications - arrhythmias
seizures
133
what are complications of malnutrition
impaired immunity
poor wound healing
growth restriction in children
unintentional weight loss - muscle mass
multi organ failure
death
134
what is an advanced directive
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
what are the advantages of an advanced directive
it enables an individual to think about what they would like to happen to them in the event they lose capacity.
136
what are limitations of an advance directive
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
when might a doctor not follow an advanced directive
- 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
what is advanced care planning
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
what is an advanced statement
it is wishes, preferences and priorities of a patient and may include nomination of a names spokes person
- not legally binding
140
what is is a lasting power of attorney
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
who might benefit from ACP conversations
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
what is osteoporosis
this is a progressive, systemic skeletal disorder characterised by reduced bone density
143
what is the precursor to osteoporosis
osteopenia
144
is the pathophysiology of osteoporosis
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
what are general risk factors for osteoporosis
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
what are medical conditions which increase the risk of osteoporosis
rheumatoid arthritis
primary hyperparathyroidism
chronic kidney disease
gastrointestinal disease - IBD, coeliac
hyperthyroidism
chronic liver disease
147
what medications increase the risk of osteoporosis
corticosteroids - any dose orally for over three months, and doses above 7.5mg/day
SSRI
PPI
anti-epileptics
anti-oestrogens
148
what is a fragility fracture
it is a low impact fracture from standing height or less
149
what are the most common sites for fragility fracture
vertebral
hip - proximal femur
wrist - distal radius
150
how do you assess fracture risk
FRAX tool - calculates the 10 year fracture probability
151
what factors does the FRAX score take into account
age
sex
BMI
previous fracture
parental hip fracture
smoking status
alcohol consumption
glucocorticoid use
rheumatoid arthritis
secondary osteoporosis
152
when should you start assessing someones fracture risk
all women over 65
all men over 75
women under 65 and men under 75 with risk factors
153
what would the management plan for someone who is at low risk of fracture in the next 10 yrs
no need to measure bone marrow density (DEXA)
give lifestyle advise and reassurance
monitor risk factors
154
what would management be for someone who is at intermediate risk for fracture in the next 10 yrs
arrange a DEXA scan and recalculate the risk score with BMD taken into account
monitor risk factors
155
what would the management be for someone who is at high risk of fracture in the next 10 years
offer treatment
arrange DEXA scan to help guide treatment
156
what populations may the risk assessment tools underestimate the fracture risk in
patients over 80
multiple previous fragility fractures
patients taking oral glucocorticoids - >7.5mg prednisolone for 3 months or more
157
what two regions are typically used for a DXA scan
the femoral neck and the spine
158
what is the T score for a DXA scan
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
what is the z score for a DXA scan
it is the number of standard deviations the patients bone density is from the mean bone density of age and gender matched control
160
what other investigations may be done for someone with suspected osteoporosis
bone profile
U+E
vitamin D
PTH
thyroid function tests
testosterone
161
what T score indicates osteopenia
-1 to -2.5
162
what T score indicates osteoporosis
< -2.5
163
what T score indicates severe osteoporosis
< -2.5 AND previous fracture
164
what lifestyle advice should be given to someone with osteoporosis
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
what should patients with vitamin D below 50nmol/L be offered
rapid correction: 300,000 IU vitamin D3 over 6-10 weeks
maintenance 800-2,000 IU vitamin D3/day
166
what is the first line treatment for patients with osteoporosis
bisphosphonates
- alendronic acid: 10mg daily or 70mg weekly
- ibandronic acid
- risendronate sodium: 5mg daily, 53mg weekly
- zoledronic acid: 5mg IV once per year
167
what advice needs to be given about taking oral bisphosphonates
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
what are the potential side effects of bisphosphonates
gastrointestinal upset - dyspepsia and reflux
atypical fractures
osteonecrosis of the jaw - swelling, pain, erythema
169
what non bisphosphonate treatment can be given to help osteoporosis
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
how long is the typical course of bisphosphonates
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
what are complications of osteoporosis
hip fractures
rib fractures
wrist fractures
vertebral fractures
chronic pain
172
what is Parkinsons disease
it is a disease causing progressive reduction in dopamine in the basal ganglia, leading to movement disorder
173
are the symptoms of parkinsons symmetrical or asymmetrical
asymmetrical
174
what is the classic triad of parkinsons disease
Resting tremor
Rigidity
Bradykinesia
175
what is the pathophysiology of parkinsons
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
what are the features of a parkinsons tremor
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
what are the features of parkinsons rigidity
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
what are features of parkinsons bradykinesia
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
what are other symptoms of parkinsons other than the core three sx
depression
sleep disturbance and insomnia
loss of the sense of smell
postural instability
cognitive impairment and memory issues
179
what are the features of benign essential tremor
symmetrical
6-12hz
improves at rest
worse with intentional movement
improves with alcohol
180
what are examples of parkinson plus syndromes
multiple system atrophy
dementia with lewy bodies
progressive supranuclear palsy
corticobasal degeneration
181
what is multiple system atrophy
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
how is parkinsons diagnosed
clinically diagnosed on the history and exam
NICE guidelines recommend the UK parkinsons disease society brain bank clinical diagnostic criteria
183
what are the treatments for parkinsons
Levodopa combined with peripheral decarboxylase inhibitors
COMT inhibitors
dopamine agonists
monoamine oxidase B inhibitors
184
How does levodopa work in parkinsons
it is a synthetic dopamine and is the most effective treatment for symptoms but becomes less effective over time
185
what is levodopa often combined with
it is usually combined with a peripheral decarboxylase inhibitor which stops it being metabolised in the body before it reaches the brain
186
what is the main side effect of levodopa
dyskinesia - abnormal movements associated with excessive motor activity
187
what are examples of dyskinesia side effects you can get from levodopa
Dystonia
chorea
athetosis
188
what is dystonia
where excessive muscle contraction leads to abnormal postures or exaggerated movements
189
what is chorea
it is abnormal involuntary movements that can be jerking and random
190
what is athetosis
it is involuntary twisting or writhing movements usually in the fingers, hands or feet
191
what can be used to manage dyskinesia associated with levodopa
amantadine - glutamate antagonist
192
what are COMT inhibitors
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
what is an example of a COMT inhibitor
entacapone
194
what are examples of dopamine agonists
bromocriptine
pergolide
cabergoline
195
what is a side effect of prolonged use of dopamine agonists
pulmonary fibrosis
196
what are monoamine oxidase B inhibitors
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
what are examples of monoamine oxidase B inhibitors
selegiline
rasagiline
198
what are symptoms can be caused polypharmacy
tiredness
sleepiness
decreased alertness
confusion
falls
depression
weakness
tremors
visual or auditory hallucinations
anxiety
dizziness
199
what can polypharmacy lead to in the elderly
adverse drug reactions
decreased medication compliance
poor quality of life
unnecessary drug expenses
200
what can be done to reduce the incidence and adverse effects of polypharmacy in the elderly
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
what are pressure ulcers
they are areas of damage to skin and the tissue underneath due extended periods of pressure on one area of the body
202
where do pressure ulcers usually form
bony parts of the body such as heels, elbows, hips and tailbone
203
what are symptoms of pressure ulcers
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
what are causes of pressure sores
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
how do pressure ulcers develop
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
how many people admitted to hospital with a sudden illness will get a pressure ulcer
around 1 in 20
207
what is the treatment for pressure ulcers
use of dressings
creams/gels to help the healing process and relieve pressure
surgery recommended for the most serious cases
208
how can you prevent pressure ulcers
regularly changing the persons position
using equipment to protect vulnerable parts of the body - mattresses and cushions
209
what is a grade 1 pressure ulcer
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
what is a grade 2 pressure ulcer
there is some epidermis or dermis damage leading to skin loss
the ulcer looks like an open wound/blister
211
what is a grade three pressure ulcer
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
what is a grade 4 pressure ulcer
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
who is at increased risk of developing pressure ulcers
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
what health conditions increase risk of pressure ulcers
type 1 and type 2 diabetes
peripheral arterial disease
heart failure
kidney failure
COPD
215
what care team will be involved in pressure ulcer management
tissue viability nurse
social worker
physiotherapist
occupational therapist
dietician
surgeons if bad enough
216
what dressings are used for pressure ulcers
hydrocolloid dressings
alginate dressings
217
what are complications of pressure ulcers
cellulitis
blood poisoning + sepsis
bone and joint infection
necrotising fasciitis
gas gangrene
218
what is the pathophysiology of squamous cell carcinoma
cancerous mutations occur in squamous keratinocytes in the epidermis which lie within the stratum spinosum
219
what are the five layers of the epidermis
stratum corneum
stratum lucidum
stratum granulosum
stratum spinosum
stratum basale
220
what is the main cause of squamous cell carcinoma
ultraviolet exposure - UVB
221
what are risk factors for squamous cell carcinoma
ultraviolet radiation
immunosuppression
Fitzpatrick skin types I and II
solid organ transplant recipients
increasing age
male sex
ionising radiation
sites of chronic inflammation
222
what is the morphology of a squamous cell lesion like
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
what is Bowens disease
it is also known as SCC in situ and it occurs when the cancerous cells are confined to the epidermis
224
what is actinic keratosis
involves the formation of precancerous scaly lesions on the skin - about a 10% risk of developing into SCC
225
how is SCC investigated
punch or incisional biopsy
ultrasound of lymph nodes and CT/MRI for staging or if metastasis is suspected
226
what classification systems exist for SCC
histopathological
clinicopathological
borders classification
227
what staging system is used for SCC
the American joint commission on cancer TNM system and are broadly catagorised as either low or high risk
228
what are high risk features for scc
size > 2mm deep
> 20mm wide
site: face, ear, genitals, hands, feet
recurrence
immunosuppressed individual
poor differentiation
perineural invasion
high tumour budding
229
what is the treatment for a squamous cell carcinoma in situ
destructive therapies - cryotherapy
topical therapies - 5 fluorouracil (chemotherapeutic agent)
230
what is the treatment for invasive SCC
conventional surgical excision with minimum 4mm margins
231
what is the treatment for metastatic SCC
surgical excision
radiotherapy
chemotherapy
232
what are complications of surgical management of SCC
bleeding
post operative bleeding
pain
scarring - keloid
nerve damage
physical deformities
233
how quickly should a potential SCC be seen in a clinic
NICE suggests a 2 week wait
234
what is a stroke
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
what is more common ischaemic or haemorrhagic stroke
ischaemic
236
what are types of ischaemic stroke
large vessel atherosclerosis
small vessel occlusion
cardioembolic ischaemic stroke
237
what is a large vessel atherosclerosis stroke
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
in western populations where is the most common site of atherosclerosis in ischaemic stroke
internal carotid artery
- circle of willis, vertebral arteries and aortic arch may also be sources
239
what are the small vessels of the brain
the small vessels are penetrating arteries that branch off larger ones of the circle of willis to supply deep subcortical and brainstem structures
240
what are small vessel occlusion ischaemic strokes caused by
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
what do small vessel occlusions in the brain lead to
lacunar strokes
242
what is a cardioembolic stroke
this is when a piece of debris from the heart shoots off into the cerebral vasculature
243
what is cardioembolic ischaemic stroke common in
atrial fibrillation
244
what are causes of cardioembolic ischaemic stroke
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
what is a haemorrhagic stroke
this is when there is bleeding into the brain itself
246
what are the most common causes of haemorrhagic stroke
hypertension
cerebral amyloid angiopathy - amyloid deposition round blood vessels leads to weakening and rupture
247
what are causes of haemorrhagic stroke
hypertension
cerebral amyloid angiopathy
bleeding disorders
drugs - anticoagulants, cocaine
vascular malformations
248
what are causes of subarachnoid haemorrhage
traumatic injury - road traffic collisions for example
spontaneous - aneurysm, arteriovenous malformation, SAH of unknown aetiology, rare disease
249
what are risk factors for subarachnoid haemorrhage
hypertension
smoking
family history
autosomal dominant polycystic kidney disease
aged over 50
female sex
250
what are the clinical features of a subarachnoid haemorrhage
sudden onset severe headache
nausea and vomiting
photophobia
251
what would you see in clinical examination in subarachnoid haemorrhage
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
when would you do a lumbar puncture in a suspected subarachnoid haemorrhage
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
what would you expect the CSF in someone who has had a subarachnoid haemorrhage to look like
yellow stained - xanthochromia
254
how is a subarachnoid haemorrhage managed
emergency - ABDCE!!!
then discuss urgently with neurosurgical team
255
what surgical intervention can be done in subarachnoid haemorrhage
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
what are complications of subarachnoid haemorrhage
obstructive hydrocephalus - blood pooling
arterial vasospasm - give nimodipine
re-bleeding of aneurysms
neurological deficits
257
what are risk factors for developing a stroke
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
what history would indicate a stroke
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
what key features are used to establish if someone is eligible for thrombolysis
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
what is the criteria for a total anterior circulation stroke
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
what is the criteria for a partial anterior circulation stroke
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
what is the criteria for lacunar syndrome (lacunar stroke)
one of the following
- pre sensory stroke
- pure motor stroke
- sensory motor stroke
- ataxic hemiparesis
263
what is the criteria for posterior circulation syndrome
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
what are differential diagnosis for stroke
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
what investigations are dine for potential stroke
Blood sugar
CT head
CT angiogram and perfusion Chest X ray
ECG
bloods
24 hour ECG
carotid dopplers
MRI
Lumbar puncture
Echo
266
what investigations should be done in a younger person with a stroke (<50)
vasculitis screen - ANA and ANCA
haematological studies
HIV and syphilis
267
what is the management of ischaemic stroke
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
how is a haemorrhagic stroke managed
anticoagulant reversal if required - vitamin K , prothrombin complex concentrate
blood pressure control - if elevated should be lowered to 130-140mmHg
neurosurgical intervention
269
what should be considered for people who are inpatients with an ischaemic stroke
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
what long term care should be put in place after someone has had a stroke
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
what are complications of stroke
aspiration events
long term neurological deficit
seizures
cerebral oedema
obstructive hydrocephalus
ischaemic stroke can undergo haemorrhagic transformation
further stroke
272
what are the two types of urinary incontinence
urge
stress
273
what is the cause of urge incontinence
overactivity of the detrusor muscle of the bladder
274
what are the symptoms of urge incontinence
suddenly feeling the urge to pass urine
having to rush to the bathroom
key in door incontinence
275
what is the cause of stress incontinence
weakening of the pelvic floor muscles and sphincter muscles which then allows urine to leak at times of increased pressure on the bladder
276
what are symptoms of stress incontinence
urinary leakage when laughing, coughing, surprised etc
277
what is mixed incontinence
it is a combination of urge and stress incontinence
278
what is overflow incontinence
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
what can cause overflow incontinence
anticholinergic medication
fibroids
pelvic tumours
neurological conditions such as ms, diabetic neuropathy and spinal cord injuries
280
is overflow incontinence more common in men or women
it is more common in men, and rare in women
281
what are risk factors for urinary incontinence
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
what modifiable lifestyle factors can contribute to incontinence symptoms
caffeine consumption
alcohol consumption
medications
BMI
283
what can be asked to assess severity of incontinence
frequency of incontinence
frequency of urination
nighttime urination
use of pads and changing of clothes
284
what should be examined when investigating incontinence
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
What is the modified oxford grading system used for pelvic muscle contraction
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
what investigations should be done for incontinence
a bladder diary
urine dipstick testing
post void residual bladder volume
urodynamic testing
287
what urodynamic tests can be done for incontinence testing
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
what management can be done for stress incontinence
avoid caffeine, diuretic and overfilling of bladder
avoid excessive or restricted fluid intake
weight loss
supervised pelvic floor exercises
surgery
duloxetine
289
what surgical options can be offered for stress incontinence
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
how is urge incontinence managed
bladder retraining
anticholinergic medication - oxybutynin
mirabegron
invasive procedures
291
what are side effects of anticholinergic medications
dry mouth, dry eyes, urinary retention, constipation, postural hypotension
can lead to cognitive decline, memory issues and worsening dementia
292
what is mirabegron
it works as a beta 3 agonist and stimulates the sympathetic nervous system to reduce symptoms of urge incontinence
293
what condition is mirabegron contraindicated in
uncontrolled hypertension as it can lead to a hypertensive crisis and increase the risk of TIA and stroke
294
what invasive options are there for urge incontinence
botulinum toxin type A injection
percutaneous sacral nerve stimulation
augmentation cystoplasty
urinary diversion
295
what is labyrinthitis
inflammation of the bony labyrinth of the inner ear, including the semicircular canals, vestibule (middle section) and cochlea
296
what is labyrinthitis normally caused by
upper respiratory tract infection
297
what is the presentation of labyrinthitis
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
How is labyrinthitis diagnosed
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
how is labyrinthitis treated
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
how is bacterial labyrinthitis treated
Antibiotics are used to treat bacterial labyrinthitis. The underlying infection (e.g., otitis media or meningitis) needs appropriate treatment.
301
can patients have lasting symptoms of labyrinthitis
Patients rarely have lasting symptoms, including permanent hearing impairment. This is more common after bacterial labyrinthitis, particularly associated with meningitis.
302
what is vestibular neuronitis
Vestibular neuronitis describes inflammation of the vestibular nerve. This is usually attributed to a viral infection.
303
what is the pathophysiology of vestibular neuritis
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
what is the presentation of vestibular neuritis
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
what is the difference between labyrinthitis and vestibular neuritis
Labyrinthitis – Loss of hearing
Neuronitis – No loss of hearing
306
what is the head impulse test
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
how does the head impulse test work
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
what will the head impulse test show if someone has a problem with their vestibular system
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
what will the head impulse test show if someone has a central cause of vertigo
nothing, the test will be normal
310
what is the management of vestibular neuritis
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
what is the prognosis of vestibular neuritis
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
what anti-emetics should be avoided in parkinsons
metoclopramide
prochlorperazine
- reduces dopamine, increases parkinsons symptoms
313
what anti-emetics are used in parkinsons
domperidone - selectively inhibits dopamine in gut and has a lesser effect on systemic dopamine
314
what is the mechanism of action of ondansetron
it is a 5-HT3 receptor antagonist
315
when would you not use ondansetron
if someone had a prolonged QT - can cause prolongation and cause heart arrhythmias
