26/9/21 Flashcards
(39 cards)
Traditionally a TIA has been had a time-based definition, how has this changed now?
Traditionally, the definition of a TIA was based on time → episode of focal neurological dysfunction, with abrupt onset, that lasted less than 24/24 and had a vascular cause.
Often patients who have had a TIA will have an infarct on MRI even if the symptoms were transient and had resolved.
As a consequence of this, the definition of a TIA is based more if there is an infarction seen on the MRI rather than the time-based definition.
What is the difference between the mild stroke and a TIA?
An episode is considered:
- A mild stroke - if infarction on MRI
- A TIA - if symptoms resolved and no infarction on MRI
How does the risk of stroke increase following a TIA? What is the time-frame of this?
Risk of Stroke - 10% at 2 weeks, half of those event occur within 48/24
What are the risk factors for increased risk of a subsequent stroke following a TIA? (5 points)
- Age >60yo
- Raised BP (>140/90)
- Motor or Speech Symptoms
- Symptoms that lasted longer than 1/24
- Diabetes
How do you manage a TIA?
If NO intracranial haemorrhoage + within 48/24 of commencement of symptoms:
- aspirin 300mg PO or via NG or PR stat → reduce dose to 100mg daily on 2nd day and continue indefinitely
How does distal oesophageal spasm present?
Distal Oesophageal Spasm - can cause regurgitation and heartburn. Also a cause of non-cardiac chest pain
3 points of treatment of distal oesophageal spasm. (1 non-pharm, 2 pharm)
- Ingestion of warm water at the onset of an attack
- Sublingual Nitrates may shorten the attack:
- Glyceryl Trinitrate Spray 400 micrograms sublingually PRN**
- If frequent or disabling:
- diltiazem controlled release 180mg PO daily, increasing to 240-360mg PO daily - depending on effectiveness and adverse effects**
Name 4 Aspects of Secondary Prevention of Ischaemic Stroke and TIA
- Blood Pressure Reduction
- Cholesterol Lowering Therapy
- Managing Carotid Stenosis
- Antiplatelet Therapy
What is the BP we aim for in secondary prevention of ischaemic stroke and TIA?
aim for systolic BP of 120-130mmHg
When do we start a statin in secondary prevention of ischaemic stroke and TIA?
consider starting statin in all patients whose stroke or TIA is presumed to be due to atherosclerotic disease REGARDLESS of initial cholesterol concentration
Criteria for Carotid Endarterectomy (6 points (give me at least 4))
- Moderate or Severe Carotid Stenosis
1. Ipsilateral TIA or nondisabling ischaemic stroke as the symptomatic event
2. Surgically accessible carotid lesion
3. Life Expectancy of at least 5 years
4. No prior ipselateral carotid endarterectomy
5. No contraindications to revascularisation
Name 3 contraindications for revascularisation of carotid stenosis.
- Severe comorbidity due to other surgical or medical illness
- An ipsilateral stroke associated with persistent disabling neurological defecits or any stroke with severe disability that precludes preservation of useful function
- Total or near total occlusion of the symptomatic ipsilateral carotid artery
CEA or Medical Management -> Stenosis of 70-99% → if symptomatic carotid stenosis with life expectancy >5 years
Carotid Revascularisation
CEA or Medical Management -> Stenosis 50-69% in Men
CEA > Medical Management
CEA or Medical Management -> Stenosis 50-69% in Women
Medical Management > CEA
CEA or Medical Management -> Stenosis <50%
Medical Management > CEA
CEA or Medical Management -> Stenosis <30%
CEA is HARMFUL.
CEA or Medical Management -> For Total Occlusion of the Symptomatic Ipsilateral Internal Carotid Artery. Decision and why?
Medical Management > CEA
- Internal carotid artery occlusion at the carotid bifurcation leads to propagation of the thrombus distally into the intracranial ICA which precludes revascularisation of the vessel.
Initial Antiplatelet Therapy for Secondary Prevention following Ischaemic Stroke or TIA (3 options)
- aspirin 100mg PO daily
- clopidogrel 75mg PO daily
- dipyridamole modified release + aspirin 200 + 25mg PO BD
What is the risk reduction of stroke (1) and subsequent vascular events (2) with use of antiplatelet therapy?
Reduces risk of subsequent stroke by approximately 13% and all vascular events by 27%
Discuss use of clopidogrel vs aspirin. In what circumstances is clopdogrel used?
Clopidogrel is modestly more effective compared to aspirin in preventing serious vascular outcomes BUT the absolute risk reduction is smaller and the drug costs more.
Therefore clopidogrel is mainly used when patients cannot tolerate aspirin or have had recurrent cerebral ischaemic events while taking aspirin.
Why not use clopidogrel + aspirin as antiplatelet therapy in secondary prevention?
Clopidogrel + Aspirin → no benefit in prevention after stroke or TIA because a reduction in ischaemic events is offset by an increased risk of serious bleeding.
What is the criteria for a migraine without aura? (3 main points) Hint: What characteristics should the headache have? What are some associated features?
Recurring Headache with at least 5 attacks fulfilling the following criteria:
- Headaches lasting 4-72 hours (treated or unsuccessfully treated
- Headache has at least 2 of the following 4 characteristics:
- Unilateral Location
- Pulsating Quality
- Moderate or Severe Pain Intensity
- Aggravation by or causing avoidance of routine physicla activity
- At least one of the following during the headaches:
- Nausea and/or vomiting
- Photophobia and phonophobia
Name the 6 categories of groups of aura symptoms. Also give me 3 specific examples of aura symptoms.
- Visual → zigzag figure near the point of fixation, can spread left or right and leave an absolute or variable degree of relative scotoma in its wake.
- Sensory → pins and needles spread from point of origin and affecting one side of the face or tongue. Numbness can occur in its wake
- Speech and/or Language → usually aphasia
- Motor
- Brainstem → dysarthria, vertigo, tinnitus, hyperacusis, diplopia, ataxia, reduced level of consciousness
- Retinal → fully reversible monocular positive and/or negative visual phenomena
