BB EOYS5 Flashcards

1
Q

Which type of seizure would you not give phenytoin or carbamazepine in order to prevent worsening of symptoms

Focal seizure
Absence seizure
Generalised Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

A

Which type of seizure would you not give phenytoin or carbamazepine in order to prevent worsening of symptoms

Focal seizure
Absence seizure
Generalised Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

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2
Q

Which type of seizure would you give carbamazepine or lamotrigine as first line treatment?

Focal seizure
Absence seizure
Generalised Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

A

Which type of seizure would you give carbamazepine or lamotrigine as first line treatment?

Focal seizure
Absence seizure
Generalised Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

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3
Q

Which type of seizure would you give sodium valproate as first line treatment? [2]

Focal seizure
Absence seizure
Generalised Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

A

Which type of seizure would you give sodium valproate as first line treatment?

Focal seizure
Absence seizure
Generalised Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

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4
Q

Which type of seizure would you give sodium valproate or ethosuximide as first line treatment?

Focal seizure
Absence seizure
Generalised Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

A

Which type of seizure would you give sodium valproate or ethosuximide as first line treatment?

Focal seizure
Absence seizure
Generalised Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

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5
Q

Which anti-epileptic treatment is teratogenic

Sodium Valproate
Ethosuximide
Lamotrigine
Levetiracetam
Lorazepam

A

Which anti-epileptic treatment is teratogenic

Sodium Valproate
Ethosuximide
Lamotrigine
Levetiracetam
Lorazepam

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6
Q

Which anti-epileptic treatment works by bind to synaptic vesicle protein SV2A causing a reduction in neurones

Sodium Valproate
Ethosuximide
Lamotrigine
Levetiracetam
Lorazepam

A

Which anti-epileptic treatment works by bind to synaptic vesicle protein SV2A causing a reduction in neurones

Sodium Valproate
Ethosuximide
Lamotrigine
Levetiracetam
Lorazepam

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7
Q

Which anti-epileptic treatment would be used to treat status epilepticus

Sodium Valproate
Ethosuximide
Lamotrigine
Levetiracetam
Lorazepam

A

Which anti-epileptic treatment would be used to treat status epilepticus

Sodium Valproate
Ethosuximide
Lamotrigine
Levetiracetam
Lorazepam & Diazepam

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8
Q

Xanthochromia occurs in

Subdural haemorrhage
Epidural haemorrhage
Subarachnoid haemorrhage
Intracerebral haemorrhage

A

Xanthochromia occurs in

Subdural haemorrhage
Epidural haemorrhage
Subarachnoid haemorrhage
Intracerebral haemorrhage

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9
Q

Which type of hematoma can present with blood in lumbar puncture?

Subdural haemorrhage
Epidural haemorrhage
Subarachnoid haemorrhage
Intracerebral haemorrhage

A

Which type of hematoma can present with blood in lumbar puncture?

Subdural haemorrhage
Epidural haemorrhage
Subarachnoid haemorrhage
Intracerebral haemorrhage

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10
Q

Which drug can be used as a prophylasix for cluster headaches if used at high dose

nifedipine
diltiazem
amlodipine
verapamil

A

Which drug can be used as a prophylasix for cluster headaches if used at high dose

nifedipine
diltiazem
amlodipine
verapamil

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11
Q

Which of the following is not used to classify if a headache is a migraine?

Light bothers person (a lot more than without a headache)
Lasts longer than 30mins
Headache limits ability to work or study
Feel nauseated or sick

A

Which of the following is not used to classify if a headache is a migraine?

Light bothers person (a lot more than without a headache)
Lasts longer than 30mins
Headache limits ability to work or study
Feel nauseated or sick

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12
Q

Triptans bind to which serotonin receptors? [2]

Are triptans agonists or antagonists? [1]

Learn

A

Agonists of 5-HT1B and 5-HT1D

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13
Q

Ditans bind to which serotonin receptors? [1]

Are they agonists or antagonists [1]

A

Agonists of 5-HT1F

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14
Q

Ditans are anti-migraine treatment that are agonists at which receptor:

5-HT1B
5-HT1C
5-HT1D
5-HT1E
5-HT1F

A

Ditans are anti-migraine treatment that are agonists at which receptor:

5-HT1B
5-HT1C
5-HT1D
5-HT1E
5-HT1F

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15
Q

Triptans are anti-migraine treatment that are agonists at which receptors [2]

5-HT1B
5-HT1C
5-HT1D
5-HT1E
5-HT1F

A

Triptans are anti-migraine treatment that are agonists at which receptors [2]

5-HT1B
5-HT1C
5-HT1D
5-HT1E
5-HT1F

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16
Q

Which anti-epileptics should not be used in absence seizures, as they may exacerbate these types of seizures? [2]

A

Phenytoin
Carbamazepine

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17
Q

Explain what is meant by phenytoin’s dose dependent / zero order / saturation kinetics characteristics

A

Most drugs have first order elimination (rate of elimination is proportional to the plasma concentration).

However, with phenytoin, as the dose of drug is increased, because of saturated enzymes, the rate of elimination is no longer proportional to the concentration of drug in the plasma (i.e. there is saturation & so only a finite amount can be eliminated).

When this happens, small increases in drugs can cause large increases in plasma concentration

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18
Q

Antiepileptic drugs:

Name three calcium channels that are used as anti-epileptic drugs [3]

A

Ethosuximide

Gabapentin / pregabalin (in the PBL)

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19
Q

AEDs

Which drug inhibits GABA metabolism? [1]

A

Vigabatrin

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20
Q

Status elipeticus is a medical emergency. Name two drugs used to treat this conditon [2]

A

Lorezepam (IV)
Diazepam (IV)

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21
Q

Alternatives to AEDs

Name 3 surgical procedures that could be used to treat epilepsy [3]

A

Lobe resection
Corpus callasotomy (reduces propogation of seizures from one cerebral hemisphere to the next)
Functional hemispherectomy

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22
Q

What is the MoA of Levetiracetam? [1]

A

Binds synaptic vesicle protein SV2A causing a reduction in conduction in neurones

SV2A protein is a part of secretory vesicle membranes that mediates calcium-dependent vesicular neurotransmitter release.

The binding of levetiracetam to SV2A appears to decrease the rate of vesicle release

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23
Q

Name a drug that predominately blocks Na+ channels, but also acts on Ca2+ channels and causes the presynaptic inhibition of glutamate release.

A

Lamotrigine

(hint: tri gated?)

24
Q

AEDs

Focal Seizures Treatment:

First line: [] or []
Second line: [] or []

A

First line: carbamazepine or lamotrigine
Second line: sodium valproate or levetiracetam

25
Management of tonic-clonic seizures is with: First line: [] Second line: [] or []
Management of tonic-clonic seizures is with: First line: **sodium valproate** Second line: **lamotrigine or carbamazepine**
26
Which drugs are used for absence seizures? [2]
**ethosuximide**, **sodium valproate**
27
Myoclonic seizures: First line: [1] Other options: [3]
First line: **sodium valproate** Other options: **lamotrigine, levetiracetam or topiramate**
28
Describe the MoA of sodium channel active drugs like phenytoin and carbamazepine [1]
**Stabilises Na+ channels inactivated state** to **decrease excitability**
29
Explain MoA of Sodium valproate [3]
Potentiates GABA receptor; Stops breakdown of GABA Blocks voltage gated sodium channels and T-type calcium channels
30
State the veins from blue & red arrow [2]
**Red arrow** = vein of Trolard (**superior anastomotic vein**) **Blue arrow** = vein of Labbe (**inferior anastomotic vein**)
31
What are the two leading causes of non-traumatic hemorrhagic stroke? [2]
HTN Aneursym
32
Describe MCA stroke if occurs on the: - Left - Right
**MCA Left stroke** * Global aphasia * Sensorimotor loss on contralateral face, upper limb and trunk **Right MCA Stroke:** * Neglect syndrome
33
# Split brain syndrome Describe how a patient with split brain syndrome would percieve & verbalise an object in their right visual field & their right hand Describe how a patient with split brain syndrome would percieve & verbalise an object in their left visual field & their left hand
Human anatomy; the right hemisphere receives visual input from the left visual field and controls the left hand Transfer of visual learning between the hemispheres is abolished **right visual field** the patient **responds correctly verbally and with his/her right hand.** **Left visual field** the patient verbally states that **he/she saw nothing**, and **identifies the object accurately with the left hand only**
34
Describe the effects of PCA stroke [3]
* **Contralateral homonymous hemianopsia** (a field loss deficit in the same halves of the visual field of each eye,) * **Reading and writing deficits** * **Impaired memory**
35
Why do TIAs commonly present with temporary blindness? [1]
**Opthalmic artery**
36
Which arteries are commonly affected during extradural (epidural) hematoma? [2]
**Middle meningeal Artery**(temperoparital area, pterion) **Ant. Ethmoidal A.** (frontal)
37
Which cranial nerve is commonly effected by extradural (epidural) hematoma [1] What happens to visual field? [1] What happens to feelings of extremities? [1]
CN III damaged Loss of visual field opposite to lesion (compress of PCA) Weakness of extremities on opposite side of lesion (crossed pyramid pathways)
38
What are the two types of cerebral aneurysm? [2]
Saccular (berry is a sub-type) Fusiform
39
What is Xanthochromia? Which type of hematoma does it occur in? [1]
**Xanthochromia** is the presence of **bilirubin in the cerebrospinal fluid** and is sometimes the only sign of an **acute subarachnoid hemorrhage.**
40
Which type of hematoma can present with blood in lumbar puncture? [1]
**Subarachnoid hematoma** Lumbar puncture - Evidence of blood in 3% of people with normal CT
41
Define primary and secondary headaches [2]
**Primary headaches** Diagnosis is made on the history in the **absence** of physical signs **Secondary headaches** Diagnosis is made on the history in the **presence** of physical signs
42
State the characteristics of cluster headaches: - How long do they last? [1] - When do they occur? [1] - Name an immediate trigger of cluster headaches [1]
- Typically last 15-180 mins - Seasonal: often last 6-8 weeks - Alcohol is an immediate trigger
43
Name acute [2] and prophylactic [1] treatment for cluster headaches
**Acute**: * **oxygen** (15L/min 100% through non-rebreather mask – acts as vasoconstrictor); * -**triptans** **Prophylactic** * : has to be quick. High dose of **verapamil**
44
# Primary headaches: Name the 3 questions need to ask for diagnosis of a migraine [need score of 2/3]
**Light bothers you** (a lot more than when you don’t have headache) Your headaches **limit your ability to work, study or do what you need to do?** You feel **nauseated or sick**
45
# Primary headaches: What is the difference of length of migraines between episodic and chronic migraines? [2]
**Episodic** * <15 days/month **Chronic** * Headache occurring on **≥15 or more days/month** for more than three months. At least **8 days/month** have the features of migraine headache
46
# Migraine pathophysiology Name 4 examples that can cross migraine threshold (& cause migraine)
- Lack of sleep - Lack of food - Dehydration - Hormonal trigger
47
Describe the NT that influences migraines [1] What urinary metabolite would be high in migraine attacks? [1]
**Seratonin** released (90% from gut, 10% platelets, 1-2% brain) Increase urinary metabolites **5HIAA** in attacks
48
Describe 5 symptoms of premonitory phase of migraine
Food craving Yawning Neck pain Heightened perception Fluid retention
49
What are the 5 stages of migraine? [5]
Premonitory Aura Heachache Resolution Recovery
50
Describe the pathophysiology of aura of migraine
A transient and local **suppression** (depression) …of spontaneous electrical activity in the **visual cortex** (cortical) …which moves slowly across the brain (**spreading**) (Note: **occurs rom visual cortex not the eyes**)
51
Describe the trigeminovascular pathways that causes migraine
Increase in **serotonin** causes **BV** on the **dura to vasodilate** This causes a release of **neuropeptides** This begins a cascade reaction causing further inflammation: particularly release of **CGRP**: potent vasodilator **CGRP activate the nerve pathways** & the nerves send pain signals to the **trigeminal ganglion** The trigeminal ganglion, once activated by CGRP, is what causes **peripheral sensitisation** which is responsible for the **throbbing pain in a migraine** Trigeminal ganglion transmits pain impulses to **SpV (spinal trigeminal nucleus caudalis)** **SpV** then relays to the **thalamus** and from the thalamus to the **cerebral cortex** where pain is decoded
52
Where do acute [1] and chronic [1] treatments for migraines target?
**Acute**: Acute medication given for migraine primarily acts **peripherally, at the trigeminal ganglion** Preventive medication for migraine acts more centrally (i.e. the trigeminal nucleus caudalis)
53
What drug classes are used to acutely treat migraine? [3]
**Triptans**: (**5HT1D**/B **agonists**) * Vasoconstrictive Agents **Ditans** (5HT1F agonists) * Neurally Active Anti-Migraine Agent **Gepants**: small molecule CGRP receptor antagonists
54
Describe the difference between peripheral and central sensitisation that occurs during migraine pathophysiology [2] come back x
**Peripheral sensitisation:** * Sensitization of peripheral **trigeminovascular neurons** in the **trigeminal ganglion** **mediates the throbbing pain**
55
Describe action of CGRP monoclonal antibodies (mAbs)
Prevent vasodilation
56
Describe MoA of triptans [1] Where are 3 possible sites of action? [3]
Triptans: * **5-HT1D/B agonists**. * 3 possible sites of action: 1. **cranial vasoconstriction, 2. peripheral neuronal inhibition and 3. inhibition of transmission through second order neurones of the trigeminal ganglion**.
57
What is the role of CGRP and when is it released? [1]
CGRP is a **potent vasodilator** released from the **meninges in response to increased serotonin-induced vasodilation** in the **premonition phase of a headache.**