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Year 3 TCDs > Transient Loss of Consciousness > Flashcards

Transient Loss of Consciousness Flashcards

1
Q

What is a transient loss of consciousness?

A
  • Blackouts
  • Fits, faints, funny turns
  • Spontaneous loss of consciousness with complete recovery
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2
Q

What are 3 causes of loss of consciousness?

A
  1. Cardiovascular (most common)
    - Cardiogenic
    - Vasovagal
  2. Neurological
    - Epilepsy
  3. Psychogenic
    - Pseudo-syncope
    - Non-epileptic attack disorder
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3
Q

What are the differentials for a 17y male with blackout occurring from sleep early one morning

A
  • Unlikely to be syncope (lying down)
  • Ask: any jerking/twitching movements in the morning? (early morning myoclonus)

Primary generalized epilepsy

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4
Q

What are the differentials for a 67y male while standing in church

A
  • Likely syncope
  • Ask: have you ever had any feelings of light headiness, dizziness, racing of heart, sweating while standing?

Vasovagal syncope

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5
Q

After a first seizure, how long before you can drive?

A

1 year seizure-free

DVLA must be informed about epilepsy

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6
Q

What is the most common side effect of lamotrogine (anti-convulsant)?

A

Hypersensitivity rash

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7
Q

What is pharmacodynamics?

A
  • Effect of drugs on the body
  • “How the drug works”
  • “What the drug does to the body”
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8
Q

What is pharmacokinetics?

A

What the body does to the drug

  • Describes the absorption, distribution, and elimination of the drug from the body
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9
Q

How do drugs work?

A
  1. Physical interactions
  2. Enzyme interactions
  3. Receptor interactions
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10
Q

Name examples of physical interactions of drugs?

A
  • Antacids (neutralise gastric acidity)

- Activated charcoal (absorption of poisons from GI tract)

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11
Q

What are 2 types of enzyme activity?

A
  1. Competitive inhibitor
    - Competitive inhibitor interferes with active site + prevents substrate from binding
  2. Non-competitive inhibitor
    - These change shape of enzyme so it cannot bind to substrate
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12
Q

What is an example drug of enzyme inhibition?

A

ACE inhibitors

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13
Q

What is the most important mechanism of drug action?

A

Receptor interactions

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14
Q

What is a receptor?

A

A molecule on the surface or within a cell that recognizes and binds with specific molecules (ligand)

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15
Q

What are the 3 main types of receptors classed by MOI?

A
  1. Altered ion permeability
    - Ligand-gated ion channels (i.e. Nicotinic ACh receptor)
  2. Regulation of gene-transcription
    - Require ligand to be lipid-soluble to cross the cell membrane (i.e. steroid hormones, thyroid hormones)
  3. Production of intermediate messenger
    - G-protein coupled receptors (i.e. opioid receptors, adrenoceptors, muscarinic acetylcholine receptors)
    - Most common
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16
Q

What is tachyphylaxis?

A

Rapid decrease in response to repeated doses over a short period of time

Commonest cause is decreasing stores of neurotransmitter

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17
Q

What is desensitization?

A

Chronic loss of response over a long period

Due to:

  • Structural change in receptor morphology
  • Decrease in receptor numbers
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18
Q

What is tolerance?

A

Phenomenom where larger doses are required to have the same effect

Due to:

  • Reduction in receptor density
  • Reduction in receptor affinity
  • Reduction in receptor numbers

eg. opioid tolerance

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19
Q

Where are seizures generated?

A

Cerebral cortex

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20
Q

What is important to note about phenytoin prescribing?

A

The concentration increases dramatically with only slight dosage changes

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21
Q

What is an example of a new anti-epileptic drug?

A

Lamotrigine

  • Linear dose-concentration relationship unlike exponential relationship with phenytoin
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22
Q

Why do anti-epileptic drugs need to be monitored (TDM)?

A

Serum + brain concentrations are in equilibrium

Loosely defined serum concentration range at which optimum therapeutic response is achieved.

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23
Q

When is monitoring important for AEDs?

A
  1. To guide dosing of AEDs with non-linear pharmacokinetics
    - ie. phenytoin
  2. To assess adherence
  3. Desired clinical outcome attained
    - Pharmacokinetic change anticipated (pregnancy, interacting drug added/removed)
  • Increased pharmacokinetic variability (drug formation changes)
24
Q

What are the metabolic interaction of AEDs?

A

Hepatic enzyme induction + inhibition of cytochrome P450 system

  1. Increases the amount of enzyme by increasing transcription
  2. Inhibition as there’s competition by drugs that bind to the same enzymatic site
25
Q

What are the 3 AED inhibitors?

A
  • Valproic acid
  • Felbamate
  • Oxcarbazepine

** The rest are inducers

26
Q

What are the idiosyncratic adverse effects of AEDs?

A
  • Idiosyncratic adverse effects (rare, serious):
  1. Rash (Steven Johnson Syndrome, Toxic epidermal necrolysis)
    - Lamotigine, carbamazepine, phenytoin
  2. Bone marrow suppression
    - Felbamate, carbamazepine
  3. Hepatic toxicity
    - Valproate, felbamate
27
Q

What are the more common neurotoxic side effects of AEDs?

A

Neurotoxic side effects:

  1. Dizziness
  2. Diplopia
  3. Ataxia
  4. Incoordination
  5. Drowsiness
  6. Cognitive slowing

**Usually dose dependent, and can be resolved by lowering the dose

28
Q

What are the more common metabolic side effects of AEDs?

A

Metabolic side effects:

  1. Weight gain (valproate) or weight loss (topimarate)
  2. Bone density (enzyme inducing AEDs - phenytoin)
    - think if prescribing to post-menopausal women
29
Q

What are other risks of AEDs?

A
  1. Psychiatric
    - 10% risk of mood disorders with topimarate + levetiracetam
  2. Cardiovascular risk
    - Increased risk in patient on enzyme induced AEDs (phenytoin)
  3. Seizure exacerbation
    - Wrong drug for seizure type!
  4. Reproductive effects
    - PCOS with valproate
    - Erectile dysfunction (carbamazapine, pregabalin)
    - Teratogenesis (pregnant women - carbamazepine, valproate, lamotrigine, phenytoin)
30
Q

What do you think is the probable diagnosis for a 64y old gentleman collapsing and losing consciousness while seated with mild jerking of the arms?

What would you like to do next?

A

The patient’s symptoms are not suggestive of epileptic seizures. His blackouts may be syncopal but he had little in the way of classical presyncopal symptoms making vasovagal syncope less likely. In addition all the attacks have occurred whilst sitting, rather than when standing (as is more often the case in vasovagal syncope).

Cardiogenic syncope is a definite possibility so a 12 lead ECG is the first line investigation.
- ie. due to complete heart block

31
Q

What is the most appropriate management step at this stage for someone with complete heart block?

A

Refer to cardiologist

This man has complete heart block and needs to be referred urgently to cardiology for consideration of a permanent pacemaker. His attacks are not consistent with epilepsy so he needs no further neurological investigations.

32
Q

What is the cause of vasovagal syncope?

A

Decrease in BP precipitated by prolonged standing, dehydration, emotional shock.

  • often have jerking in the limbs

Not pathological in all cases

33
Q

What is the cause of cariogenic syncope?

A
  • Arrhythmia
  • Cardiomyopathy

More serious

34
Q

What is the cause of seizure?

A

Abnormal/excessive discharge of electrical activity from the cerebral cortex

  • Provoked: alcohol withdrawal/excess, recreational drugs (cocaine, amphetamines), prescription drugs (tramadol)
  • Unprovoked: epilepsy
35
Q

What is a psychogenic non-epileptic attack?

A

NEAD (non-epileptic attack disorder)

  • Episodes caused by subconscious psychological episodes
36
Q

What are some rare causes of fits/faints/funny turns?

A
  • Migranous events
  • Vestibular disorders
  • Cerebrovascular events
  • Sleep disorders
37
Q

What should you ask in a loss of consciousness history?

A
  • Pre-syncopal symptoms (light headedness, sweating, dizzy, visual/auditory aura, deja vu)
  • During episode (incontinence, jerking, warnings, colour change, biting tongue)
  • Post-ictal (confusion, tired, unconscious)
38
Q

What motor activity is associated with vasovagal syncope?

A
  • Twitching of limbs
  • Stiffening and jerking
  • Tongue biting + incontinence can occur

Clear presyncopal symptoms (PPP) distinguish vasovagal from cardiogenic syncope:

  • pain, dehydration, emotional shock
  • Light-headed, ringing in ears, dizzy, pale
  • < 1min duration and no confusion following episode
39
Q

What is the definition of syncope?

A

Loss of consciousness caused by lack of cerebral blood supply

40
Q

Explain NEAD (psychogenic syncope)

A

Periods of unconsciousness with no abnormality on EEG, which distinguishes it from epilepsy.

  • Bilateral limb movements, no loss of consciousness, often thrusting/back arching
  • Slumping and remaining still, no abnormalities in heart rate

Tx = psychogenic therapy

41
Q

What demographic usually have absence seizures?

A
  • Occurs in children
42
Q

What is myoclonic jerks?

A
  • Generalised twitching of limbs (commonly arms) due to periods of sleep deprivation alcohol excess
  • Infrequent generalized tonic/clonic seizures
  • Needs treatment + avoid sleep deprivation/ alcohol excess
43
Q

What are the 5 categories of diagnostic errors?

A
  1. Framing
    - Piece of info is given early in history and you overvalue it
  2. Anchoring
    - Place probability of diagnosis far too near 100% certain or 0% and don’t adjust with additional data
  3. Availability
    - Making diagnoses on ease of recall of previously seen cases
  4. Representativeness
    - Ignoring how common/rare diseases are
  5. Blind Obedience
    - Over-relience on tests when we know these can be fallible
44
Q

What are the 4 first line treatments for ongoing epilepsy?

A
  1. Sodium valproate (valproic acid)
  2. Lamotrigine
  3. Carbamazepine
  4. Topimarate
45
Q

What is the initial treatment for someone presenting with an acute seizure?

A

Lorazepam

If this doesn’t work, can try phenytoin

46
Q

An 84 year old man attends his GP following a collapse the night before. He had been walking back from the toilet at 02.00am when he collapsed. He recalls feeling lightheaded when urinating and then remembers nothing until his wife was standing over him in the bathroom doorway. She described hearing him collapse to the floor and observed some brief jerks before he began to open his eyes and come round.

Choose the most likely diagnosis.

A

Micturition syncope

The feeling of lightheadedness is key here; it is a pre-syncopal symptom often felt by someone before they blackout. Other pre-syncopal symptoms include nausea, sweating and ‘closing down’ of vision. Micturition syncope is a common syndrome and is a form of vasovagal syncope. The history that details the events leading up to the blackout are key to making the diagnosis. Brief jerks of the limbs are commonly seen in syncope.

47
Q

A 24 year old woman attends her GP due to episodes noted by her new boyfriend. He describes her as seeming to stare into space and chew her lip for 1-2 minutes. She then seems confused for about 5minutes before returning to normal. The patient sometimes feels that she knows when an attack is going to happen but finds it hard to describe this feeling.

Choose the most likely diagnosis.

A

Complex partial seizures

The description given is compatible with complex partial seizures. There is a loss of awareness, but not a loss of consciousness. The chewing movements of the mouth are a form of automatism. Patients with focal onset seizures may find it very difficult to put into words the feeling they get before a seizure.

48
Q

A patient presents to A+E with a first generalized tonic clonic seizure, there is no known neurological illness and normal neurological examination. 12 lead ECG is normal, as are routine blood tests.

What is the next most appropriate management step?

A

Refer to first seizure clinic

Patients presenting to A+E with a suspected generalized tonic clonic seizure should be referred promptly to a first seizure clinic or a general neurology clinic. They should always be advised not to drive and to take a witness of the attack to their clinic appointment wherever possible. Patients having a first seizure are not usually given antiepileptic medication unless there is evidence of a condition that makes seizure recurrence very likely (Eg a tumour on brain scanning).

49
Q

A 24 year old male patient presents to A+E with recurrent generalized tonic clonic seizures. Between seizures he fails to regain full consciousness and the Emergency medicine consultant assesses him as being in status epilepticus.

Choose the most appropriate first line treatment.

A

IV lorazepam

Benzodiazepines are first line treatment for status epilepticus. Practice varies, but intravenous lorazepam is commonly used. Buccal midazolam is a good option where IV access has not been obtained.

50
Q

Which anti-epileptic drug has the most teratogenic potential in pregnancy?

A

Sodium valproate

Most antiepileptic drugs are considered to give rise to an increased risk of foetal malformations when pregnant mothers are exposed to them. However, the rates of significant problems seem much higher with sodium valproate than these other drugs. This drug is therefore avoided wherever possible in women of childbearing age.

51
Q

A 52 year old man with known advanced alcoholic liver disease is admitted to A+E with a low GCS following a witnessed generalized tonic clonic seizure at home.

Choose the most appropriate initial investigation

A

Blood glucose

In any patient presenting with altered conscious level a blood glucose is a vital initial test. In this patient hypoglycaemia could be the cause of both the seizure and the reduced GCS. Patients with advanced liver disease are at increased risk of hypoglycaemia due to faulty hepatic gluconeogenesis.

52
Q

A 92 year old woman is four days post op on the orthodaedic ward following a fractured neck of femur. She has struggled to eat and drink since her surgery and has been on IV fluid replacement. She has had two generalized tonic clonic seizures in the early hours of the morning.

Bedside blood glucose reading is 9.2.

Choose the most appropriate initial investigation

A

Serum sodium

Hyponatraemia is a common complication in the post operative period, especially amongst the elderly. Injudicious use of intravenous fluids that don’t contain enough sodium (IV dextrose, for example) can be a contributing factor. Significant hyponatraemia (or hypernatraemia) can trigger seizures, especially if the sodium level changes over a short period of time.

53
Q

What is the prevalence of epilepsy in the population?

A

Epilepsy affects between 0.5 and 1% of the population so cannot be considered a rare disease.

It is one of the conditions seen most commonly in neurology clinics and is also a frequent cause for acute admissions to hospital. Details on the National Audit of Seizures in Hospitals can be found at: www.nashstudy.org.uk

54
Q

Is it mandatory to disclose the diagnosis of epilepsy to an employer?

A

No

Disclosing a diagnosis of epilepsy to an employer can be a positive step and may allow companies to make suitable adjustments for people with epilepsy. However, it is not mandatory for an employee to do so. It is important that someone with epilepsy makes a reasoned judgment about this and if they feel their condition could put themselves or others at risk in the workplace they should tell their employer. Charities like Epilepsy Action provide helpful advice on these sorts of matters.

55
Q

Describe the pathophysiology of epileptic seizures

A

A disruption in the normal balance between excitatory and inhibitory currents or neurotransmission in the brain resulting in hypersynchronous neuronal discharge .

Hypersynchronous neuronal discharges are thought to be the pathophysiological hallmark of epileptic seizures.

Antiepileptic drugs work by altering the balance of excitatory and inhibitory neurotransmitter signals in the brain.

Year 3 TCDs (24 decks)

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