Exam revision Flashcards
What is a TIA?
TIA is defined as transient neurological dysfunction caused by focal brain, spinal cord, or retinal ischaemia, without evidence of acute infarction. It is a medical emergency
What is is risk of a patient developing stroke following a TIA?
within the first week following a TIA, the risk of stroke is up to 10%. The estimated incidence of TIA within the UK is 50 per 100,000 people per year.
What is the diagnostic criteria for TIA?
Traditionally, transient neurological dysfunction with resolution within 24 hours was diagnostic of TIA. However, up to a third of patients whose symptoms have resolved within 24 hours have evidence of infarction on imaging. Consequently, the definition is now ‘tissue-based’ rather than ‘time-based’ with the incoporation of the phrase ‘without evidence of acute infarction’. Thus, the end-point is biological tissue damage, not an arbitrary time cut-off.
What is the aetiology of TIA?
TIA is caused by temporary blockage to blood flow, which leads to ischaemia.
Ischaemia refers to the absence of blood flow to an organ, which deprives it of oxygen. Cerebral ischaemia may be due to in situ thrombosis, emboli, or rarely, dissection.
Thrombosis: local blockage of a vessel due to atherosclerosis. Precipitated by cardiovascular risk factors (e.g. hypertension, smoking) or small vessel disease (e.g. vasculitis, sickle cell). Listen for bruits
Emboli: propagation of a blood clot that leads to acute obstruction and ischaemia. Typically due to atrial fibrillation or carotid artery disease. valve disease prosthetic valves
Dissection: a rare cause of cerebral ischaemia from tearing of the intimal layer of an artery (typically carotid). This leads to an intramural haematoma that compromises cerebral blood flow. May be spontaneous or secondary to trauma.
Hyperviscosity-polycythemia,sickle cell,myeloma
Vasculitis-SLE,PAN,syphilis
During a TIA, there is a transient reduction in blood flow to an area of cerebral tissue that causes neurological symptoms. TIA commonly occurs secondary to embolisation from atrial fibrillation or carotid artery disease.
What are the risk factors for TIA?
TIA is a cardiovascular disease, and as such, it shares many common risk factors with conditions such as ischaemic heart disease and peripheral vascular disease.
Smoking Diabetes mellitus Hypertension Hypercholesterolaemia Obesity Atrial fibrillation Carotid artery disease Age Thrombophilic disorders (e.g. antiphospholipid syndrome) Sickle cell disease Family history
How does TIA present?
A TIA presents with sudden, focal neurological deficit that reflects the area of the brain devoid of blood flow.
A variety of neurological deficits can present in TIA, but the majority of symptoms will resolve within 1-2 hours.
Neurological deficit
Unilateral weakness or sensory loss
Dysphasia
Ataxia, vertigo, or incoordination
Amaurosis fugax: see below
Homonymous hemianopia: visual field loss on the same side of both eyes
Cranial nerve defects: particularly if associated with contralateral sensory/motor deficits
What are the differentials for amaurosis fugax
Amaurosis fugax
This is a classical syndrome of short-lived monocular blindness, which is often described as a black curtain coming across the vision. It is a term usually reserved for transient visual loss of ischaemic origin.
The principle cause of amaurosis fugax is transient obstruction of the ophthalmic artery, which is a branch of the internal carotid artery. However, other ischaemic causes to consider include giant cell arteritis (i.e. temporal arteritis) and central retinal artery occlusion. An important differential of transient visual loss, particularly in young patients, is migraine.
How can TIA be diagnosed?
Diagnosis
Any patient with ongoing symptoms requires urgent referral to a stroke unit.
TIA is a clinical diagnosis based on the history as the majority of patients will have complete resolution of symptoms. Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit.
Key aspects to making the diagnosis of TIA include:
Onset & duration of symptoms: collateral history may be needed
Associated symptoms (suggest alternative diagnosis): headache, vomiting, syncope, seizures
Neurological deficit: see clinical features
Cardiovascular risk factors: hypertension, diabetes, smoking, high cholesterol, family history
Co-morbidities: heart disease, atrial fibrillation, carotid disease, previous stroke/TIA
Anticoagulation history
Clinical examination: cardiovascular exam including BP, neurological examination, fundoscopy
NOTE: patients on anticoagulation with new neurological deficits require urgent admission and exclusion of intracerebral bleeding
The Face Arm Speech Time Test (FAST test)
A rapid diagnostic screen to assess for features of TIA/stroke used in the community. Anyone with a positive screen should be assessed urgently at a stroke unit. The test is positive if any of the following are met:
New facial weakness
New arm weakness
New speech difficulty
What are the differentials for TIA and
Numerous conditions can present similarly to TIA, which are collectively referred to as ‘stroke mimics’.
Toxic/metabolic: hypoglycaemia, drug and alcohol consumption
Neurological: seizure, migraine, Bell’s palsy
Space occupying lesion: tumour, haematoma
Infection: meningitis/encephalitis, systemic infection with ‘decompensation’ of old stroke
Syncope: extremely uncommon presentation of TIA, consider causes of syncope
When would you refer patient with TIA?
All patients with a suspected TIA should be referred to a specialist TIA clinic and be seen within 24 hours.
At the TIA clinic, patients should have a comprehensive medical assessment including blood tests, electrocardiogram (ECG) and imaging. If the episode occurred > 1 week ago, the assessment should be within 7 days.
The ABCD2 is a prognostic score that was traditionally used to identify people at high risk of stroke after a TIA score. It was originally used to triage the urgency of TIA referrals and treatment with aspirin. NICE no longer recommend its use.
What investigations are done for TIA?
Investigations
MRI is the key investigation in a patient with suspected TIA.
Bloods
Haematology: full blood count (FBC), HbA1c +/- haemoglobin electrophoresis
Routine biochemistry: Urea & electrolytes (U&Es), bone profile, liver function tests (LFTs), lipid profile
Coagulation: routine clotting
Special (as indicated): ‘young stroke screen’ (e.g. thrombophilia screen, Fabry’s)
Cardiac investigations
ECG: assessment for arrhythmias, especially atrial fibrillation
Echo: not routinely offered unless suspicion of heart disease or confirmed stroke
Imaging
MRI head with diffusion-weighted imaging (DWI): preferred to CT unless alternative diagnosis suspected that CT could detect. Enables detection of small infarcts.
Carotid dopplers: all patients who are candidates for carotid endarterectomy.
When is urgent admission warranted?
Certain features warrant urgent admission to hospital because of the high risk of stroke, bleeding or deterioration.
≥1 suspected TIA (crescendo TIA): typically within the last 7 days
Suspected cardioembolic source or severe carotid stenosis
Vulnerable patient: lack of reliable observer at home to monitor for worsening symptoms
Bleeding disorder or taking an anticoagulant
Any patient with ongoing symptoms needs to be treated as an acute stroke and urgently referred to a stroke unit.
ABCD2 SCORE 4 HIGH RISK,greater than 6 very high risk
How can TIA be managed?
Management
Any patient with a suspected TIA should be treated with 300 mg of aspirin unless contraindicated.
The management of TIA can be divided into acute treatment, secondary prevention and lifestyle measures.
Acute treatment
The principle management for TIA is 300 mg of aspirin that is usually continued for two weeks. This is followed by treatment with 75 mg of clopidogrel as long-term vascular prevention.
Patients with atrial fibrillation or significant carotid artery disease require a different treatment pathway.
Atrial fibrillation (AF): should be offered and counselled about starting an oral anticoagulant
Carotid artery disease (CAD): urgent referral for consideration of carotid endarterectomy if significant disease. Based on NASCET or ECST criteria for stenosis.
NASCET: 50-99% stenosis
ECST: 70-99% stenosis
Secondary prevention
Patients with a TIA should be offered secondary prevention treatments to optimise their cardiovascular risk
Anti-hypertensives: as per hypertension guidelines (tolerate higher if significant bilateral CAD)
Lipid modification: offer high-dose statin therapy unless contraindication.
Diabetic control: treat any new diagnosis of diabetes and optimise control of pre-existing disease
Obstructive sleep apnoea: referral to specialist sleep medicine/respiratory clinic if suspected
Pre-menopause: use of combined oral contraceptive pill contraindicated.
Lifestyle measures
Basic advice on physical activity, smoking cessation, diet optimisation and alcohol intake should be given to all patients
What is recommended for driving with TIA?
Driving
It is vital to advise all patients to stop driving if they have had a suspected, or confirmed, TIA.
Patients should always be advised to check the DVLA for the most up to date recommendations on driving.
Cars and motorcycles: stop driving one month, do not need to inform DVLA Larger vehicles (e.g. buses, lorries): stop driving, inform the DVLA
When should aspirin not be given?
Immediate antithrombotic therapy:
give 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
When should carotid endarterectomy be done in TIA?
With regards to carotid artery endarterectomy:
recommend if patient has suffered stroke or TIA in the carotid territory and are not severely disabled
should only be considered if carotid stenosis > 70% according ECST* criteria or > 50% according to NASCET** criteria
within 2 weeks
What is aspirin is contraindicated?
aspirin 75mg od with dipyridamole
What are the most common sites of crescendo attacks?
critical intracranial stenosis-superior division of MCA
What are the stroke mimics?
Differential diagnosis
M8S:
Migraine
Sugar: hypoglycaemia.
Seizures, especially Todd’s palsy.
Sepsis, encephalitis.
Syncope
SDH
Space occupying lesion.
OldStrokes with intercurrent illness.
Somatisation
Where is asbestos found?and how can it affect the lung?
Asbestos widely used to construct ceiling, walls and flooring of houses/ buildings
Provide insulation and fire protection
Latency period
Several years before pleural thickening develops
>20 years for fibrosis & plaque
Asbestos is a fibre-like material that was once used in buildings for insulation, flooring and roofing. Its use has been fully banned in the UK since 1999.
While asbestos can be dangerous, it’s not harmful if left alone. But if material containing asbestos is damaged, it can release a fine dust that contains asbestos fibres.
When the dust is breathed in, the asbestos fibres enter the lungs and can gradually damage them over time.
What are the different lung presentations of asbestos?
Asbestos can cause a variety of lung disease from benign pleural plaques to mesothelioma.
Pleural plaques
Pleural plaques are benign and do not undergo malignant change. They, therefore don’t require any follow-up. They are the most common form of asbestos-related lung disease and generally occur after a latent period of 20-40 years.
Pleural thickening
Asbestos exposure may cause diffuse pleural thickening in a similar pattern to that seen following an empyema or haemothorax. The underlying pathophysiology is not fully understood.
Asbestosis
The severity of asbestosis is related to the length of exposure. This is in contrast to mesothelioma where even very limited exposure can cause disease. The latent period is typically 15-30 years. Asbestosis typically causes lower lobe fibrosis. As with other forms of lung fibrosis the most common symptoms are shortness-of-breath and reduced exercise tolerance.
Mesothelioma
Mesothelioma is a malignant disease of the pleura. Crocidolite (blue) asbestos is the most dangerous form.
Possible features
progressive shortness-of-breath
chest pain
pleural effusion
Patients are usually offered palliative chemotherapy and there is also a limited role for surgery and radiotherapy. Unfortunately the prognosis is very poor, with a median survival from diagnosis of 8-14 months.
Lung cancer
Asbestos exposure is a risk factor for lung cancer and also has a synergistic effect with cigarette smoke.
What is asbestosis?
Asbestosis is a diffuse interstitial lung fibrosis that manifests in patients with pleural plaque disease ≥10 years following exposure to asbestos.
What are the CXR findings for asbestosis?
Takes >10 years for radiographic changes to develop
Small, irregular, oval opacities
Diffuse interstitial fibrosis
“Shaggy heart border” sign
Cardiac silhouette ill-defined on chest radiograph
Implies pleural disease on mediastinal interface
How can asbestosis be diagnosed?symptoms,signs,examination and investigation findings?
History of asbestos exposure, typically 20 or more years prior
Symptoms: dyspnoea, cough
Signs: crepitations on auscultation, finger clubbing, cyanosis, reduced chest expansion
Chest x-ray: linear interstitial fibrosis, pleural plaques, pleural thickening, atelectasis
Pulmonary function tests: may be normal or show a restrictive pattern (reduced forced vital capacity (FVC) and total lung capacity (TLC) with a normal FEV1/FVC ratio) or obstructive pattern (reduced FEV1).
High resolution CT: pleural thickening, pleural plaques
Bronchoscopy + biopsy: limited use as normally cannot sample enough tissue for a diagnosis
Open lung biopsy: for definitive diagnosis if cancer is suspected