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Practice Exams > 26/9/21 > Flashcards

26/9/21 Flashcards

1
Q

Traditionally a TIA has been had a time-based definition, how has this changed now?

A

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.

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2
Q

What is the difference between the mild stroke and a TIA?

A

An episode is considered:

  • A mild stroke - if infarction on MRI
  • A TIA - if symptoms resolved and no infarction on MRI
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3
Q

How does the risk of stroke increase following a TIA? What is the time-frame of this?

A

Risk of Stroke - 10% at 2 weeks, half of those event occur within 48/24

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4
Q

What are the risk factors for increased risk of a subsequent stroke following a TIA? (5 points)

A
  • Age >60yo
  • Raised BP (>140/90)
  • Motor or Speech Symptoms
  • Symptoms that lasted longer than 1/24
  • Diabetes
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5
Q

How do you manage a TIA?

A

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

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6
Q

How does distal oesophageal spasm present?

A

Distal Oesophageal Spasm - can cause regurgitation and heartburn. Also a cause of non-cardiac chest pain

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7
Q

3 points of treatment of distal oesophageal spasm. (1 non-pharm, 2 pharm)

A
  • 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**
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8
Q

Name 4 Aspects of Secondary Prevention of Ischaemic Stroke and TIA

A
  1. Blood Pressure Reduction
  2. Cholesterol Lowering Therapy
  3. Managing Carotid Stenosis
  4. Antiplatelet Therapy
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9
Q

What is the BP we aim for in secondary prevention of ischaemic stroke and TIA?

A

aim for systolic BP of 120-130mmHg

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10
Q

When do we start a statin in secondary prevention of ischaemic stroke and TIA?

A

consider starting statin in all patients whose stroke or TIA is presumed to be due to atherosclerotic disease REGARDLESS of initial cholesterol concentration

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11
Q

Criteria for Carotid Endarterectomy (6 points (give me at least 4))

A
  • 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
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12
Q

Name 3 contraindications for revascularisation of carotid stenosis.

A
  1. Severe comorbidity due to other surgical or medical illness
  2. An ipsilateral stroke associated with persistent disabling neurological defecits or any stroke with severe disability that precludes preservation of useful function
  3. Total or near total occlusion of the symptomatic ipsilateral carotid artery
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13
Q

CEA or Medical Management -> Stenosis of 70-99% → if symptomatic carotid stenosis with life expectancy >5 years

A

Carotid Revascularisation

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14
Q

CEA or Medical Management -> Stenosis 50-69% in Men

A

CEA > Medical Management

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15
Q

CEA or Medical Management -> Stenosis 50-69% in Women

A

Medical Management > CEA

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16
Q

CEA or Medical Management -> Stenosis <50%

A

Medical Management > CEA

17
Q

CEA or Medical Management -> Stenosis <30%

A

CEA is HARMFUL.

18
Q

CEA or Medical Management -> For Total Occlusion of the Symptomatic Ipsilateral Internal Carotid Artery. Decision and why?

A

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.

19
Q

Initial Antiplatelet Therapy for Secondary Prevention following Ischaemic Stroke or TIA (3 options)

A
  • aspirin 100mg PO daily
  • clopidogrel 75mg PO daily
  • dipyridamole modified release + aspirin 200 + 25mg PO BD
20
Q

What is the risk reduction of stroke (1) and subsequent vascular events (2) with use of antiplatelet therapy?

A

Reduces risk of subsequent stroke by approximately 13% and all vascular events by 27%

21
Q

Discuss use of clopidogrel vs aspirin. In what circumstances is clopdogrel used?

A

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.

22
Q

Why not use clopidogrel + aspirin as antiplatelet therapy in secondary prevention?

A

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.

23
Q

What is the criteria for a migraine without aura? (3 main points) Hint: What characteristics should the headache have? What are some associated features?

A

Recurring Headache with at least 5 attacks fulfilling the following criteria:

  1. Headaches lasting 4-72 hours (treated or unsuccessfully treated
  2. Headache has at least 2 of the following 4 characteristics:
    1. Unilateral Location
    2. Pulsating Quality
    3. Moderate or Severe Pain Intensity
    4. Aggravation by or causing avoidance of routine physicla activity
  3. At least one of the following during the headaches:
    1. Nausea and/or vomiting
    2. Photophobia and phonophobia
24
Q

Name the 6 categories of groups of aura symptoms. Also give me 3 specific examples of aura symptoms.

A
  1. 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.
  2. Sensory → pins and needles spread from point of origin and affecting one side of the face or tongue. Numbness can occur in its wake
  3. Speech and/or Language → usually aphasia
  4. Motor
  5. Brainstem → dysarthria, vertigo, tinnitus, hyperacusis, diplopia, ataxia, reduced level of consciousness
  6. Retinal → fully reversible monocular positive and/or negative visual phenomena
25
Q

What are 4 characteristics that are part of the criteria for an aura? How many need to be positive for it to fit the criteria?

A
  1. At least one aura symptom spread gradually over 5 mins
  2. Each individual aura symptoms lasts 5-60mins
  3. At least one aura symptoms is unilateral
  4. Aura is accompanied by, or followed within 60 mins by a headache
26
Q

What is the first line therapy for a migraine? Give me one example.

A

Non-Opioid Analgesia -> Aspirin 900-1000mg PO → wait 4-6/24 prior to repeating dose (max 4g in 24/24)
- If response to non-opioid is sub-optimal → add anti-emetic as it can increase drug absorption

27
Q

What is 1st line therapy for an Intractable Migraine?

A

sumatriptan 6mg subcutaneously (only if a triptan has not been given in the last 2 hours and a parenteral triptan has not been trialled

28
Q

If the patient is in hospital, what options do we have for treatment of the migraine?

A
  • 12.5mg Chlorpromazine in NaCl 0.9% 100ml over 30/60 → can repeat infusion 2 times up to 37.5mg
29
Q

Prophylaxis of Tension Type Headache

A
  • amytriptilline 10mg nocte → increased dose by 10mg up ot max 75mg PO nocte for 8/52 then review
30
Q

How does Calcium Pyrophosphate Deposition occur?

A

Excessive calcium pyrophosphate → local supersaturation + subsequent crystallisation

31
Q

Even though patients are often asymptomatic, how do patients with Calcium Phosphate Deposition present? (3 points)

A
  1. Osteoarthritis with calcium pyrophosphate deposition
  2. Acute Calcium Pyrophosphate Crystal Arthritis → Pseudogout which is the most common cause of an acute monoarthritis in the older patient
    • acutely inflamed joint - most commonly wrist and knee
    • can also mimick septic arthritis as can have associated fever and leukocytosis
  3. Chronic calcium pyrophosphate crystal inflammatory arthritis
32
Q

How do you diagnose Calcium Phosphate Deposition?

A

Joint aspirate of synovial fluid to identify calcium pyrophosphate dihydrate crystals
- weakly positive birefringent CPP crystals in synovial fluid analysis

33
Q

Calcium Phosphate Deposition: Name 3 associated conditions (there are 5) and what serum screening tests need to be completed in patients diagnosed with this. (5 tests)

A
  • Haemochromatosis
  • Hyperparathyroidism
  • Hypomagnesemia
  • Hypophosphatasia
  • Familial Hypocalciuric Hypercalcemia
  • Calcium, Magnesium, Phosphate
  • Alkaline Phosphatase (ALP)
  • Ferritin → Fe Studies
34
Q

How do you treat Calcium Phosphate Deposition?

A

Nil evidence for optimal treatment of pseudogout so treat as per acute gout guidelines.

Given it is the older population that get pseudogout and therefore patients are more likely to have age related co-morbidities → intra-articular steroid injection may be the safest treatment option

35
Q

How is DMD inherited? Male vs Female? What does it affect?

A

Genetic condition > X-linked recessive pattern

Affecting muscles that leads to muscle wasting that gets worse overtime

Males > Females

36
Q

What is the diagnostic triad for DMD?

A

Diagnostic Triad → male child + gait disorder + bulky calves

37
Q

What are the situations in which to suspect DMD? (3 points)

A
  • evidence of delated motor milestones in a young child with a positive family history of DMD
  • child not walking by 16-18 months + presence of Gower’s sign, toe walking or calf walking
  • unexplained increases in transaminases (AST, ALT)
38
Q

What are other signs and symptoms assocaited with DMD? (give me 3..there are 10)

A
  • not running by age 3
  • abnormal gait
  • learning difficulties and behavioural issues
  • poor head control
  • frequent trips or falls
  • muscle pain or cramps
  • struggling to hop, climb stairs, or get up from the floor in school aged children
  • episodes of myoglobinura
  • speech and language delay
  • autism spectrum disorder
39
Q

How do you diagnose DMD?

A

If DMD is suspected → CK should be obtained → genetic analysis

Practice Exams (45 decks)

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