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BB2 > BB2 Revision5 > Flashcards

BB2 Revision5 Flashcards

1
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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2
Q

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

A

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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3
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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4
Q

Antiepileptic drugs:

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

A

Ethosuximide

Gabapentin / pregabalin (in the PBL)

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5
Q

AEDs

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

State clonazepams MoA [1]

A

Benzodiazepines - GABA(A) receptor

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

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6
Q

AEDs

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

What is MoA? [1]

A

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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7
Q

AEDs

Which drug inhibits GABA metabolism? [1]

A

Vigabatrin

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8
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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9
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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10
Q

Alternatives to AEDs

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

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

A

Keto diet

Cannabidiol

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11
Q

Which of the following type of channel does pregabalin target?

Ca2+
GABA
Na+
Glutamate

A

Which of the following type of channel does pregabalin target?

Ca2+
GABA
Na+
Glutamate

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12
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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13
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?)

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14
Q

AEDs

Focal Seizures Treatment:

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

A

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

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15
Q

Management of tonic-clonic seizures is with:

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

A

Management of tonic-clonic seizures is with:

First line: sodium valproate
Second line: lamotrigine or carbamazepine

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16
Q

Which drugs are used for absence seizures? [2]

A

ethosuximide, sodium valproate

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17
Q

Myoclonic seizures:

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

A

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

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18
Q

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

A

Stabilises Na+ channels inactivated state to decrease excitability

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19
Q

Explain MoA of Sodium valproate [3]

A

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

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20
Q

State the veins from blue & red arrow [2]

A

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

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21
Q

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

A

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

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22
Q

Name the leading causes of hemorrhagic stroke [5]

A

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

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23
Q

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

A

HTN
Aneursym

24
Q

Describe MCA stroke if occurs on the:

  • Left
  • Right
A

MCA Left stroke
* Global aphasia
* Sensorimotor loss on contralateral face, upper limb and trunk

Right MCA Stroke:
* Neglect syndrome

25
Q

Which artery is effected here? [1]

A

Lenticulostriate

26
Q

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

A

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

27
Q

Describe the effects of PCA stroke [3]

A
  • Contralateral homonymous hemianopsia (a field loss deficit in the same halves of the visual field of each eye,)
  • Reading and writing deficits
  • Impaired memory
28
Q

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

A

Opthalmic artery

29
Q

Which type of intra-axial bleed causes the most mortality? [1]

Which type of veins are commonly ruptered to cause this? [1]

A

Subdural hematoma - due to bridging veins rupturing

30
Q

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

A

Middle meningeal Artery(temperoparital area, pterion)

Ant. Ethmoidal A. (frontal)

31
Q

Which cranial nerve is commonly effected by extradural (epidural) hematoma [1]

What happens to visual field? [1]

What happens to feelings of extremities? [1]

A

CN III damaged

Loss of visual field opposite to lesion (compress of PCA)

Weakness of extremities on opposite side of lesion (crossed pyramid pathways)

32
Q

Describe the onset of SAH [1]

Describe pain experienced in SAH [1]

A

Rapid onset: thunderclap headache

33
Q

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

A

Saccular (berry is a sub-type)
Fusiform

34
Q

Which artery supplies the midbrain & thalamus? [1]

A

PCA

35
Q

What is Xanthochromia?

Which type of hematoma does it occur in? [1]

A

Xanthochromia is the presence of bilirubin in the cerebrospinal fluid and is sometimes the only sign of an acute subarachnoid hemorrhage.

36
Q

Which type of hematoma can present with blood in lumbar puncture? [1]

A

Subarachnoid hematoma
Lumbar puncture - Evidence of blood in 3% of people with normal CT

37
Q

Label A-C

A

A: ICH
B: SDH
C: SAH

38
Q

Which the following is SAH and which is ICH?

A

L: SAH
R: ICH

39
Q

Define primary and secondary headaches [2]

A

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

40
Q

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]
A
  • Typically last 15-180 mins
  • Seasonal: often last 6-8 weeks
  • Alcohol is an immediate trigger
41
Q

Define cluster headaches

A

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

42
Q

Name acute [2] and prophylactic [1] treatment for cluster headaches

A

Acute:
* oxygen (15L/min 100% through non-rebreather mask – acts as vasoconstrictor);
* -triptans

Prophylactic
* : has to be quick. High dose of verapamil

43
Q

Primary headaches:

Name the 3 questions need to ask for diagnosis of a migraine [need score of 2/3]

A

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

44
Q

Primary headaches:

What is the difference of length of migraines between episodic and chronic migraines? [2]

A

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

45
Q

Migraine pathophysiology

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

A
  • Lack of sleep
  • Lack of food
  • Dehydration
  • Hormonal trigger
46
Q

Describe the NT that influences migraines [1]

What urinary metabolite would be high in migraine attacks? [1]

A

Seratonin released (90% from gut, 10% platelets, 1-2% brain)

Increase urinary metabolites 5HIAA in attacks

47
Q

Describe 5 symptoms of premonitory phase of migraine

A

Food craving
Yawning
Neck pain
Heightened perception
Fluid retention

48
Q

What are the 5 stages of migraine? [5]

A

Premonitory
Aura
Heachache
Resolution
Recovery

49
Q

Describe the pathophysiology of aura of migraine

A

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)

50
Q

Describe the trigeminovascular pathways that causes migraine

A

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

51
Q

Where do acute [1] and chronic [1] treatments for migraines target?

A

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)

52
Q

What drug classes are used to acutely treat migraine? [3]

A

Triptans: (5HT1D/B agonists)
* Vasoconstrictive Agents

Ditans (5HT1F agonists)
* Neurally Active Anti-Migraine Agent

Gepants: small molecule CGRP receptor antagonists

53
Q

Describe the difference between peripheral and central sensitisation that occurs during migraine pathophysiology [2]

come back x

A

Peripheral sensitisation:
* Sensitization of peripheral trigeminovascular neurons in the trigeminal ganglion mediates the throbbing pain

54
Q

Name first line treatment for migraine? [1]

A

Sumatriptan

55
Q

Describe action of CGRP monoclonal antibodies (mAbs)

A

Prevent vasodilation

56
Q

Describe MoA of triptans [1]
Where are 3 possible sites of action? [3]

A

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
Q

What is the role of CGRP and when is it released? [1]

A

CGRP is a potent vasodilator released from the meninges in response to increased serotonin-induced vasodilation in the premonition phase of a headache.

BB2 (65 decks)

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