Neurology Flashcards

1
Q

What is shingles also known as?

A

Herpes Zoster Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes shingles?

A

reactivation of varicella zoster virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Key risk factors for shingles

A

increasing age, immunosuppressive conditions, HIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

typical presentation of shingles

A

acute, unilateral, painful blistering rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Which dermatomes are commonly affected in shingles

A

T1- L2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Features of shingles

A

prodromal period

  • 2-3day hx of burning pain over the dermatomes affected
  • may have fever, headache, lethargy

Rash

  • erythematous, macular rash which becomes vesicular
  • demarcated by dermatome and doesnt cross the midline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is shingles diagnosed?

A

clinical diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the medical management of shingles?

A

Analgesia

  • paracetemol and NSAIDs
  • amitriptyline if first line insufficient
  • oral corticosteroids if not responding to the above

Antivirals within 72hrs unless <50yo and mild rash/pain with no risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Advice given to patient with shingles

A

remind them they are infectious until vesicles have crusted over usually 5-7 days following onset (avoid pregnant and immunosuppressed people)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the complications of shingles

A
  • post- herpetic neuralgia
  • herpes zoster ophthalmicus
  • herpes zoster oticus (Ramsay Hunt syndrome):
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is syncope?

A

transient loss of consciousness with spontaneous complete recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the main causes of syncope?

A
  • Reflex mediated (neurally mediated)
  • Cardiac (arrhythmias and structural causes)
  • Orthostatic (iatrogenic, dementia, volume depletion)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which investigations should be carried out in syncope?

A
  • ECG (?prolonged QT)
  • lying standing BP / tilt table test
  • Glucose
  • Electrolytes
  • FBC
  • Underlying illness (CXR, CT, LP, ECHO etc)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of cardiac syncope

A
arrhythmias 
- bradycardia / tachycardia 
structural
- valvular
- MI
- HOCM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Treatment of cardiac syncope

A

treat the problem

  • medicine (beta blockers, atropine)
  • electrical cardioversion
  • catheter ablation
  • pacemaker
  • implantable cardioverter defibrillator (ICD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is vasovagal syncope?

A

triggered by emotion, pain or stress. Often referred to as ‘fainting’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is subarachnoid haemorrhage?

A

presence of blood in the subarachnoid space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the causes of SAH?

A

head injury (traumatic SAH) is the most common cause

spontaneous SAH (non-traumatic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes of spontaneous SAH

A
  • Intracranial aneurysm( ruptured ‘berry’ aneurysms)

- Arterial dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Which conditions are associated with berry aneurysms?

A
  • Adult Polycystic Kidney Disease

- coarctation of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Classical presentation of SAH

A
  • Thunderclap headache
  • N&V
  • Meningism (photophobia, stiff neck)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How can a SAH be confirmed?

A

CT head
LP if CT Head if negative
Neuro referral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which findings on an LP are indicative of SAH

A

xanthochromia (result of RBC breakdown) and normal or raised opening pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

After SAH is confirmed, which investigations can be carried out to identify a causative pathology?

A

CT inter-cranial angiogram (vascular lesion e.g aneurysm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What is Multiple sclerosis?
autoimmune disorder characterised by demyelination in the central nervous system
26
Who is at higher risk of MS
women ages 20-40 living at higher latitude
27
How can MS be diagnosed
refer to neuro and bloods to exclude other causes
28
What are the most common initial presentations of MS
- optic neuritis - transverse myelitis (inflammation within spinal cord) - cerebellar sx ( dysmetria, ataxia, vertigo) sx disseminated in time and space
29
Which investigations should be carried out for MS?
MRI
30
How is an acute relapse of MS treated?
High dose steroids (methylprednisolone) to shorten duration of relapse
31
What is a venous sinus thrombosis?
occurs when a blood clot forms in the brain's venous sinuses. This prevents blood from draining out of the brain. As a result, blood cells may break and leak blood into the brain tissues, forming a hemorrhage.
32
What are the symptoms of venous sinus thrombosis?
- headaches - n&v - blurred vision - LOC - seizures
33
How is venous sinus thrombosis diagnosed?
MRI venography CT venography
34
Treatment of venous sinus thrombosis
Heparin | Warfarin for long term
35
What is a Cavernous sinus thrombosis
the formation of a clot within the cavernous sinus
36
What is the most common cause of CST
infection
37
Common clinical features of CST
headache, unilateral periorbital oedema, proptosis (eye bulging), photophobia and cranial nerve palsies
38
Which nerve is most commonly affected in CST
abducens nerve (CN VI)
39
Complication of CST
Where the cause is infection, thrombosis of the cavernous sinus can rapidly progress to meningitis.
40
Investigations requested in suspected CST
CT Head/ MRI FBC Blood culture ?LP
41
How is CST treated
Abx for causative infection
42
Which seizures last a few seconds and are associated with a quick recovery
Absence
43
What may provoke an absence seizure
hyperventilation or stress
44
Who is most commonly affected by absence seizures?
3-10 years old and girls are affected twice as commonly as boys
45
How are absence seizures managed?
sodium valproate and ethosuximide are first-line treatment
46
Prognosis of absence seizures
good prognosis - most become seizure free in adolescence
47
Status epilepticus is defined as...
a single seizure lasting >5 minutes OR | >= 2 seizures within a 5-minute period without the person returning to normal between them
48
Why is the priority in Status epilepticus to terminate seizure activity
can lead to irreversible brain damage
49
What is the immediate management of Status epilepticus?
ABC | IV benzodiazepines
50
What may be used in management if there is ongoing status epilepticus
phenytoin or phenobarbital infusion
51
What is a febrile convulsion?
seizures provoked by fever in otherwise normal children
52
clinical features of febrile convulsion
usually occur early in a viral infection usually lasting less than 5 minutes most commonly tonic-clonic
53
How can a generalise seizure be further classified
Motor- e.g tonic-clonic | Non-motor - e.g absence
54
Sx of epilepsy
bite their tongue incontinence of urine post-ictal phase
55
Which investigations are ordered following a patients first seizure?
EEG and MRI
56
First line tx for generalised seizure
sodium valproate
57
First line tx for focal seizure
carbamazepine
58
What are the guidelines for driving post seizure?
- Generally patients cannot drive for 6 months following a seizure. - For patients with established epilepsy they must be fit free for 12 months before being able to drive
59
What is the difference between a generalised and focal seizure?
Focal onset seizures start in one area and can spread across the brain and cause mild or severe symptoms, depending on how the electrical discharges spread. Generalized seizures can start as focal seizures that spread to both sides of the brain.
60
What happens in tonic-clonic seizure?
``` Tonic - muscles stiffen - LOC - tongue biting Clonic - rhythmical jerking ```
61
What is Bell's palsy?
Acute, unilateral facial nerve (CN VII) paralysis | - rapid onset ( < 72 hours)
62
Features of Bell's palsy
- Lower motor neuron facial nerve : forehead affected - Post-auricular pain (preceding paralysis) - Altered taste - Dry eyes Facial muscle weakness (unilateral): - drooping of the eyebrows - corner of the mouth - loss of the nasolabial fold
63
What is the bell's phenomenon?
The eye can't be closed- eyeball rotates upwards and outwards
64
What is the management of bell's palsy?
- oral prednisolone within 72 hours - Seek specialist advice - Eyecare: prescription of artificial tear + eye lubricants
65
What is the follow-up for bell's palsy?
If paralysis shows no improvement after 3 week, refer to ENT urgently
66
What is the prognosis for bell's palsy?
Full recovery within 3-4 months
67
What dose of prednisolone is given in bell's palsy?
50 mg for 10 days
68
What are the two main ascending tracts of the spinal cord and what information do they carry?
Dorsal - fine touch, proprioception, vibration sense | Spinothalamic - pain and temperature
69
What is the descending tract of the spinal cord called and what does it carry?
corticospinal tract carries motor information
70
Which signs indicate there is a problem with the spinal cord rather than with the other parts of the nervous system?
often bilateral and asymmetrical mixed upper and lower motor neuron signs as the spinal cord is part of both the CNS and PNS - upper signs : increased tone, clonus, hyperreflexia - lower signs: muscle wasting, flaccid paralysis, reduced reflexes sphincter involvement (e.g urinary retention/constipation) autonomic dysfunction indicates lesion is above T6
71
How to tell where in the spinal cord the problem is
cervical if all 4 limbs affected thoracic if only lower limbs affected above C3 if resp difficulties and diaphragm affected
72
What is Amyotrophic lateral sclerosis
(motor neuron disease) affects both upper (corticospinal tracts) and lower motor neurons results in a combination of upper and lower motor neuron signs
73
What features are seen in neoplastic spinal cord decompression?
back pain, may be worse on coughing or lying down - lower limb weakness - sensory loss or numbness - neuro signs dependent on level of lesion - -above L1 usually UMN in legs and sensory - - below L1 usually LMN in legs and perianal numbness
74
Which investigation should be requested following suspected neoplastic spinal cord decompression?
urgent whole MRI spine within 24hrs of presentation
75
Management of neoplastic spinal cord decompression
high-dose oral dexamethasone urgent oncological assessment for consideration of radiotherapy or surgery
76
What are the symptoms of diabetic peripheral neuropathy?
Sensory loss: - Tingling - Numbness - unable to feel light touch - Cannot feel pain - Unable to detect change in temperature
77
Management of diabetic peripheral neuropathy
1st line = amitriptyline, duloxetine, gabapentin or pregabalin - glycaemic control - referral to podiatry
78
What are the presentations of diabetic foot disease?
1. neuropathy: loss of sensation | 2. ischaemia: absent foot pulses, reduced ankle-brachial pressure index (ABPI), intermittent claudication
79
What is involved in annual diabetic foot check?
1. screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse 2. screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot
80
What is guillain-barre syndrome?
immune-mediated demyelination of the peripheral nervous system often triggered by an infection
81
What infection triggers guillain-barre syndrome?
campylobacter jejuni
82
What are the characteristic features of guillain-barre syndrome?
Progressive, symmetrical weakness of all limbs - usually ascending (leg first) - reflexes reduced or absent - mild sensory symptoms
83
What are the other features for guillain-barre syndrome?
1. Weakness - Maximum severity at 2 weeks after initial onset , stops progressing after 5 weeks - Facial weakness, dysphasia, dysarthria - May lead to resp failure 2. Pain – neuropathic pain esp in legs, possible back pain 3. Reflexes – may be reduced or absent 4. Sensory symptoms – paraesthesia & sensory loss starting in the lower extremities 5. Autonomic symptoms – reduced sweating, heat tolerance, urinary hesitancy
84
How do you diagnose GBS?
Clinical assessment
85
What investigations may be helpful in diagnosing GBS?
1. Nerve conduction studies – most useful confirmatory test, if initially normal should be repeated after 2 weeks. 2. Lumbar puncture – elevated level of CSF protein with normal white cell count, week 1 after symptom onset
86
Management of GBS
1. Admission to hospital, preferably hospital with Neuro Critical Care capabilities 2. Intravenous Immunoglobulin or Plasmapheresis. - -> IVIG - contraindicated in IgA deficiency or renal impairment 3. DVT prophylaxis – until able to walk independently 4. Watch pt. closely for need of intubation 5. Initiate cardiac monitoring – 6. HTN management 7. Pain control – gabapentin, opiates, carbamazepine 8. Physical Therapy to avoid contractures, maintain flexibility 9. Rehabilitation MDT approach Psychological support for pt. and family
87
What does Chronic IDP stand for?
chronic inflammatory demyelinating polyneuropathy
88
Symptoms of Chronic IDP
1. Initially present with some limb weakness which will slowly progress to symmetrical weakness in muscles of the hands, feet, shoulder and hip. 2. Symptoms may be progressive, episodic or monophasic (1-3 years). 3. Symptoms should last > 8 weeks 4. Loss of sensation, numbness, tingling, pins and needles
89
Clinical features of Chronic IDP
1. Muscle atrophy in hands, feet, shoulders and hips 2. Absent or diminished deep tendon reflexes 3. Impaired responses to sensory stimulation 4. Ataxic gait 5. Some cranial nerve involvement such as dysphagia or diplopia
90
Investigations of Chronic IDP
- NCS - Lumbar Puncture - Peripheral nerve biopsy
91
Management of Chronic IDP
Conservative: - Physical and occupational therapy to prevent accumulating disability over time and encouraging active lifestyle. Medical : 1st line: - Intravenous Immunoglobulin (IVIG) - Plasma exchange – may only be effective for several weeks and therefore may require an intermittent treatment schedule. - Corticosteroids – used in with immunosuppressants. 1. Long term immunosuppression : Takes the attack off the peripheral nerves 2. Pharmacotherapy for neuropathic pain : e.g. gabapentin & pregabalin
92
Features of migraine
1. a severe, unilateral, throbbing headache - -> attacks may last up to 72 hours 2. associated with nausea, photophobia and phonophobia 3. patients characteristically go to a darkened, quiet room during an attack 4. 'classic' migraine attacks are precipitated by an aura. 5. typical aura are visual, progressive, last 5-60 minutes and are characterised by transient hemianopic disturbance or a spreading scintillating scotoma
93
Management of migraine
Headache diary, avoid triggers – sleep, stress, hydrate, regular meals 1. Acute: - -> 1st line: triptan and NSAID - -> simple analgesia – ibuprofen, aspirin, paracetamol before onset - -> Anti-emetic: metoclopramide - -> Follow-up within 2-8 weeks 2. Preventative: propranolol, topiramate or amitriptyline 3. Refer: migraine > 72 hours, typical aura: motor weakness, poor balance, headache changes
94
What medication is contraindicated in migraine with aura?
COCP
95
Symptoms of tension headache
* often described as a 'tight band' around the head or a pressure sensation. * bilateral * tends to be of a lower intensity than migraine * may be related to stress
96
Management of tension headache
- Acute: 1st line (aspirin, paracetamol or an NSAID) - Prophylaxis: 10 sessions of acupuncture over 5-8 weeks - -> Low dose amitriptyline (10-75mg) - ----->Not responsive – stop and discuss neuro - ----->Responsive – attempt withdrawal 4-6 months
97
Symptoms of cluster headache
1. Unilateral periorbital pain 2. Ipsilateral autonomic symptoms: eyelid oedema, facial sweating or flushing, nasal congestion, conjunctival injection, lacrimation 3. Brief attacks of < 3 hours duration 4. pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours 5. clusters typically last 4-12 weeks
98
Management of cluster headache
1. acute: 100% oxygen, subcutaneous triptan 2. prophylaxis: verapamil is the drug of choice. 3. Seek specialist advice from a neurologist if a patient develops cluster headaches with respect to neuroimaging
99
What is essential tremor?
Autosomal dominant condition which usually affects both upper limbs
100
Features of essential tremor
- postural tremor: worse if arms outstretched | - improved by alcohol and rest
101
Management of essential tremor
1st line = propanolol at low dose
102
What is parkinson's disease?
Progressive neurodegenerative condition caused by degeneration of dopaminergic neurons in the substantia nigra
103
What is the classic triad of features of parkinson's disease?
1. Bradykinesia - short, shuffling steps - difficulty initiating movement 2. Tremor - worse when stessed or tired - 'pill-rolling' 3. Rigidity - lead pipe
104
How is parkinson's diagnosed?
usually clinical
105
What investigation can distinguish between essential tremor and parkinson's?
- Single-photon emission computed tomography
106
How do you differentiate between parkinson's disease and drug-induced parkinsonism?
In drug-induced parkisonism: - motor symptoms are generally rapid onset and bilateral - rigidity and rest tremor are uncommon
107
Management of parkinson's disease
Only specialist should initiate treatment: 1st line: Levodopa - if motor symptoms affecting QOL Dopamine agonist - if motor symptoms not affecting QOL
108
What is huntington's disease?
- inherited neurodegenerative condition. | - progressive and incurable condition that typically results in death 20 years after the initial symptoms develop.
109
Features of huntington's disease
Typically develop after 35 years of age: - chorea - personality changes (e.g. irritability, apathy, depression) and intellectual impairment - dystonia - saccadic eye movements
110
What can peripheral neuropathy conditions be divided into?
1. Motor loss | 2. Sensory loss
111
What conditions cause motor loss in peripheral. neuropathy?
1. Guillain-Barre syndrome 2. lead poisoning 3. chronic inflammatory demyelinating polyneuropathy (CIDP) 4. diphtheria
112
What conditions cause sensory loss in peripheral. neuropathy?
1. diabetes 2. uraemia 3. leprosy 4. alcoholism 5. vitamin B12 deficiency 6. amyloidosis
113
What nerve damage causes a foot drop?
Peroneal nerve (L4-L5, S1-S2)
114
What nerve damage causes a wrist drop?
Radial nerve
115
What is carpel tunnel syndrome?
When carpel tunnel is swollen/inflammed - the median nerve is affected
116
Symptoms of carpel tunnel syndrome
- Aching, tingling, pins & needles - Symptoms can spread up the arm - Worse on movement - temporary relief by hanging had out of bed at night or shaking vigorously
117
What examination tests do you carry out for carpel tunnel syndrome?
Phalens - hold wrist fully palmarflexed - tap on wrist reproduces symtpoms Tinel's sign - tapping over dorsum of the wrist percipitates pain
118
What does wasting of the thenar eminence indicate?
Median nerve affected
119
What investigation can be carried out for carpel tunnel syndrome?
NCS
120
Management of carpel tunnel syndrome
- Spontaneously resolves 3-6 months < 30 y/o - Splint - Steroid injection? - Referral for surgical decompression
121
What do you not prescribe for carpel tunnel syndrome?
NSAIDs
122
What is myasthenia gravis?
Autoimmune disorder from insufficient functioning ACh receptors Affect women > men
123
What is the key feature of myasthenia gravis?
muscle fatigability - worsens with activity - improves after rest
124
What other features can you get with myasthenia gravis?
- extraocular muscle weakness: diplopia - proximal muscle weakness: face, neck, limb girdle - ptosis - dysphagia
125
What is the diagnostic test for myasthenia gravis?
- Serological testing for ACh receptor antibodies | - Repetitive EMG
126
Management of myasthenia gravis
1st line = pyridostigmine (long-acting acetylcholinesterase inhibitors) - Eventually immunosuppression : prednisolone
127
Management of myasthenic crisis
- plasmapheresis | - IV immunoglobulins
128
What is cerebral palsy?
disorder of movement and posture due to a non-progressive lesion of the motor pathways in the developing brain
129
What is the classification of cerebral palsy?
1. Spastic 2. dyskinetic 3. ataxic 4. mixed
130
What non-motor problems can children with cerebral palsy develop?
1. learning difficulties (60%) 2. epilepsy (30%) 3. squints (30%) 4. hearing impairment (20%)
131
What are the possible manifestations of cerebral palsy?
1. abnormal tone early infancy 2. delayed motor milestones 3. abnormal gait 4. feeding difficulties.
132
Management of cerebral palsy?
1. MDT approach 2. Oral diazepam - for spasticity 3. Anticonvulsant , analgesia
133
What is stroke?
sudden interruption in the vascular supply of the brain
134
What are the types of stoke?
1. Ischaemic - subtype: TIA - ' blockage in blood vessel' 2. Haemorrhagic - blood vessel burst leading to reduction in blood
135
What are the symptoms of a stroke?
1. Motor weakness 2. speech problems (dysphasia) 3. swallowing problems 4. visual field defects 5. balance problems
136
What are some symptoms more common with haemorrhagic stroke than ischaemic?
- decrease in consciousness - headache - N & V - Seizures
137
What is the FAST campaign?
1. Face - 'Has their face fallen on one side? Can they smile?' 2. Arms - 'Can they raise both arms and keep them there?' 3. Speech - 'Is their speech slurred?' 4, Time - 'Time to call 999 if you see any single one of these signs.'
138
What are the 2 types of imaging used in stroke?
CT MRI 1st line = non-contrast CT head
139
What criteria needs to be met for immediate treatment of ischaemic stroke?
Criteria 1. patients present with 4.5 hours of onset of stroke symptoms 2. the patient has not had a previous intracranial haemorrhage, uncontrolled hypertension, pregnant etc
140
What is the immediate management of ischaemic stroke?
Alteplase (< 4.5 hours) Aspirin 300mg within 24 hours
141
What is the management of confirmed haemorrhagic stroke?
Neurosurgical consultation Those not suitable for surgery: 1. Supportive: stop anticoag + antithrombotic meds 2. ? lower BP acutely
142
What is the surgical option for acute ischaemic stroke?
Thrombectomy
143
Secondary prevention for stroke
1st line = Clopidogrel 2nd line = aspirin + modified-release (MR) dipyridamole
144
What other factors need to be treated in stroke?
1. fluid management 2. Glycaemic control 3. BP 4. Feeding assessment + management
145
What is TIA?
a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without acute infarction. (<24 hours)
146
Clinical features of TIA
- unilateral weakness or sensory loss. - aphasia or dysarthria - ataxia, vertigo, or loss of balance symptoms typically resolve within 1 hour
147
Immediate management of TIA | Contraindications
Aspirin 300 mg immediately, unless 1. the patient has a bleeding disorder or is taking an anticoagulant (needs immediate admission for imaging to exclude a haemorrhage) 2. the patient is already taking low-dose aspirin regularly: continue the current dose of aspirin until reviewed by a specialist 3. Aspirin is contraindicated: discuss management urgently with the specialist team
148
What is the advice on driving for TIA?
Do not drive until seen by specialist
149
What investigation should be carried out for TIA?
1. MRI - to detect territory of ischaemia 2. Urgent carotid doppler CT should be done unless alternative diagnosis
150
Management of TIA
1st line = Clopidogrel
151
What is raised intracranial pressure?
Additional volume in the brain + ventricles
152
Features of raised ICP
1. headache 2. vomiting 3. reduced levels of consciousness 4. papilloedema 5. Cushing's triad - widening pulse pressure - bradycardia - irregular breathing
153
What investigations should be carried out for raised ICP?
1. Neuroimaging = underlying causes | 2. Invasive ICP monitoring
154
Management of raised ICP
1. Head elevation to 30 degrees 2. IV mannitol 3. Controlled hyperventilation 4. Removal of CSF
155
What is temporal arteritis?
Large vessel vasculitis which overlaps with polymyalgia rheumatica (PMR).
156
Features of temporal arteritis
1. Jaw claudication 2. temporal headache 3. eventually leads to vision loss as optic nerve loses blood supply as large to medium vessels becomes narrowed. 4. Can be systemically unwell. 5. Hard, non-pulsating temporal artery (normal = pulsating, able to palpate and doesn’t feel hard)
157
What is the gold standard investigation for temporal arteritis?
USS and biopsy - raised ESR > 50mm/hr
158
Management of temporal arteritis
Urgent steroid course = high dose glucocorticoids - as soon as diagnosis is suspected before biopsy 1. no visual loss = high dose prednisolone 2. visual loss = IV methylprednisolone before high-dose prednisolone
159
What is vasculitis?
Inflammation of small vessels | - May be drug reaction
160
Symptoms of vasculitis
- Itching, burning purpuritic rash | - 1-3mm lesions, often on legs
161
Treatment of vasculitis
1. Treat underlying cause, if known 2. Compression stockings, elevation 3. Sedating antihistamine 4. Colchicine/Dapsone if no systemic involvement 5. High-dose steroid if systemic involvement, +/- methotrexate, azathioprine
162
What is Alzheimers?
progressive degenerative disease of the brain
163
Non-pharmacological management of Alzheimers
offer wellbeing services and group cognitive stimulation therapy
164
pharmacological management of Alzheimers
First line: acetylcholinesterase inhibitors (donepezil, galantamine, rivastigmine) Second line: memantine (an NMDA receptor antagonist)
165
When should antipsychotics be given to patients with Alzheimers?
when pt is at risk of harming themselves or others or has delusions/hallucinations causing them severe distress
166
What is the most common causative pathogen in enchephalitis?
HSV-1
167
Symptoms of enchephalitis
``` confusion or disorientation. seizures or fits. changes in personality and behaviour. difficulty speaking. weakness or loss of movement in some parts of the body. loss of consciousness. ```
168
Which investigations should be requested in ?encephalitis
CSF PCR for HSV MRI EEG
169
What might you see in CSF of encephalitic patient
lymphocytosis, elevated protein
170
What is the tx of all cases of suspected encephalitis?
IV Aciclovir
171
Life threatening complication of meningitis
septicaemia resulting in permanent damage of nerves or brain
172
Symptoms of meningitis
headache, neck stiffness, photophobia, confusion, fevers, non-blanching rash
173
Gold standard investigation for meningitis
lumbar puncture
174
Characteristic CSF findings in bacterial meningitis
cloudy, low glucose, high protein
175
What should be given to patients with suspected meningococcal disease in a pre-hospital setting?
IM benzylpenicillin
176
When should you suspect hiv ?
- unusually severe/prolonged symptoms that are recurrent or unexplained - conditions related to immunosuppression (shingles/oral candidiasis) - lymphadenopathy - pyrexia - weight loss
177
HIV risk factors
- coming from high prevalence area - sex between men and men - injecting drug use
178
When should asymptomatic patients with HIV be tested after possible exposure?
at 4 weeks
179
How is HIV monitored
HIV viral load and CD4 lymphocyte cell count
180
What are people with CD4 count <200 at a higher risk of?
HIV-related opportunistic infections and cancers
181
How is HIV treated
antiretrovirals - suppresses viral replication but does not eliminate HIV therefore treatment is lifelong
182
The causative pathogen of tuberculosis
Mycobacterium tuberculosis
183
Which vaccine offers protection against TB
BCG
184
What are the 2 types of TB
PRIMARY infection occurring in previously uninfected host , usually asymptomatic SECONDARY If the host becomes immunocompromised the initial infection may become reactivated.
185
Gold standard investigation for active TB
Sputum culture
186
What investigations may be requested in ?active TB
Sputum culture -GOLD STANDARD CXR NAAT
187
What is a classical finding in CXRs in active TB
Upper lobe cavitation and hilar lymphadenopathy
188
What is the standard therapy for treating active TB and how long should they be given
``` first 2 months: Rifampicin Isoniazid Pyrazinamide Ethambutol ``` continue for further 4 months: Rifampicin Isoniazid
189
How is latent TB treated
3 months of isoniazid (with pyridoxine) and rifampicin OR 6 months of isoniazid (with pyridoxine) pyridoxine reduces the occurence of isoniazid side effects
190
Give key side effects for TB drugs
Rifampicin : red/orange secretions Isoniazid: peripheral neuropathy Pyrazinamide: hyperuricaemia=gout Ethambutol : optic neuritis
191
Primary and secondary features of syphilis
Primary features - chancre - lymphadenopathy Secondary features - occurs 6-10 weeks after primary infection - systemic symptoms: fevers, lymphadenopathy - rash on trunk, palms and soles - condylomata lata (painless, warty lesions on the genitalia )
192
Investigations for ?syphilis
clinical diagnosis and GUM referral for serology and microscopic
193
Management of syphilis
IM Benzathine penicillin
194
How is lyme disease spread
ticks
195
key features of lyme disease
``` erythema migrans (bulls eye rash) systemic features (headaches, lethargy, fever) ```
196
How is lyme disease diagnosed
clinical if erythema migrans is present | ELISA antibodies to Borrelia burgdorferi
197
Management of lyme disease
doxycyline/amox (pregnancy)
198
What is a prion disease and what is the most common
A prion is a type of protein that can trigger normal proteins in the brain to fold abnormally. Creutzfeldt-Jakob disease
199
features of prion disease
rapid onset dementia and myoclonus
200
What is Whipples disease
Whipple disease is a rare bacterial infection that most often affects your joints and digestive system. Whipple disease interferes with normal digestion by impairing the breakdown of foods, and hampering your body's ability to absorb nutrients, such as fats and carbohydrates.
201
If no response in status epilepticus within 45 minutes, what is the next step?
Induction of general anaesthesia
202
2nd line for generalised tonic-clonic seizures
Lamotrigine | Carbamzepine
203
2nd line for focal seizures
levetiracetam
204
Specific types of generalised seziures
``` tonic-clonic (grand mal) tonic clonic typical absence (petit mal) atonic ```
205
Classifications of seizures
Focal Generalised Unknown onset