BB2 Revision5 Flashcards by patrick ellis

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

Phenytoin
Carbamazepine

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Explain the DDI effect that phenytoin and carbamazepine have on other drugs [3]

Phenytoin and carbamazepine:
* both induce metabolizing liver enzymes.
* These liver enzymes are involved of transformation of many drugs / increased metabolism
* which may result in the loss of efficacy of other drugs (other drugs may need an increase in dose as a response)

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

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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Antiepileptic drugs:

Name two calcium channels that are used as anti-epileptic drugs [2]

Ethosuximide

Gabapentin / pregabalin (in the PBL)

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AEDs

What type of drug class does clonazepam belong to? [1]

State clonazepams MoA [1]

Benzodiazepines - GABA(A) receptor

positive allosteric modulators: enhance the frequency of GABA channel opening. (more GABA; causes more inhibition)

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AEDs

What type of drug class does phenobarbitone and stiripentol belong to? [1]

What is MoA? [1]

phenobarbitone and stiripentol:

Drug class: Barbiturates: GABAA receptor positive allosteric modulators
. Phenobarbitone (leads to microsomal enzyme induction)
Enhances the duration of GABA channel opening. (more GABA; causes more inhibition

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AEDs

Which drug inhibits GABA metabolism? [1]

Vigabatrin

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

Lorezepam (IV)
Diazepam (IV)

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Alternatives to AEDs

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

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

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Alternatives to AEDs

Name a type of diet that could help epilepsy [1]

Name a drug class for a potential new AED [1]

Keto diet

Cannabidiol

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Which of the following type of channel does pregabalin target?

Ca2+
GABA
Na+
Glutamate

Which of the following type of channel does pregabalin target?

Ca2+
GABA
Na+
Glutamate

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What is the MoA of Levetiracetam? [1]

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

Lamotrigine

(hint: tri gated?)

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AEDs

Focal Seizures Treatment:

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

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

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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

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Which drugs are used for absence seizures? [2]

ethosuximide, sodium valproate

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Myoclonic seizures:

First line: [1]
Other options: [3]

First line: sodium valproate
Other options: lamotrigine, levetiracetam or topiramate

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Describe the MoA of sodium channel active drugs like phenytoin and carbamazepine [1]

Stabilises Na+ channels inactivated state to decrease excitability

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Explain MoA of Sodium valproate [3]

Potentiates GABA receptor;
Stops breakdown of GABA
Blocks voltage gated sodium channels and T-type calcium channels

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State the veins from blue & red arrow [2]

Red arrow = vein of Trolard (superior anastomotic vein)
Blue arrow = vein of Labbe (inferior anastomotic vein)

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What are the two types of strokes [2] & their causes [2]

Ischaemic (thrombotic; embolic): 80%
Haemorrhagic stroke (trauma; spontaneous): 20%

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Name the leading causes of hemorrhagic stroke [5]

Major causes of hemorrhagic stroke
* Hypertension
* Aneurysm
* Elderly
* Head injury (trauma)
* Alcoholics
* Arteriovenous malformation

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What are the two leading causes of non-traumatic hemorrhagic stroke? [2]

HTN
Aneursym

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

Which artery is effected here? [1]

Lenticulostriate

# 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**

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**

Why do TIAs commonly present with temporary blindness? [1]

**Opthalmic artery**

Which type of intra-axial bleed causes the most mortality? [1] Which type of veins are commonly ruptered to cause this? [1]

**Subdural hematoma** - due to bridging veins rupturing

Which arteries are commonly affected during extradural (epidural) hematoma? [2]

**Middle meningeal Artery**(temperoparital area, pterion) **Ant. Ethmoidal A.** (frontal)

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)

Describe the onset of SAH [1] Describe pain experienced in SAH [1]

**Rapid** onset: **thunderclap headache**

What are the two types of cerebral aneurysm? [2]

Saccular (berry is a sub-type) Fusiform

Which artery supplies the midbrain & thalamus? [1]

PCA

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.**

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

Label A-C

A: ICH B: SDH C: SAH

Which the following is SAH and which is ICH?

L: SAH R: ICH

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

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

Define cluster headaches

a neurological disorder characterized by recurrent severe headaches on one side of the head, typically around the eye(s).

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**

# 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**

# 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

# Migraine pathophysiology Name 4 examples that can cross migraine threshold (& cause migraine)

- Lack of sleep - Lack of food - Dehydration - Hormonal trigger

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

Describe 5 symptoms of premonitory phase of migraine

Food craving Yawning Neck pain Heightened perception Fluid retention

What are the 5 stages of migraine? [5]

Premonitory Aura Heachache Resolution Recovery

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**)

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

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)

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

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**

Name first line treatment for migraine? [1]

Sumatriptan

Describe action of CGRP monoclonal antibodies (mAbs)

Prevent vasodilation

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**.

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.**