Geratology Flashcards
1
Q
What factors may predispose patients to developing pressure ulcers?
A
Malnourishment
Incontinence: urinary and faecal
Lack of mobility
Pain (leads to a reduction in mobility)
2
Q
What scoring system is used to screen for patients who are at risk of developing pressure areas?
A
Waterlow score
3
Q
What is a Waterlow score used for?
A
Used to screen for patients who are at risk of developing pressure areas
4
Q
How would you describe a grade 1 pressure ulcer?
A
Non-blanchable erythema of intact skin.
Discolouration of the skin, warmth, oedema, induration or hardness may also be used as indicators, particularly on individuals with darker skin
5
Q
How would you describe a grade 2 pressure ulcer?
A
Partial thickness skin loss involving epidermis or dermis, or both.
The ulcer is superficial and presents clinically as an abrasion or blister
6
Q
How would you describe a grade 3 pressure ulcer?
A
Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
7
Q
How would you describe a grade 4 pressure ulcer?
A
Extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures with or without full thickness skin loss
8
Q
Non-blanchable erythema of intact skin would be what grade pressure ulcer?
A
Grade 1
9
Q
Partial thickness skin loss involving epidermis or dermis, or both.
A
Grade 2
10
Q
Full thickness skin loss involving damage to or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia.
A
Grade 3
11
Q
Extensive destruction, tissue necrosis, or damage to muscle, bone or supporting structures with or without full thickness skin loss
A
Grade 4
12
Q
What is the management for pressure ulcers?
A
A moist wound environment encourages ulcer healing.
Hydrocolloid dressings and hydrogels may help facilitate this.
The use of soap should be discouraged to avoid drying the wound
Consider referral to the tissue viability nurse
13
Q
What should not be done routinely for pressure ulcers?
A
Wound swabs should not be done routinely as the vast majority of pressure ulcers are colonised with bacteria.
The decision to use systemic antibiotics should be taken on a clinical basis (e.g. Evidence of surrounding cellulitis)
14
Q
What are the risk factors for squamous cell carcinoma of the skin?
A
Excessive sunlight exposure
Actinic keratoses and Bowen’s disease
Immunosuppression e.g. renal transplant / HIV
Smoking
Long-standing leg ulcers
15
Q
What are the classical features of squamous cell carcinoma of the skin?
A
Typically on sun exposed sites - head, neck, hands, arms
Rapidly expanding painless, ulcerate nodules
May have cauliflower like appearance
May be areas of bleeding
16
Q
What is the management of squamous cell carcinoma of the skin?
A
Surgical excision with 4mm margins if lesion <20mm in diameter.
Surgical excision with 6mm margins if lesion >20mm in diameter.
17
Q
What management for squamous cell carcinoma can be used if the patient is high risk or concerned about cosmetic importance?
A
Mohs micrographic surgery
18
Q
What hormones are released when the body gets too cold and where from?
A
TSH and ACTH from the hypothalamus
19
Q
Define mild hypothermia?
A
Mild hypothermia: 32-35°C
20
Q
Define moderate-severe hypothermia?
A
Moderate or severe hypothermia: < 32°C
21
Q
What are the features of hypothermia?
A
Shivering
Cold and pale skin
Slurred speech
Confusion / impaired mental state
22
Q
What are the specific features of mild hypothermia?
A
Tachypnoea, tachycardia and hypertension
23
Q
What are the specific features of moderate hypothermia?
A
Respiratory depression, bradycardia and hypotension
24
Q
What changes may be seen on an ECG if a patient has hypothermia?
A
Hyopthermia = Jesus Quist It’s Bloody Freezing
Osborne (J) Waves (small hump at the end of QRC complex)
QT interval - prolonged
Irregular Rhythm
Bradycardia
First Degree Heart Block
25
What is the initial management for hypothermia?
Removing the patient from the cold environment and removing any wet/cold clothing,
Warming the body with blankets
Securing the airway and monitoring breathing,
If the patient is not responding well to passive warming, you may consider maintaining circulation using warm IV fluids or applying forced warm air directly to the patient's body
26
What must you be wary of when performing rapid re-warming of patients?
Rapid re-warming can lead to peripheral vasodilation and shock
In severe cases, be prepared to conduct CPR. IV drugs should be avoided if possible, as the patient is more likely to have a drastic response to the drug.
27
When performing ALS in a patient with hypothermia, what is the protocol?
In cases of hypothermia causing cardiac arrest, defibrillation is less effective and only 3 shocks should be administered before the patient is rewarmed to 30 degrees centigrade
28
What are the three definitions of malnutrition?
A Body Mass Index (BMI) of less than 18.5, or
Unintentional weight loss greater than 10% within the last 3-6 months, or
A BMI of less than 20 and unintentional weight loss greater than 5% within the last 3-6 months
29
What would a MUST score of 0 indicate in clinical care?
Low risk - Repeat screening
- Hospital – weekly
- Care Homes – monthly
- Community – annually for special groups e.g. those >75
30
What would a MUST score of 1 indicate in clinical care?
Medium risk - Observe
- Document dietary intake for 3 days
- If adequate – little concern and repeat screening
- If inadequate – clinical concern – follow local policy
31
What would a MUST score of 2 indicate in clinical care?
High risk - Treat
- Refer to dietitian, Nutritional Support Team or implement local policy
- Set goals, improve and increase overall nutritional intake
- Monitor and review care plan
32
What must be measured and then calculated for a MUST score?
Height (m) and weight (kg) and therefore BMI
Weight / Height^2
33
Define constipation?
Defecation that is unsatisfactory because of infrequent stools (< 3 times weekly), difficult stool passage (with straining or discomfort), or seemingly incomplete defecation.
34
What are first-line laxatives for constipation?
Ispaghula husk - a bulk forming laxative
35
What are second-line laxatives for constipation?
Macrogol - an osmotic laxative
36
Name some types of bulk forming laxatives?
Ispaghula husk
Methylcellulose
37
Name some types of osmotic laxatives?
Lactulose
Macrogol
38
Name some types of stimulant laxatives?
Senna
Bisacodyl
39
Name a stool softener laxative?
Docusate sodium
40
Name some laxative suppositories?
Glycerol
Bisacodyl
41
Name some enema laxatives?
Phosphate
Sodium citrate
Docusate
42
What is the mechanism of action of bulk forming laxatives?
They increase the bulk of the stool, usually take 2-3 days to work. It is important to drink plenty of water alongside bulk laxatives
43
What is the mechanism of action of stimulant laxatives?
Stimulate the local nervous system within the gut wall which increase colonic contractility and secretions. They work in 6-12 hours. Better for those with difficulty emptying more so than infrequent motions
44
What is the mechanism of action of osmotic laxatives?
These are poorly absorbable molecules that cause an osmotic effect drawing water into bowel lumen. Very commonly used and very effective in faecal impaction and infrequent bowel motions
45
What is the mechanism of action of stool softening laxatives?
Lowers the surface tension, leading to water and fasts penetrating the stool.
46
What is the mechanism of action of suppository laxatives?
Used to aid rectal emptying by stimulating the anal sphincter and initiating peristalsis.
Used when there is an inadequate response to oral, incomplete emptying, incontinence, or altered rectal sensitivity. Causes more rapid evacuation
47
What is the mechanism of action of enema laxatives?
Include osmotic, softeners, and/or weak stimulants. A phosphate enema contains 128mL of liquid whereas other mini ones have 5mL. Act quickly to bring about a more rapid evacuation.
48
What are the risk factors for urinary incontinence?
Advancing age
Previous pregnancy and childbirth
High BMI
Hysterectomy
Family history
49
What are the different types of urinary incontinence?
Urge incontinence
Stress incontinence
Mixed incontinence
Overflow incontinence
Functional incontinence
50
What is an urge incontinence and what is it caused by?
The urge to urinate quickly followed by an uncontrollable leakage ranging from a few drops to complete emptying
Due to detrusor muscle overactivity
51
What is an stress incontinence and what is it caused by?
Leaking small amounts when coughing or laughing
52
The urge to urinate quickly followed by an uncontrollable leakage ranging from a few drops to complete emptying would be what?
Urge incontinence
53
Leaking small amounts when coughing or laughing would be what?
Stress incontinence
54
What is mixed incontinence?
Both urge and stress incontinence
55
What is overflow incontinence?
Due to bladder outlet obstruction e.g. prostate enlargement
56
What is functional incontinence?
Comorbid physical conditions impair the patient's ability to get to a bathroom in time
57
What are some causes of functional incontinence?
Dementia
Sedating medication
Injury / illness resulting in decreased ambulation
58
Incontinence due to bladder outlet obstruction e.g. prostate enlargement would be what?
Overflow incontinence
59
Incontinence due to comorbid physical conditions impair the patient's ability to get to a bathroom in time would be what?
Functional incontinence
60
What are the initial investigations for urinary incontinence?
Bladder diaries for a minimum of 3 days
Vaginal examination
Kegel exercises
Urine dipstick and culture
Urodynamic studies
61
What is the first line management for urge incontinence?
Bladder retraining for a minimum of 6 weeks
62
What is the first-line pharmacological management for urge incontinence?
Oxybutynin (immediate release)
63
What are the second line pharmacological agents used for urge incontinence?
Tolterodine (immediate release)
Darifenacin (once daily preparation)
64
What class of drugs are used first line in urge incontinence?
Antimuscarinics (anticholinergics)
65
In what demographic should oxybutynin be avoided?
Frail older women due to anticholinergic side-effects
66
What pharmacological agent should be used in 'frail older women' in urge incontinence?
Mirabegron
67
What class of drug is mirabegron?
A beta-3-agonist
68
What is the first line management for stress incontinence?
Pelvic floor retraining (Kegel exercises)
8 contractions performed 3 times per day for a minimum of 3 months
69
What is the second line management for stress incontinence?
Surgical procedures: e.g. retropubic mid-urethral tape procedures
70
What is the second line management for women for stress incontinence if they decline surgical procedures?
Duloxetine
71
What class of drug is duloxetine?
A combined noradrenaline and serotonin reuptake inhibitor
72
What is the mechanism of action of duloxetine?
Increased synaptic concentration of noradrenaline and serotonin within the pudendal nerve → increased stimulation of urethral striated muscles within the sphincter → enhanced contraction
73
List some risk factors for falls in the elderly?
Lower limb muscle weakness
Vision problems
Balance/gait disturbances (diabetes, rheumatoid arthritis and parkinson's disease etc)
Polypharmacy (4+ medications)
Incontinence
>65
Have a fear of falling
Depression
Postural hypotension
Arthritis in lower limbs
Psychoactive drugs
Cognitive impairment
74
List some medications that may cause postural hypotension?
Nitrates
Diuretics
Anticholinergic medications
Antidepressants
Beta-blockers
L-Dopa
ACE inhibitors
75
List some medications that may be associated with falls due to mechanisms other than postural hypotension?
Benzodiazepines
Antipsychotics
Opiates
Anticonvulsants
Codeine
Digoxin
Other sedative agents
76
What is osteoporosis?
Osteoporosis is a disorder affecting the skeletal system characterised by loss of bone mass.
WHO defines as presence of bone mineral density (BMD) of less than 2.5 standard deviations (SD) below the young adult mean density
77
What are the risk factors for osteoporosis?
Corticosteroid use
Smoking
Alcohol
Low BMI
Family history
78
What screening tool is used to measure a patients 10-year risk of developing a fragility fracture?
FRAX score
79
A FRAX score is used to assess what?
Used to measure a patients 10-year risk of developing a fragility fracture
80
What investigation is used to assess bone mineral density?
Dual-energy X-ray absorptiometry (DEXA)
81
What bones does a DEXA scan look at?
Hip and lumbar spine.
82
What is the first-line management for osteoporosis?
Alendronate OR
Risedronate OR
Etidronate
Vitamin D and calcium if deficient
83
What class of drug is alendronate and Risedronate?
Oral bisphosphonates
84
Explain the DEXA scan algorithm?
Step 1: Is a fragility fracture present?
- No = move on to step 2
- Yes = Make clinical diagnosis of osteoporosis if age ≥ 75 OR perform DEXA scan if age > 50
Step 2: Perform Fragility fracture risk assessment
- Low Risk = Repeat fragility fracture assessment in 5 years
- Intermediate-High Risk = perform DEXA scan
85
What does intermediate-high risk on FRAX scoring indicate for investigation?
Perform DEXA scan
86
What QFracture score would indicate a DEXA scan would be arranged?
>10%
87
What is the T score in a DEXA scan based off?
Based on bone mass of young reference population
88
What does a T score of -1 indicate for a DEXA scan?
-1.0 means bone mass of one standard deviation below that of young reference population
Osteopenia
89
What does a T score of -2.5 indicate for a DEXA scan?
-2.5 means bone mass of 2.5 standard deviations below that of young reference population
Osteoporosis
90
What is a Z score in a DEXA scan?
Z score is adjusted for age, gender and ethnic factors
91
What is the mechanism of action of bisphosphonates?
Bisphosphonates bind to hydroxyapatite in bone, inhibiting osteoclast-mediated bone resorption
92
What advice should be given when prescribing oral bisphosphonates?
Oral bisphosphonates should be taken with a full glass of water, on an empty stomach, and the patient should remain upright for at least 30 minutes afterwards
93
What is the second line management for osteoporosis?
Denosumab injection every 6 months
94
What are the potential third-line managements for osteoporosis?
Strontium ranelate
Raloxifene
Teriparatide
Romosozumab
95
What is the mechanism of action of denosumab?
Human monoclonal antibody that inhibits RANK ligand, which in turn inhibits the maturation of osteoclasts
96
At what level of corticosteroids should osteoporosis management be commenced anticipatorily?
Equivalent of prednisolone 7.5mg a day for 3 or more months.
97
What is normal pressure hydrocephalus? What is it thought to be caused by?
Normal pressure hydrocephalus is a reversible cause of dementia seen in elderly patients. It is thought to be secondary to reduced CSF absorption at the arachnoid villi.
98
What is the classic triad of features seen in normal pressure hydrocephalus?
Urinary incontinence
Dementia and bradyphrenia
Gait abnormality (may be similar to Parkinson’s disease)
99
What would the triad of urinary incontinence, dementia and bradyphrenia, gait abnormality (may be similar to Parkinson’s disease) suggest?
Normal pressure hydrocephalus
100
What would normal pressure hydrocephalus present with on imaging?
Hydrocephalus with ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement
101
Ventriculomegaly without sulcal enlargement on imaging of the brain would indicate what?
Normal pressure hydrocephalus
102
What is the management of normal pressure hydrocephalus?
Ventriculoperitoneal shunting
103
What are the complications of ventriculoperitoneal shunting?
Around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhages
104
What are some non-pharmacological managements of Alzheimer’s disease?
A range of activities to promote wellbeing that are tailored to the person’s preference
Group cognitive stimulation therapy for patients with mild and moderate dementia
Group reminiscence therapy and cognitive rehabilitation
105
What types of drugs are donepezil, galantamine and rivastigmine?
Acetylcholinesterase inhibitors
106
What pharmacological management can be given for mild to moderate Alzheimer’s disease?
Donepezil, Galantamine and Rivastigmine
107
What second line pharmacological management can be given for Alzheimer’s disease?
Memantine
108
What type of drug is memantine?
NMDA receptor antagonist
109
Under what conditions can the second line pharmacological management be used for Alzheimer’s disease?
For moderate Alzheimer’s who are intolerant of, or have a contraindication to, acetylcholinesterase inhibitors.
As an add-on drug to acetylcholinesterase inhibitors for patients with moderate or severe Alzheimer’s.
Monotherapy in severe Alzheimer’s
110
What feature would contraindicate use of donepezil?
Bradycardia
111
What is an adverse effect of donepezil?
Insomnia
112
What is the characteristic pathological feature of lewy-body dementia?
Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas.
113
Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas would suggest what?
Lewy-body dementia
114
What are the features of lewy-body dementia?
Progressive cognitive impairment which typically occurs before parkinsonism, but usually both features occur within a year of each other.
Cognition may be fluctuating (different to other dementias)
Parkinsonism
Visual hallucinations + dementia = lewy -body dementia
115
Visual hallucinations + dementia would indicate what?
Lewy body dementia
116
What pharmacological management can be given for mild to moderate lewy body dementia?
Donepezil and Rivastigmine
117
What second line pharmacological management can be given for Lewy body dementia?
Memantine
118
What class of drugs should be avoided in lewy body dementia and why?
Antipsychotics should be avoided in Lewy body dementia as patients are extremely sensitive and may develop irreversible parkinsonism.
E.g, Risperidone and Haloperidol.
119
What is frontotemporal lobular degeneration?
Frontotemporal lobar degeneration (FTLD) is the third most common type of cortical dementia after Alzheimer’s and Lewy body dementia.
120
What are the three recognised types of FTLD?
Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (chronic progressive aphasia, CPA)
Semantic dementia
121
What are the common features of FTLD?
Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills
Personality change and social conduct problems
122
What are the most common features of Frontotemporal dementia (Pick’s disease)?
Characterised by personality change and impaired social conduct.
123
What axillary features ‘may’ be present in Frontotemporal dementia (Pick’s disease)?
Hyperorality
Disinhibition
Increased appetite
Perseveration behaviours
124
What would you see on imaging for frontotemporal dementia (Pick’s disease)?
Focal gyral atrophy with a knife-blade appearance.
Macroscopic - Atrophy of the frontal and temporal lobes
Microscopic: Pick bodies - spherical aggregations of tau protein (silver-staining)
Gliosis
Neurofibrillary tangles
Senile plaques
125
What is the most common feature of chronic progressive aphasia (CPA)?
Here the chief factor is non fluent speech. They make short utterances that are agrammatic. Comprehension is relatively preserved.
126
What is the most common feature of semantic dementia?
A fluent progressive aphasia. The speech is fluent but empty and conveys little meaning. Unlike in Alzheimer’s memory is better for recent rather than remote events.
127
Define Alzheimer’s disease?
Alzheimer’s disease (AD) is a progressive degenerative disease of the brain accounting for the majority of dementia seen in the UK
128
What are the risk factors for Alzheimer’s disease?
Increasing age
Family history
Inherited autosomal trait
Apoprotein E allele E4
Caucasian ethnicity
Down syndrome
129
What autosomal dominant traits are associated with an increased risk of Alzheimer’s disease?
Mutations in:
- The amyloid precursor protein (chromosome 21)
- Presenilin 1 (chromosome 14)
- Presenilin 2 (chromosome 1) genes
130
What genetic condition is associated with an increased risk of Alzheimer’s disease?
Down syndrome
131
What macroscopic pathological changes are seen in Alzheimer’s disease?
Widespread cerebral atrophy, particularly involving the cortex and hippocampus
132
What microscopic pathological changes are seen in Alzheimer’s disease?
Cortical plaques due to deposition of type A-Beta-amyloid protein and intraneuronal neurofibrillary tangles caused by abnormal aggregation of the tau protein
Hyperphosphorylation of the tau protein has been linked to AD
133
What biochemical pathological changes are seen in Alzheimer’s disease?
There is a deficit of acetylcholine from damage to an ascending forebrain projection
134
What is the difference between Parkinson’s disease dementia and Lewy-body dementia?
Motor symptoms will be present before dementia symptoms for PDD.
PDD is diagnosed if a patient had a Parkinson’s disease diagnosis for at least 1 year.
135
What is Creutzfeldt-Jakob disease?
Creutzfeldt-Jakob disease (CJD) is rapidly progressive neurological condition caused by prion proteins.
136
What is the pathophysiology of Creutzfeldt-Jakob disease?
Prion proteins induce the formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases.
137
What are the features of Creutzfeld-Jakob disease?
Dementia with rapid onset
Myoclonus
138
What would you see on imaging with an individual with Creutzfeldt-Jakob disease?
MRI - hyperintense signals in the basal ganglia and thalamus.
139
Hyperintense signals in the basal ganglia and thalamus of an MRI would indicate what?
Creutzfeldt-Jakob disease
140
What is vascular dementia?
It is not a single disease but a group of syndromes of cognitive impairment caused by different mechanisms causing ischaemia or haemorrhage secondary to cerebrovascular disease.
141
What is the second most common form of dementia?
Vascular dementia
142
What are the subtypes of vascular dementia?
Stroke-related VD
Subcortical VD
Mixed dementia
143
What is stroke-related VD?
Vascular dementia caused by a multi-infarct or single-infarct dementia
144
What is subcortical VD?
Vascular dementia caused by small vessel disease.
145
What is mixed dementia?
The presence of both VD and Alzheimer's disease
146
What are the risk factors for vascular dementia?
History of stroke or transient ischaemic attack (TIA)
Atrial fibrillation
Hypertension
Diabetes mellitus
Hyperlipidaemia
Smoking
Obesity
Coronary heart disease
A family history of stroke or cardiovascular
147
In what disease would vascular dementia be inherited?
CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopath)
148
What is the typical presentation of vascular dementia?
Several months or several years of a history of a sudden or STEPWISE DETERIORATION of cognitive function.
149
What may some features of vascualar dementia be?
Focal neurological abnormalities e.g. visual disturbance, sensory or motor symptoms
The difficulty with attention and concentration
Seizures
Memory disturbance
Gait disturbance
Speech disturbance
Emotional disturbance
150
What criteria is used to diagnose vascular dementia?
NINDS-AIREN criteria
151
The NINDS-AIREN criteria is used for what?
For a diagnosis of vascular dementia
152
Outline the NINDS-AIREN criteria?
Presence of cognitive decline that interferes with activities of daily living, not due to secondary effects of the cerebrovascular event
Cerebrovascular disease defined by neurological signs and/or brain imaging
A relationship between the above two disorders inferred by:
- The onset of dementia within three months following a recognised stroke
- An abrupt deterioration in cognitive functions
fluctuating, stepwise
- Progression of cognitive deficits
153
What is the management for for vascular dementia?
Include: cognitive stimulation programmes, multisensory stimulation, music and art therapy, animal-assisted therapy
154
List some causes of Parkinsonism?
Parkinson's disease
Drug-induced e.g. antipsychotics, metoclopramide*
Progressive supranuclear palsy
Multiple system atrophy
Wilson's disease
Post-encephalitis
Dementia pugilistica (secondary to chronic head trauma e.g. boxing)
Toxins: carbon monoxide, MPTP
155
What is the cause of parkinsonism?
Parkinson's disease is a progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra.
156
What is the classic triad of parkinson's disease?
The reduction in dopaminergic output results in a classical triad of features: bradykinesia, tremor and rigidity.
The symptoms of Parkinson's disease are characteristically asymmetrical.
157
Describe the bradykinesia seen in Parkinson's disease?
Poverty of movement also seen, sometimes referred to as hypokinesia
Short, shuffling steps with reduced arm swinging
Difficulty in initiating movement
158
Describe the tremor seen in Parkinson's disease?
Most marked at rest, 3-5 Hz
Worse when stressed or tired, improves with voluntary movement
Typically 'pill-rolling', i.e. in the thumb and index finger
159
What are some other 'axillary' characteristics seen in Parkinson's disease?
Mast-like facies
Flexed posture
Micro-graphia
Drooling of saliva
Impaired olfaction
REM sleep disturbance
Fatigue
Postural hypertension
160
What is the first line management for Parkinson's disease if motor symptoms are affecting the quality of life?
Levodopa nearly always combined with a decarboxylase inhibitor (e.g. carbidopa or benserazide)
161
Why is levodopa combined with a decarboxylase inhibitor for Parkinson's therapy?
This prevents the peripheral metabolism of levodopa to dopamine outside of the brain and hence can reduce side effects
162
List some common side effects of levodopa?
Dry mouth
Anorexia
Palpitations
Postural hypotension
Psychosis
163
What pharmacological agent can be given for excessive salivation in Parkinson's disease?
Glycopyrronium bromide
164
What pharmacological agent should be considered if a patient with Parkinson's disease develops orthostatic hypotension? What is the mechanism of this drug?
Midodrine - acts on peripheral alpha-adrenergic receptors to increase arterial resistance
165
What pharmacological agent should be considered if excessive daytime sleepiness occurs in a patient with Parkinson's disease?
Modafinil
166
What is the first line management for Parkinson's disease if motor symptoms are NOT affecting the quality of life?
Dopamine agonist (non-ergot derived - ropinirole, apomorphine)
Levodopa
Monoamine oxidase B (MAO-B) inhibitor
167
What would a blood test show for osteoporosis?
Normal ALP
Normal calcium
Normal phosphate
Normal PTH
168
List some dopamine receptor agonists that are used in the treatment of Parkinson's disease?
Bromocriptine
Ropinirole
Cabergoline
Apomorphine
169
What investigations should be organised before prescribing ergot-derived dopamine receptor agonists?
Echocardiogram
ESR
Creatinine
Chest x-ray
Due to being associated with pulmonary, retroperitoneal and cardiac fibrosis
170
What class of Parkinson's drugs have potential for impulse control disorders?
Dopamine receptor agonists
171
What is the mechanism of action of MAO-B inhibitors? Give an example of this class of drug?
Monoamine Oxidase-B inhibitors work by inhibiting the breakdown of dopamine secreted by the dopaminergic neurones.
Selegiline
172
Give some examples of COMT inhibitors for Parkinson's disease?
Entacapone
Tolcapone
173
What is the mechanism of action of COMT inhibitors?
Catechol-O-Methyl Transferase inhibitors - an enzyme involved in the breakdown of dopamine, and hence may be used as an adjunct to levodopa therapy
174
What is 'end-of-dose' wearing off phenomenon in Parkinson's disease management?
Symptoms often worsen towards the end of dosage interval. This results in a decline of motor activity
175
What is 'on-off phenomenon' in Parkinson's disease management?
Large variations in motor performance, with normal function during the 'on' period, and weakness and restricted mobility during the 'off' period
176
What side-effects may be seen at peak dose of levadopa?
Dystonia, chorea and athetosis (involuntary writhing movements)
177
What is benign paroxysmal positional vertigo?
One of the most common causes of vertigo encountered.
It is characterised by the sudden onset of dizziness and vertigo triggered by changes in head position.
178
What are the classical features of benign paroxysmal positional vertigo?
Vertigo triggered by change in head position (e.g. rolling over in bed or gazing upwards)
May be associated with nausea
Each episode lasts for approximately 10-20 seconds
179
What investigation can be used to assess for benign paroxysmal positional vertigo?
Dix-Hallpike manoeuvre - rapidly lower the patient to the supine position with an extended neck. Positive test recreates symptoms. There is also rotary nystagmus
180
What is the management for benign paroxysmal positional vertigo?
Epley manoeuvre
181
Define stroke?
A stroke (also known as cerebrovascular accident, CVA) represents a sudden interruption in the vascular supply of the brain.
182
What about the metabolism of neural tissue means that strokes are devastating?
Neural tissue is completely dependent on aerobic metabolism so any problem with oxygen supply can quickly lead to irreversible damage.
183
What are the two types of stroke?
Ischeamic - 85% - 'Blockage' in the blood vessel stops blood flow
Haemorrhagic - 15% - Blood vessel 'bursts' leading to reduction in blood flow
184
What is the difference between a stroke and TIA?
TIA describes the sudden onset of a focal neurologic symptom and/or sign lasting typically less than an hour, brought on by a transient decrease in blood flow. A stroke on the other had will cause permanent damage.
185
What are the subtypes of ischaemic stroke?
Thrombotic stroke - thrombosis from large vessel
Embolic stroke - blood clot, fat, air, bacteria
186
What are the subtypes of haemorrhagic stroke?
Intracerebral haemorrhage - bleeding within the brain
Subarachnoid haemorrhage - bleeding on the surface of the brain
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What is heart failure?
Heart failure may be defined as a clinical syndrome where the heart is unable to pump enough blood to meet the metabolic needs of the body.
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What classification system is used to classify the severity of heart failure?
The New York Heart Association (NYHA) classification
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What is the The New York Heart Association (NYHA) classification used for?
Used to classify the severity of heart failure.
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NYHA Class I would indicate what?
No symptoms
No limitation
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NYHA Class II would indicate what?
Mild symptoms
Slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
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NYHA Class III would indicate what?
Moderate symptoms
Marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
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NYHA Class IV would indicate what?
Severe symptoms
Unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
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What is heart failure with reduced ejection fraction defined as?
Left ventricular ejection fraction is typically defined as < 35 to 40%
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What type of dysfunction do patients with HF-pEF have?
Diastolic dysfunction (impaired ventricular filling during diastole).
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Diastolic dysfunction (impaired ventricular filling during diastole) would be what type of heart failure?
HF-pEF
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What type of dysfunction do patients with HF-rEF have?
HF-rEF patients typically have systolic dysfunction (impaired myocardial contraction during systole)
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Systolic dysfunction (impaired myocardial contraction during systole) would be what type of heart failure?
HF-rEF
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What is the most common reason for a heart failure patient to present to the Emergency Department?
The most urgent symptoms are often due to left ventricular failure, resulting in pulmonary oedema.
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Left ventricular failure would present with what symptoms?
Pulmonary oedema:
Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
Bibasal fine crackles
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Right ventricular failure would present with what symptoms?
Peripheral oedema - ankle/sacral oedema
Raised jugular venous pressure
Hepatomegaly
Weight gain due to fluid retention
Anorexia ('cardiac cachexia')
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What are the first line investigations for heart failure?
N-terminal pro-B-type natriuretic peptide (NT-proBNP)
B-type natriuretic peptide (BNP)
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What would normal levels of NTproBNP and BNP be?
BNP - < 100 pg/m
NTproBNP - < 400 pg/ml
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What would raised levels of NTproBNP and BNP be?
BNP - 100-400 pg/ml
NTproBNP - 400-2000 pg/ml
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What would high levels of NTproBNP and BNP be?
BNP - > 400 pg/ml
NTproBNP - > 2000 pg/ml
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What would the interpretation be of a raised NTproBNP blood test?
Arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
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What would the interpretation be of a high NTproBNP blood test?
Arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
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What is the first-line pharmacological management of heart failure?
ACE-Inhibitor
Beta-blocker
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What are some examples of beta-blockers that may be used in treatment of heart failure?
Bisoprolol
Carvedilol
Nebivolol
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What are the second-line therapies for heart failure?
Aldosterone antagonist
SGLT-2 inhibitors
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What are some examples of aldosterone antagonists used in heart failure?
Spironolactone
Eplerenone
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What should you be conscious of when prescribing both ACE inhibitors and aldosterone antagonists in heart failure patients?
They both cause hyperkalaemia - therefore potassium should be monitored
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What are some examples of SGLT-2 inhibitors?
Canagliflozin
Dapagliflozin
Empagliflozin
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What is the mechanism of action of SGLT-2 inhibitors?
Reduce glucose reabsorption and increase urinary glucose excretion
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What class of drugs have not been shown to reduce mortality in heart failure?
No long-term reduction in mortality has been demonstrated for loop diuretics such as furosemide
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What would the symptoms of a cerebral hemisphere infarct be?
Contralateral hemiplegia: Initially flaccid then spastic
Contralateral sensory loss
Homonymous hemianopia
Dysphasia
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What would the symptoms of a brainstem infarct be?
May result in more severe symptoms including quadriplegia and lock-in-syndrome
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What would the symptoms of a lacunar infarct be?
May result in pure motor, pure sensory, mixed motor and sensory signs or ataxia
219
What classification system is used to classify strokes based on the initial symptoms?
Oxford stroke classification (also known as the Bamford classification)
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What is the Oxford stroke classification (Bamford classification) used for?
Used to classify strokes based on the initial symptoms
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What criteria are assessed in the Oxford stroke classification (Bamford classification)?
1. Unilateral hemiparesis and/or hemisensory loss of the face, arm & leg
2. Homonymous hemianopia
3. Higher cognitive dysfunction e.g. dysphasia
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How would a total anterior circulation infarct present and what arteries would be involved?
All three of the Oxford stroke classification (Bamford classification)
Involves the middle and anterior cerebral arteries
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How would a partial anterior circulation infarct present and what arteries would be involved?
2/3 of the Oxford stroke classification (Bamford classification)
Involves the smaller arteries of anterior circulation e.g. upper and lower division of the middle cerebral arteries
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How would a lacunar infarct present and what arteries would be present?
1 of the following:
1. Unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. Pure sensory stroke.
3. Ataxic hemiparesis
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How would a posterior circulation infarct present and what arteries would be involved?
Presents with 1 of the following:
1. cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia
Involves the vertebrobasilar arteries
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What symptoms may be useful to differentiate between a ischaemic or haemorrhagic stroke?
Haemorrhagic stroke patients are more likely to have:
Decreased level of consciousness.
Headache
Nausea and vomiting
Seizures
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What is the first line investigation for a stroke?
Non contrast CT of the head
MRI can also be used
228
What is the first line management for an ischaemic stroke?
300mg aspirin*
*only if a haemorrhagic stroke has been excluded with brain imaging
Cholesterol >3.5 mmol/l then give statin
229
What is the criteria for thrombolysis for stroke?
Administered within 4.5 hours of onset of stroke symptoms
Haemorrhagic stroke has been excluded
Blood pressure to be lowered to 185/110 mmHg
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What pharmacological agents are given for thrombolysis in stroke?
Alteplase
Tenecteplase
231
What is the secondary prevention pharmacological agent for stroke?
Clopidogrel
Aspirin + modified-release (MR) dipyridamole if contraindicated
